LIBRARY 

OF  THE 

University  of  Illinois. 

CLASS.  BOOK.  VOLUME). 


Accession  No. 


✓ 


- 


tf  ^ ' 


LIBRARY 

OF  THE 

UNIVERSITY  af  ILLINOIS. 


Small  capillary 
vein  in  the  inter- 
glandular  con- 
nective tissue, 
between  first  and 
second  gland 
tubule. 


Capillary. 


Small  vein 'aris- 
ing from  muscu- 
laris  mucosae 
in  center  of  the 
drawing. 


Longitudinal  and 
cross-section  of 
the  museularis 


Mucoid  degener- 
ation of  free 
ends  of  cylindri- 
cal epithelium. 


Cylindrical  epi- 
thelium of  the 
gastric  surface. 


Vestibule 

(Vorraum.) 


Exit  of  gland 
duct. 


The  darker 
stained  are  the 
parietal,  border 
or  oxyntic  cells,* 
showing  commu- 
nication with  the 
central  gland 
duct.  The  lighter 
are  the  central, 
chief  or  ferment 
cells. 


Break  in  contin- 
uity of  central 
duct,  due  to  curv- 
ing away  of  the 
gland  tubule  =, 
from  the  plane 
of  .section. 


Between  the 
longitudinal  tu- 
bules 2 cross  and 
2 tangent  sec- 
tions of  peptic 


Fibres  of  the 
museularis  mu- 
cosae embracing 
base  of  the  peptic 
gland. 


HEMMETER  DEI/. 


Hoen  & Co.,  Lith. 


VERTICAL  SECTION  THROUGH  NORMAL  HUMAN 


GASTRIC  MUCOSA. 


DISEASES 

OF  THE 

STOMACH 


THEIR  SPECIAL  PATHOLOGY,  DIAGNOSIS,  AND  TREATMENT, 
WITH  SECTIONS  ON  ANATOMY,  PHYSIOLOGY,  CHEMI- 
CAL AND  MICROSCOPICAL  EXAMINATION  OF 
STOMACH  CONTENTS,  DIETETICS,  SUR- 
GERY OF  THE  STOMACH,  ETC. 


BY 

JOHN  C.  HEMMETER,  M.D.,  Philos.D. 

PROFESSOR  IN  THE  MEDICAL  DEPARTMENT  OF  THE  UNIVERSITY  OF  MARYLAND,  BALTIMORE;  CONSULTANT 
TO  THE  UNIVERSITY  HOSPITAL,  AND  DIRECTOR  OF  THE  CLINICAL  LABORATORY,  ETC. 


WITH  MANY  ORIGINAL  ILLUSTRATIONS 

A NUMBER  OF  WHICH  ARE  IN  COLORS 

AND  A LITHOGRAPH  FRONTISPIECE 


Seconfc  jEnlaroefr  anfc  IRevtsefc  BMtion 

WITH  NEW  CHAPTERS  AND  ADDITIONAL  ILLUSTRATIONS 


PHILADELPHIA 

P.  BLAKISTON’S  SON  & CO. 

IOI2  WALNUT  STREET 
1900 


Copyright,  1900,  by  P.  Blakiston’s  Son  & Co. 


PRESS  OF  WM.  F.  FELL  & CO., 
1220-24  Sansom  Street, 

PHILADELPHIA. 


o o '$ 


k>  llo,  33 
H 3 7 d 2- 


REMOTE  STORAGE 


THE  BELLY  AND  THE  MEMBERS 

The  members  of  the  body  rebelled  against  the  Belly,  and 
said,  “Why  should  we  be  perpetually  engaged  in  administer- 
ing to  your  wants,  while  you  do  nothing  but  take  your  rest 
and  enjoy  yourself  in  luxury  and  self-indulgence?”  The 
members  carried  out  their  resolve,  and-  refused  their  assistance 
to  the  Belly.  The  whole  body  quickly  became  debilitated, 
and  the  hands,  feet,  mouth,  and  eyes,  when  too  late,  repented 
of  their  folly. — AUsop. 


tJ 

cn 

X 

-x 


mo?. 


TO 

PROFESSOR  WILLIAM  OSLER,  M.D., 

OF  BALTIMORE 

(II  maestro  di  color  che  sanno. — Dante), 

THIS  VOLUME  IS  RESPECTFULLY 


DEDICATED.  * 


PREFACE  TO  SECOND  EDITION. 


The  exhaustion  of  the  first  edition  of  this  book  made  a call  for  a 
revision  necessary  in  a little  over  one  year  from  the  date  of  its  pub- 
lication. Owing,  however,  to  serious  illness  in  the  author’s  im- 
mediate family,  it  was  impossible  to  comply  promptly  with  the 
request  of  the  publishers.  The  whole  book  has  been  gone  over 
critically  four  times  by  the  author  and  his  associate,  Dr.  Harry 
Adler,  and  there  are  probably  not  fifty  pages  in  which  some  im- 
portant insertion  or  alteration  has  not  been  made.  About  two- 
thirds  of  the  book  has  been  actually  reconstructed,  and  a large 
amount  of  new  material  added,  of  which  the  following  articles  are 
the  most  important:  Hypertrophic  Stenosis  of  the  Pylorus, 

Obstruction  of  the  Orifices,  The  Use  and  Abuse  of  Rest  and  Exer- 
cise in  the  Treatment  of  Digestive  Diseases,  part  of  the  chapter  on 
Motor  Insufficiency,  Electrodiaphany,  Hemorrhage  from  Stomach, 
and  the  articles  on  Gastroptosis  and  Enteroptosis  have  been  en- 
tirely rewritten. 

New  illustrations  and  plates,  being  the  work  of  Mr.  Louis 
Schmidt  and  Mr.  Herman  Becker,  have  been  inserted  on  the  fol- 
lowing subjects:  Hypertrophic  Stenosis  of  the  Pylorus  from 

Chronic  Stenosing  Gastritis  ; Actual  Size  and  Configuration  of  the 
Stomach  in  a State  of  Hyperplastic  Stenosing  Gastritis  ; Malforma- 
tion and  Distortion  of  Thorax  and  Stomach  Caused  by  Lacing, 
Tight  Clothing,  etc. ; Adhesions  Causing  Motor  Insufficiency ; 
Gastric  Distention  by  C02,  Showing  the  Stomach  in  a State  of 
Gastroptosis  ; Connective-tissue  Hyperplasia  Separating  Remnants 
of  Peptic  Glands;  Detachment  of  Secretory  Cells;  Mechanism 
Effecting  Vertical  Position  of  the  Stomach. 

A text-book  that  undergoes  subsequent  editions  is  the  product 
of  the  evolution  of  thought,  not  only  of  its  author,  but  of  that  part 
of  the  medical  profession  which  is  active  in  its  special  domain. 
While  the  book  bears  the  impress  of  the  author’s  individuality,  it 

vii 


Vlll 


PREFACE  TO  SECOND  EDITION. 


should,  if  possible,  be  an  exponent  of  the  total  practical  knowledge 
that  has  been  gained.  As  Riegel  says, 

“ The  final  object  of  all  medical  activity  is  to  help  and  to  heal.  The  practitioner  has 
the  right  to  estimate  the  progress  in  any  domain  of  medicine  by  the  gain  that  has  accrued 
to  the  healing  art.” 

In  the  author’s  opinion  the  most  useful  feature  of  this  second 
edition  is  the  repeated  and  thorough  application  of  mature  and 
critical  judgment  to  the  entire  subject-matter  of  the  book.  It  is 
not  intended  that  this  should  be  a scientific  work  in  the  technical 
sense  of  the  term,  the  question  that  weighed  most  heavily  upon  the 
author’s  conscience  being,  “ How  much  can  I aid  the  practitioner 
in  his  efforts  toward  helping  and  healing  others?” 

I am  indebted  to  the  distinguished  American  clinician,  to  whom 
this  book  is  dedicated,  Professor  William  Osier,  for  much  cordial 
encouragement  and  many  useful  suggestions,  given  both  person- 
ally and  by  correspondence.  To  my  associate,  Dr.  Harry  Adler, 
I wish  to  express  thanks  for  the  unceasing  vigilance  which  he 
exercised  in  the  proof-reading  and  for  the  application  of  conserva- 
tive critical  judgment  throughout  the  entire  book,  and  especially  to 
the  paragraphs  on  Clinical  Pathology.  To  Dr.  F.  P.  Mall  for 
advice  relating  to  chapter  on  the  Anatomy  of  the  Digestive 
Organs.  To  Dr.  Edward  L.  Whitney  I am  indebted  for  rewriting 
the  chemical  section  of  Part  I.  To  Dr.  Henry  W.  Nolte  (now  of 
Newark,  N.  J.)  and  Mr.  Thomas  H.  Cannon  for  arranging  the  index 
of  subjects  and  index  of  authors.  To  the  medical  faculty  of  the 
University  of  Maryland  I am  indebted  for  the  unrestricted  use  of 
the  clinical  and  pathological  material  of  the  University  Hospital 
and  their  generous  support  of  the  clinical  laboratory,  in  which 
much  of  the  newer  material  was  clinically  and  experimentally 
tested. 

The  almost  daily  association  with  clinicians  of  experience  and 
ability  gives  a feeling  of  enthusiasm,  which  is  a powerful  auxiliary 
to  an  author,  and  marvelously  diminishes  his  toil ; in  the  language 
of  Ovid — 

“ Scribentem  juvat  ipse  favor,  minuitque  laborem  ; 

Cumque  suo  crescens  pectora  fervet  opus.” 

The  Author. 

Baltimore,  March.,  igoo. 


PREFACE  TO  FIRST  EDITION. 


The  tendency  of  modern  science — not  only  of  medical  science — 
is  toward  specialization. 

Diseases  of  the  stomach  alone  is  not  a field  sufficiently  large  to 
constitute  a genuine  specialty.  It  is  generally  associated  with  the 
study  of  the  diseases  of  all  digestive  organs,  particularly  of  the 
intestines,  liver,  and  pancreas.  The  diseases  of  metabolism  consti- 
tute a legitimate  field  naturally  falling  into  the  domain  of  the 
digestive  clinical  pathologist. 

In  an  address  before  the  Medical  and  Chirurgical  State  Faculty 
of  Maryland  in  April,  1896,  Professor  Da  Costa,  in  speaking  of  the 
manner  in  which  medical  libraries  build  up  and  increase,  said  that 
“ books  attract  books,  and,  as  a rule,  any  new  work  in  any  par- 
ticular class  has  a striking  family  resemblance  to  those  already 
published.” 

If  this  new  contribution  to  the  pathology  and  treatment  of 
organic  diseases  of  the  stomach  does  not  conform  to  Da  Costa’s 
generalization,  it  is  not  because  of  any  premeditated  plan  to  make 
it  different  from  other  works  on  the  same  subject,  but  because  a 
number  of  entirely  new  methods  of  diagnosis  have  entered  into  it, 
and  because  an  attempt  has  been  made  to  do  justice  to  the  work  of 
American  clinicians  in  this  special  department.  My  chief  effort 
has  been  to  furnish  the  general  practitioner  with  a work  from 
which  he  can  readily  acquaint  himself  with  all  that  has  been  done 
in  this  important  branch  of  medicine,  to  fit  himself  to  make  exam- 
inations, to  take  advantage  of  new  methods  of  diagnosis,  and  to  treat 
this  very  difficult  class  of  diseases  rationally  and  successfully. 

With  this  end  in  view  I have  endeavored  to  treat  the  subject 
systematically  and  concisely,  giving  first  the  special  anatomy  and 
physiology  of  the  digestive  organs,  methods  of  diagnosis  and 
general  therapy,  including  dietetics,  following  this  by  a methodical 
discussion  of  the  various  diseases  affecting  the  stomach,  with  their 
symptomatology,  diagnosis,  prognosis,  pathology,  and  treatment. 

ix 


X 


PREFACE  TO  FIRST  EDITION. 


The  illustrations,  of  which  many  are  from  original  drawings,  have 
been  selected  because  of  their  practical  bearing  upon  the  matter  in 
hand. 

Aside  from  the  fact  that  the  pathology,  diagnosis,  and  therapy 
of  diseases  of  the  human  organs  have  become  so  extensive  that  it 
is  absolutely  impossible  for  one  mind  to  master  them  all,  genuine 
advances  in  any  particular  department  have  hitherto  been  made 
only  by  such  scholars  as  could  concentrate  and  focus  their  mental 
energy  upon  a limited  subject. 

Experience  of  the  last  twenty-five  years  has  demonstrated  that 
the  general,  fundamental  stock  of  medical  knowledge  has  not  been 
injured,  but,  on  the  contrary,  it  has  been  wonderfully  enlarged  and 
strengthened  by  the  progress  in  strictly  special  fields  of  work. 

To  read  the  history  of  the  development  of  medical  sciences,  the 
frequently  astonishing  results  and  indefatigable  perseverance  of 
“ the  grand  old  men  of  medicine,”  is  not  only  a healthy  training 
for  prospective  investigators,  but  can  not  fail  to  polish  down  the 
pride  of  the  overambitious. 

Speaking  purely  from  a therapeutic  standpoint,  however,  our 
medical  ancestors  of  the  beginning  of  this  century  were  for  the 
greater  part  divided  into  two  extreme  classes  : First,  the  poly- 
pharmacists ; second,  the  skeptics,  the  therapeutic  nihilists.  It  is 
largely  the  credit  of  the  specialties  that  Asclepiads  have  evolved 
from  this  confused  opposition.  It  was  an  unspeakable  comfort  to 
be  reassured  by  Virchow  and  others  that,  after  all,  the  end  object, 
the  fundamental  purpose,  of  all  medical  progress  must  be  the  relief 
of  suffering  and  the  cure  of  disease,  not  simply  the  development 
of  abstract  science.  A further  step  in  the  evolution  of  therapy 
was  the  realization  that  the  object  of  medical  study  and  treatment 
must  not  be  the  “ disease,”  but  the  diseased  patient.  Specialties 
can  not  make  the  adept  one-sided,  nor  obscure  his  view  of  the 
general  body  of  medical  knowledge;  on  the  contrary,  the  detailed 
development  of  the  intellect  which  results  from  concentration  of 
energy  upon  one  subject  will  enlarge  his  powers  of  observation 
and  analysis  and  insure  a more  comprehensive  understanding  of 
the  totality  of  general  medicine.  Boerhaave  could  claim  to  be 
master  of  all  applied  medical  branches;  Langenbeck  and  Frerichs 
were  credited  with  absolute  mastership  in  three  or  four  hetero- 
geneous branches  of  medicine.  Medicine  has  been  enormously 
developed  since  those  days.  Who  will  claim  such  mastery  at 
the  present  time?  Bach,  Mozart,  and  Haydn  were  acknowledged 


PREFACE  TO  FIRST  EDITION. 


XI 


virtuosi  on  five  or  six  instruments.  Where  is  such  a phenomenal 
genius  of  the  present  day  in  music  ? The  enlargement  of  any 
branch  of  human  knowledge  or  art  brings  specialization  with  it 
as  a natural  sequence;  that  this  tendency  is  a blessing  for  the 
central,  fundamental  stock  of  knowledge,  science,  or  art  has  been 
proved  in  many  branches.  Perhaps  as  good  an  evidence  of  this 
fact  as  any  is  the  advantage  which  general  medicine  is  just  begin- 
ning to  reap  from  the  brilliant  results  of  bacteriology. 

When  the  printing  of  this  book  was  begun,  there  was  no  work 
of  American  origin  on  this  subject.  Since  then  the  volume  by 
Einhorn  has  appeared,  being  a compilation  of  the  monographs  by 
this  author  in  the  “Twentieth  Century  Practice  of  Medicine.” 

We  already  have  a large  number  of  eminently  qualified  and 
versatile  clinicians,  men  with  acute  observing  powers  and  analytical 
minds,  who  have  worked  in  this  interesting  field.  The  names  of 
Austin  Flint,  Pepper,  Osier,  and  Delafield  Fitz  are  as  well  known 
in  this  department  in  our  country  as  those  of  Kussmaul,  Senator, 
Nothnagel,  Leube,  Ewald,  and  Boas  in  Germany,  or  Hayem, 
Bouveret,  Debove,  and  Mathieu  in  France. 

Among  those  who  have  made  contributions  of  note  to  this  special 
line  of  work  are  S.  Meltzer,  Einhorn,  George  Dock,  W.  D.  Booker, 
Charles  G.  Stockton,  Allen  Jones,  D.  D.  Stewart,  Julius  Frieden- 
wald,  Francis  P.  Kinnicut,  F.  B.  Turck,  Charles  E.  Simon,  and 
other  gifted  experimenters  and  clinicians. 

The  anatomy  of  the  stomach  has  received  a lasting  benefit 
through  the  intellect  of  F.  Mall,  of  Baltimore. 

The  surgery  of  the  alimentary  tract  has  many  very  creditable 
representatives  in  our  country,  among  whom  may  be  mentioned 
W.  W.  Keen,  Robert  F.  Weir,  N.  Senn,  John  B.  Deaver,  McBurney, 
Roswell  Park,  F.  Lang,  R.  Abbe,  W.  Meyer,  Murphy,  Bull, 
Maurice  H.  Richardson,  W.  S.  Halsted,  Gerster,  and  John  M.  T. 
Finney.  The  literary  and  practical  contributions  of  a number  of 
these  men  have  reached  a classic  standard  and  compelled  foreign 
admiration. 

The  physiological  chemistry  of  digestion  and  internal  secretion 
has  received  the  benefit  of  the  work  of  Bowditch,  Chittenden, 
Howell,  Vaughn,  Adami,  Able,  and  others,  and  dietetics  has  its 
versatile  representative  in  Gilman  Thompson. 

To  Messrs.  Blakiston,  Son  & Co.,  the  publishers,  the  author  feels 
sincerely  grateful.  It  would  be  a neglect  to  omit  an  expression  of 
this  feeling.  The  manner  in  which  they  have  executed  their  part 


Xll 


PREFACE  TO  FIRST  EDITION. 


of  the  work  speaks  for  itself.  It  is  a great  pleasure  for  an  author 
to  be  able  to  work  with  such  intelligent  and  enthusiastic  pub- 
lishers. 

To  Dr.  Edward  L.  Whitney,  my  associate,  it  becomes  my  pleasant 
duty  to  express  thanks  for  the  able  manner  in  which  he  has  written 
the  chemical  section  of  part  first,  and  also  for  much  kind  assistance 
throughout  the  work. 

Pathology  has  its  men  now  universally  acknowledged  for  the 
integrity  and  dignity  of  their  work  in  our  esteemed  teachers,  Welch 
and  Councilman.  Already  an  American  School  of  Pathology  is 
forming,  with  these  men  and  Prudden,  Flexner,  and  others.  But 
in  the  special  pathology  of  the  digestive  organs  the  workers  are 
few;  a very  creditable  beginning,  however,  has  been  made;  the 
foundation  is  an  honor  to  the  prospective  builders,  but  the  land  to 
be  explored  is  exceedingly  large  in  its  extent,  and  “ the  harvest  is 
plenteous , but  the  laborers  are  few!' 

JOHN  C.  HEMMETER. 

Baltimore,  1897. 


“ Heard  are  the  voices, 

Heard  are  the  sages, 

The  worlds  and  the  ages ; 
Choose  well,  your  choice  is 
Brief  and  yet  endless. 

“ Here  eyes  do  regard  you 
In  eternity’s  stillness, 
Here  is  all  fullness, 

Ye  brave,  to  reward  you  ; 
Work  and  despair  not!' 

— Goethe. 


LIST  OF  ILLUSTRATIONS 


PLATE  PAGE 

Normal  Histology  of  the  Gastric  Mucosa, Frontispiece. 


I.  Three  Sections  of  Stomach-walls  Placed  Side  by  Side  to  Show  the  Positions 
of  Blood-vessels  and  Lymphatics  to  the  Different  Layers  (Colored), 

. Opposite  Page  28 

II.  Reconstruction  of  a Small  Portion  of  the  Middle  Zone  of  the  Stomach 

(Colored), Opposite  Page  29 

III.  Patient  with  Intragastric  Bag  within  Stomach  and  Pneumograph  in  Place, 

Both  Connected  with  the  Kymograph, Opposite  Page  72 

IV.  Apparatus,  not  Including  Kymograph, Opposite  Page  73 

V.  Phlegmonous  Gastritis  in  the  Sequence  of  Ulcus  Carcinomatosum, 

Opposite  Page  434 

VI.  Bacterial  Invasion  of  Gastric  Epithelium.  From  a Case  of  Diphtheric 

Gastritis  (Colored), Opposite  Page  438 

VII.  Carcinomatous  Ulcer  of  the  Pyloric  Antrum,  ......  Opposite  Page  490 

VIII.  Ulcus  Carcinomatosum  of  the  Pylorus, Opposite  Page  506 

IX.  Syphilitic  Gastritis,  Showing  Degeneration  and  Loss  of  the  Superficial 

Columnar  Epithelium  and  That  of  the  Vestibules,  etc. , . Opposite  Page  596 

X.  Hypertrophic  Stenosis  of  the  Pylorus  from  Chronic  (Stenosing)  Gastritis, 

Opposite  Page  618 

XI.  Stenosing  Hypertrophic  Gastritis,  Actual  Size  and  Configuration  of  Stom- 
ach Opened  along  the  Lesser  Curvature  from  Esophagus  to  Duodenum, 

Opposite  P.age  620 

XII.  Malformation  and  Distortion  of  the  Stomach  Caused  by  Lacing  or  Tight 


Clothing,  Belts,  etc. Opposite  Page  628 

XIII.  Gastrectasia,  Transillumination  of  the  Stomach, Opposite  Page  640 

XIV.  Adhesions,  Causing  Motor  Insufficiency  but  Retaining  Stomach  in  Normal 

Position, Opposite  Page  642 

FIG.  PAGE 

1-3.  Sections  of  Deep  Ends  of  Fundus  Glands  of  the  Cat  in  Different  Secretive 

Phases, 26 

4.  Plaster  Casts  of  Duodenum  of  Infant  and  Adult,  39 

5.  Hemmeter’s  Apparatus  for  Obtaining  Intestinal  Contents, 53 

6.  Pressure  Bottles  for  Distending  the  Intragastric  Bag  during  Duodenal  Intuba- 

tion,   54 

7.  Intragastric  Tissue  Rubber  Bag,  with  Three  Distinct  Parts, 80 

• 8.  Location  of  the  Stomach — Dorsal  View  (Colored), 99 

9.  Location  of  the  Stomach — Anterior  View  (Colored), 100 

10.  Normal  Percussion  Limits  of  the  Adult  Stomach, 101 

11.  Stomach  Distended  by  Air  or  C02,  Showing  Stomach  in  State  of  Gastrop- 

tosis,  103 


XIV 


LIST  OF  ILLUSTRATIONS. 


FIG. 

12.  The  Electrodiaphane, 

13.  Hemmeter’s  Double-current  Stomach  Lavage  Tube, 

14.  Illustrating  the  Principle  of  Siphonage, 

15.  Bulb  Used  for  the  Aspiration  of  Test-meals  with  Patients  Having  Very  Relaxed 

Abdominal  Walls,  

16.  The  Esophageal  Tubal  Probe,  

17.  Stomach-pump  Used  Only  for  Rapid  Evacuation  of  Poisons, 

18.  Modified  Ewald  Tube,  with  Numerous  Smaller  and  Larger  Lower  Openings,  . 

19.  Oppler-Boas  Bacillus  from  Contents  of  a Carcinomatous  Stomach, 

20.  Fragment  of  Mucosa  Showing  a Normal  Condition  of  Glands, 

21.  Hypertrophy  and  Proliferation  of  Glandular  Elements, 

22.  Atrophy  and  Vacuolization  of  Glandular  Elements,  etc., 

23.  Strauss’  Mixing  Funnel  for  Lactic  Acid  Determinations,  . . . 

24.  Gastroscope, 

25.  Esophagoscope,  Obturator,  Esophageal  Forceps,  Esophageal  Applicator,  . . . 

26.  Recurrent  Gastric  Needle  Spray  or  Douche, 

27.  The  Intragastric  Spray, 

28.  Rectal  Electrode, 

29.  Einhorn’s  Intragastric  Electrode, 

30.  Abdominal  Electrode, 

31.  Massage  of  the  Stomach  in  Dilatation  or  Gastroptosis, 

32.  Massage  for  Improving  Gastric  Tonicity, 

33.  Massage  of  the  Stomach  and  Colon, 

34.  Atrophy  and  Vacuolization  of  Glandular  Elements,  etc., 

34  A.  Connective-tissue  Hyperplasia  Separating  Remnants  of  Glands  Which  Show 

a Small  Nucleus  Surrounded  by  a Thin  Shell  of  Protoplasm, 

34  B.  Detachment  of  Remnants  of  Secretory  Cells  Containing  Vacuoles  from 
Lumen  of  Peptic  Duct, 

35.  Cancerous  Invasion  of  the  Glandular  Layer.  A Portion  of  the  Mucous  Coat, 

36.  Cancerous  Infiltration  of  the  Muscularis.  Section  of  a Portion  of  the  Muscular 

Coat  of  the  Stomach, 

37.  A Portion  of  an  Area  in  the  Submucosa,  Largely  Composed  of  Groups  of 

Cancer  Cells,  *. 

38.  Section  of  Tissue  Near  the  Base  of  a Carcinomatous  Ulcer,  Showing  Micro- 

organisms ( Colored ), 

39.  Diagrammatic  Illustration  of  the  Mechanism  Effecting  Vertical  Position  of  the 

Stomach, . . . ' 

40.  Dilation  of  the  Stomach, 


105 

116 

117 

1 1 7 
121 

123 

124 
129 
140 

142 

143 
169 
179 

183 

299 

300 
303 
303 
3°7 
309 
3IQ 
3ii 
452 

473 

474 

528 

529 

531 

532 
628 

63s 


*»  1 


TABLE  OF  CONTENTS. 


PART  FIRST. 


ANATOMY  AND  PHYSIOLOGY  OF  THE  DIGESTIVE  ORGANS.- 
METHODS  AND  TECHNICS  OF  DIAGNOSIS. 


CHAPTER  I.  Page 

Anatomy  of  the  Stomach, 17-24 


Muscular  Layer. — Structure  of  the  Mucous  Membrane. — Three  Kinds 
of  Cells  of  the  Peptic  Glands. 


CHAPTER  II. 

Histology  of  the  Stomach, 24-31 

Mucosa. — Vessels  and  Nerves. 

CHAPTER  III. 

The  Small  Intestine, 31-41 

Structure.  — Valvulte  Conniventes.  — Villi.  — Lacteals.  — Glands.  — 
Blood-vessels. — Lymph-vessels. — Relations  of  the  Duodenum. — Jeju- 
num and  Ileum. 

CHAPTER  IV. 

Physiology  of  Digestion, 41-48 

Food  Substances. — Caloric  Values. — Ptyalin  Digestion. — Digestion  of 
Starches. — Gastric  Juice. 

CHAPTER  V. 


Pepsinogen  and  Pepsin. — Rennin  Zymogen  and  Rennin. — 

Intestinal  Digestion. — Duodenal  Intubation,  . . 49-58 

Rennin,  Chymosin,  or  Pexin. — Physiology  of  Intestinal  Digestion. — 

The  Pancreas  : Its  Secretion  and  Pancreatic  Digestion. 

CHAPTER  VI. 

The  Bile. — The  Succus  Entericus. — Intestinal  Fermen- 
tation. — Putrefaction.  — Formed  or  Organized 
Ferments, 59-64 

CHAPTER  VII. 

Effects  of  the  Action  of  the  Several  Digestive  Secre- 
tions.— Methods  for  Testing  the  Motor  Func- 
tions of  the  Stomach,  . . 65-71 

Qualitative  and  Quantitative  Methods  for  Testing  the  Motor  Functions 
of  the  Stomach. 


XV 


Xvi  TABLE  OF  CONTENTS. 

CHAPTER  VIII. 

Methods  for  Testing  the  Gastric  Peristalsis,  .... 

CHAPTER  IX. 

Hemmeter’s  Method  for  Testing  the  Gastric  Peris- 
talsis, . 

Theories  Concerning  the  Movements  of  the  Ingesta. 

CHAPTER  X. 

Absorption  from  the  Stomach, 

Penzoldt’s  and  Faber’s,  Herschel’s,  Julius  Miller’s,  and  Hemmeter’s 
Tests  for  Gastric  Resorption. 

CHAPTER  XI. 

Methods  for  Determining  the  Location,  Size,  and 
Capacity  of  the  Stomach, 

Percussion  and  Auscultation. — Location,  Size,  and  Capacity. — Gastro- 
diaphany  of  Einhorn. — Literature. 

CHAPTER  XII. 

The  Stomach-tube  and  Technics  of  Its  Introduction,  . . 
Examination  of  Stomach  Contents. — Test-meals:  Their  Effect  upon 
the  Amount  of  Acid  Secreted.— Literature. 

CHAPTER  XIII. 

Methods  for  Qualitative  and  Quantitative  Analysis 
of  Stomach  Contents, 

Presence  of  Bits  of  Gastric  Mucosa. — Examination  of  Stomach  Con- 
tents for  Mucus,  Saliva,  Bile,  Duodenal  Secretions,  Blood,  and  Pus. — 
Tests  for  Blood  in  Stomach  Contents. — Demonstration  of  the  Presence 
of  Iron  in  Stomach  Contents  or  Vomited  Matter. — Spectroscopical  Ex- 
amination of  Stomach  Contents  for  Blood. — Examination  of  Portions 
of  Mucosa  or  Tissue  Found  in  the  Wash-water  or  Vomited  Matter. — 
Character  and  Amount  of  Undigested  Food. — Bacteria. — Literature. 

CHAPTER  XIV. 

The  Diagnostic  Significance  of  Fragments  of  Gastric 
Mucosa, 

Deductions  from  Fifty  Cases. 


CHAPTER  XV. 

The  Chemistry  of  Gastric  Digestion, 

Occurrence  of  Secretions  in  the  Empty  Stomach. — Stimulations  to 
Secretions  of  Gastric  Juice. — Significance  of  Foam. — Preparation  of 
Gastric  Contents. — Quantitative  Analysis. — Methods. — Standard  or 
Normal  Solutions. — Indicators. — Titration. — Apparatus. 

CHAPTER  XVI. 

Chemical  Examination  of  Gastric  Juice, 

Tests  for  Presence  of  Free  Acids. — Tests  for  Free  Hydrochloric  Acid. 
— The  Dimethyl-amido-azo-benzol  Test. — The  Resorcin  Test. — Com- 
bined Hydrochloric  Acid. — Lactic  Acid  : Formation,  Significance, 
Detection. — The  Phloroglucid- Vanillin  Test. 


Page 

72-78 

79-90 

90-97 

98-1x3 

114—126 

127-139 

139-148 

148-155 

i56~i63 


TABLE  OF  CONTENTS.  Xvii 

CHAPTER  XVII.  Page 

Quantitative  Analysis  of  the  Stomach  Acids, 163-171 


Topfer’s  Method. — Method  of  Martius  and  Lttttke. — Leo’s  Method. — 

Boas’  Method. — Lactic  Acid  : Quantitative  Estimation,  Boas’  Method. 

— Quantitative  Estimation  of  Fatty  Acids. — Total  Organic  Acids.  • 

CHAPTER  XVIII. 

Digestive  Ferments. — Products  of  Digestion. — Tests  for 

Same, 171-177 

Saliva. — Pepsin. — Pepsinogen. — Chymosin  or  Rennin  and  Rennin 
Zymogen. — Action  of  Pepsin  on  Proteids. 

CHAPTER  XIX. 

Gastroscopy, 178-184 

Description  of  the  Instrument. 


PART  SECOND. 


THERAPY  AND  MATERIA  MED1CA  OF  STOMACH  DISEASES. 


CHAPTER  I. 

The  Principles  of  Dietetic  Treatment  of  Gastric 

Diseases, 185-227 

Preparations  of  the  Foods. — The  Diet  as  Influenced  by  the  State  of  the 
Secretion. — The  Dietetics  of  Gastric  Ulcer  and  Erosions. — The  Indica- 
tions for  Predigested  Foods:  Peptones,  Albumoses,  Dextrose,  etc. — 

Rectal  Alimentation. — The  Occurrence  of  Proteolytic  Ferments  in  the 
Colon  and  Rectal  Contents. — Preparation  of  Rectal  Enemata. — Indica- 
tions Necessitating  Rectal  Feeding. — Tables  of  Dietetics. 

CHAPTER  II. 

Dietetic  Kitchen. — Diet  Lists,  228-287 

Effects  of  Cooking  on  Food. — Indications  of  the  Palate. — Dietetical 
Cooking. — The  Use  and  Abuse  of  Rest  and  Exercise  for  the  Digestive 
Organs. — Mental  Rest. — Dietetic  Exercise. 

CHAPTER  III. 

The  Dietetics  of  Alcohol  and  Alcoholic  Beverages,  . 

Action  of  Alcohol  on  Pancreatic  Digestion. — Action  of  Alcohol  on 
Salivary  Digestion. — Action  of  Alcohol  on  Gastric  Peristalsis. — Effect 
on  Absorption. 

CHAPTER  IV. 

Lavage  and  the  Gastric  Douche, 

The  Gastric  Douche. — Electricity  in  the  Treatment  of  Gastric  Diseases. 

— Hydrotherapeutic  and  Orthopedic  Methods. — Gastric  Massage. — 

Combination  of  Massage  and  Medicated  Irrigations  of  Stomach  and 
Colon. 

CHAPTER  V. 

Mineral  Springs, 

The  Uses  and  Abuses  of  Natural  Mineral  Waters  in  Diseases  of  the 
Digestive  Organs. — Useful  Mineral  Springs  of  the  United  States,  with 
Analyses  and  Mode  of  Action. 


287-297 


297-313 


3 1 3-3 2 8 


XV111 


TABLE  OF  CONTENTS. 


CHAPTER  VI.  PAGE 

Important  Medicinal  Agents  in  Gastric  Therapy,  . . . 328-347 

Hydrochloric  Acid. — The  Alkalies. — The  Bitter  Tonics  and  So-called 
Stomachic  Remedies. — Digestive  Ferments. 


CHAPTER  VII. 

Surgical  Treatment  of  Organic  Gastric  Diseases,  . . 348-373 

Various  Forms  of  Operations  Practised  upon  the  Stomach.  — The 
Fundamental  Factors  Influencing  the  Rate  of  Mortality  in  Gastric 
Operations. — Operative  Statistics. 

CHAPTER  VIII. 

Influence  of  Gastric  Diseases  upon  Other  Organs  and 


on  Metabolism, „ 374-400 

The  Influence  of  Diseases  of  Other  Organs  on  the  Stomach. — Literature. 

CHAPTER  IX. 

The  Blood  and  Urine  in  Stomach  Diseases, 400-413 

The  Gases  of  the  Stomach. — Urinary  Changes  in  Stomach  Diseases. 


PART  THIRD. 


THE  GASTRIC  CLINIC. 


CHAPTER  I. 

Acute  Gastritis, 414-443 

Simple  Acute  Gastritis. — Phlegmonous  or  Purulent  Gastritis. — Suppur- 
ative Inflammation  of  the  Gastric  Mucosa. — Abscess  of  the  Stomach. 

— Infectious  Gastritis. — Gastritis  Mycotica  or  Parasitaria. — Gastritis 
Diphtherica  and  Crouposa. — Toxic  Gastritis. — Gastritis  Venenata. 

CHAPTER  II. 

Chronic  Gastritis, 443-486 

Literature. 

CHAPTER  III. 

Ulcer  of  the  Stomach, 486-526 

Ulcus  Ventriculi,  Pepticum,  Rotundum,  Perforans,  Rodens,  Corrosivum, 
e Digestione. — Literature. 

CHAPTER  IV. 

Malignant  Tumors  of  the  Stomach, 527-589 

Carcinomata.— Sarcomata. — Literature. — Table  of  Differential  Diag- 


TABLE  OF  CONTENTS. 


XIX 


CHAPTER  V.  PACK 

Stomach  Diseases  Caused  by  Infectious  Granulomata,  . 590-606 

Tuberculosis  of  the  Stomach. — Syphilis  of  the  Stomach. — Literature. 

CHAPTER  VI. 

Benign  Tumors  of  the  Stomach, 606-623 

Myomata.  — Fibromata. — Lipomata. — Polypi. — Myxomata. — Papillo- 
mata.— Lymphadenomata. — Pedunculate  Tumors. — Foreign  Bodies. — 

Gastroliths. — Hypertrophic  Stenosis  of  the  Pylorus. — Literature. 

CHAPTER  VII. 

Motor  Insufficiency, 624-682 

Gastric  Atony  or  Myasthenia. — Gastrectasis  (Dilation  of  the  Stom- 
ach).— Obstruction  of  the  Orifices. — Literature. 

CHAPTER  VIII. 

Hemorrhage  from  the  Stomach  (Gastrorrhagia),  . . . 682-694 

CHAPTER  IX. 

Enteroptosis — Gastroptosis, 695-732 

History  and  Pathogenesis  of  Enteroptosis. — Observation  on  Gastrop- 
tosis.— Observation  on  Dislocation  of  the  Colon. — Observation  on  Dis- 
location of  the  Liver. — Literature. 

CHAPTER  X. 

Neuroses  of  the  Stomach,  733~794 

General  Considerations.  — Cardiospasm.  — Pyloric  Spasm.  — Gastro- 
spasm.  — Gastric  Hyperperistalsis.  — Nervous  Eructation.  — Nervous, 

Habitual,  or  Reflex  Vomiting. — Insufficiency  or  Incontinence  of  the 
Cardia. — Rumination,  or  Merycism. — Insufficiency  or  Incontinence  of 
the  Pylorus, — Atony  of  the  Stomach. — Literature. 

CHAPTER  XI. 

Sensory  Neuroses, 794-816 

Hyperesthesia. — Gastralgia.  — Bulimia,  or  Hyperorexia. — Acoria. — 

Nervous  Anorexia. 

CHAPTER  XII. 

Neuroses  of  Secretion, 817-849 

Hyperchylia. — Periodic  Atypical  Flow  of  Gastric  Juice. — Chronic 
Continuous  Flow  of  Gastric  Juice. — Literature. — Subacidity. 

CHAPTER  XIII. 

Achylia  Gastrica, 850-864 

CHAPTER  XIV. 

Nervous  Dyspepsia  (Leube). — Neurasthenia  Gastrica 

(Ewald),  865-876 

Heterochylia. 

List  of  Authors, 879 

List  of  Subjects, 889 


Diseases  of  the  Stomach. 


PART  FIRST. 

ANATOMY  AND  PHYSIOLOGY  OF  THE  DIGESTIVE 
ORGANS.— METHODS  AND  TECHNICS 
OF  DIAGNOSIS. 


CHAPTER  I. 

ANATOMY  OF  THE  STOMACH. 

The  organic  diseases  which  affect  the  human  stomach  produce 
decided  and  characteristic  changes  in  its  structure.  For  the  proper 
comprehension  of  these,  a brief  outline  of  the  normal  anatomy  and 
histology  is  indispensable.  Even  a short  reference  to  the  embry- 
ology of  the  human  stomach  will  have  to  be  made,  but  this  will  be 
limited  to  the  two  diseases — viz.,  enteroptosis  and  gastroptosis,  the 
pathogenesis  of  which  will  become  more  intelligible  by  a review 
of  the  fetal  development  of  this  organ. 

Many  valuable  contributions  to  the  subject  of  the  macroscopical 
and  microscopical  anatomy  of  the  stomach  have  been  made  during 
recent  years.  In  the  subjoined  brief  synopsis  we  have  availed 
ourselves  of  the  valuable  researches  of  F.  Mall,  and  of  the  works 
quoted  by  him  in  the  bibliography  given  in  his  article  in  the  “ Johns 
Hopkins  Hospital  Reports,”  volume  I.  The  comprehensive  works 
of  Oppel,  Spalteholz,  and  others  which  have  appeared  during 
i896-’99,  have  also  been  consulted. 

The  stomach  is  the  dilated,  sac-like  portion  of  the  digestive 
tract,  between  the  esophagus  and  the  small  intestine.  One  can 
distinguish  a lower  convex  arch,  the  greater  curvature,  which  is 
directed  toward  the  left  and  downward ; and  an  upper  concave 
arch,  the  lesser  curvature,  which  is  directed  toward  the  right  and 
upward.  The  broad  left  end  of  the  greater  curvature  is  called  the 
2 17 


ANATOMY  OF  THE  STOMACH. 


fundus,  the  size  of  which  varies  according  to  age.  Between  the 
fundus  and  the  lesser  curvature  is  situated  the  cardia,  being 
the  continuation  and  funnel-shaped  expansion  of  the  esophagus. 
While  it  is  not  marked  on  the  outside  of  the  organ,  there  is  a 
distinct  limiting  line  internally  on  the  mucous  membrane,  which  is 
caused  by  a change  in  the  structure  of  the  epithelial  lining.  This 
zigzag  line  separates  the  cardia  from  the  esophagus.  At  this  point 
the  arrangement  of  the  muscular  fibers  and  veins  is  also  different 
from  that  in  the  esophagus. 

The  location  of  the  cardia  in  the  adult  is  at  the  twelfth  dorsal 
vertebra.  At  about  the  height  of  the  bifurcation  of  the  bronchi, 
the  spiral  curving  of  the  esophagus  around  the  aorta  begins.  By 
executing  this  curve,  the  convexity  of  which  is  toward  the  right, 
the  esophagus  gets  to  the  left  side  of  the  aorta,  and  passes 
through  the  diaphragm  in  the  foramen  cesophageum,  near  the 
spinal  column. 

The  stomach  becomes  narrower  from  the  fundus  toward  the 
pylorus.  Near  the  pylorus  there  is  a constriction,  caused  by  a 
ring-like  formation  of  muscular  tissue,  which  corresponds  to  the 
pyloric  valve.  The  muscular  tissue  is  covered  internally  by  the 
gastric  mucous  membrane,  the  latter  forming  the  pyloric  valve, 
the  opening  of  which  is  of  varying  diameter.  The  part  of  the 
stomach  in  advance  of  the  pylorus  is  called  the  pyloric  antrum, 
and  is  frequently  separated  from  the  greater  curvature  by  an  inden- 
tation or  depression.  This  antrum  may  be  elongated  so  as  to 
assume  resemblance  to  the  intestine ; this  is  more  frequently  the 
case  in  the  female. 

On  the  anterior  and  posterior  walls  of  the  stomach,  running 
along  between  the  muscular  and  serous  coats  of  the  organ,  are  two 
band-like  stripes,  consisting  of  elastic,  smooth,  muscular  fibers, — 
the  pyloric  ligaments. 

The  size  of  the  stomach  depends  upon  age,  sex,  and  individuality, 
and  upon  the  degree  of  its  distention.  The  long  axis  varies 
from  25  to  35  cm.  The  greatest  vertical  measurement,  at  the  cardia, 
is  15  cm.,  and  the  greatest  straight  diameter  is  from  11  to  12  cm.; 
the  smallest,  at  the  pyloric  antrum,  is  from  3 to  4 cm.  In  the 
female  it  is  generally  smaller  and  more  slender. 

The  capacity  varies  considerably:  Ewald  considers  from  1600 
to  1700  c.c.  to  be  the  normal  limit.  Three-fourths  of  the  stomach 
belongs  to  the  left  half  of  the  body  and  one-fourth  to  the  right 
half.  The  cardia  is  located  behind  the  median  edges  of  the  fifth 


DIAPHRAGM — PANCREAS. 


>9 


and  sixth  ribs.  The  fundus,  the  largest  part  of  the  body  of  the  organ , 
is  in  the  left  hypochondrium  ; the  rest,  with  the  pyloric  part,  is  in 
the  epigastrium.  The  pylorus  lies  in  the  right  half  of  the  body,  but 
occasionally  changes  to  the  middle  line  at  the  level  of  the  seventh 
and  eighth  ribs,  in  a line  with  the  ensiform  cartilage.  The  lesser 
curvature  runs  along  to  the  left,  and  near  the  spinal  column.  The 
vaulting  dome  of  the  fundus,  which  applies  itself  to  the  concavity 
of  the  diaphragm,  is  the  highest  point.  The  deepest  point  of  the 
stomach  is  in  the  greater  curvature,  in  the  inferior  half  of  an  imagi- 
nary straight  line  connecting  the  ensiform  cartilage  with  the  umbili- 
cus. Both  the  highest  and  lowest  parts  of  the  stomach  are  moved 
about  according  to  the  level  of  the  diaphragm  and  the  distention  of 
the  stomach.  In  an  empty  condition,  the  stomach  is  withdrawn 
into  the  upper  portion  of  the  abdomen  ; but  when  filled,  it  distends 
in  all  directions,  but  mostly  in  the  direction  of  its  long  axis,  from 
the  left  above,  downward,  and  to  the  right.  In  a state  of  moderate 
distention  about  forty  centimeters  of  its  anterior  wall  come  in 
contact  with  the  inner  surface  of  the  anterior  abdominal  wall. 

The  diaphragm  covers  the  fundus  and  the  largest  part  of  the 
left  segment,  while  the  left  lobe  of  the  liver,  up  to  the  sulcus  inter- 
lobularis,  covers  the  smallest  part — that  is,  the  lesser  curvature 
and  the  pyloric  portion.  From  this  fact  arises  the  difficulty  in 
palpating  tumors  in  the  latter  places,  which  is  impossible  except 
when  gastroptosis,  or  descent  of  the  stomach,  moves  it  away  from 
the  liver.  In  the  state  of  expansion  or  dilatation,  the  stomach  moves 
out  from  behind  the  liver;  but  the  lesser  curvature  can  not  change 
its  location  to  any  considerable  extent,  and  the  change  of  location 
of  the  whole  stomach  caused  by  filling  is  produced  almost  exclu- 
sively by  an  extension  of  the  greater  curvature. 

The  pancreas  extends  along  the  posterior  wall  of  the  stomach. 
At  the  upper  edge  of  the  pancreas  are  the  splenic  artery  and  vein. 
The  transverse  colon  runs  along  the  greater  curvature,  and  its  left 
flexure  fills  the  remaining  space  in  the  left  hypochondrium.  The 
location  of  the  stomach  is  fixed  by  a ligamentous  attachment  of  the 
cardia,  by  the  pylorus,  and  also  by  a number  of  suspensory  liga- 
ments, which  are  all  formations  of  the  peritoneum.  Some  authors 
say  that  the  stomach  is  supported  in  this  position  by  intra- 
abdominal pressure.  The  experiments  of  Moritz,  of  Munich,  and 
the  author  have  proved  that  intra-abdominal  pressure  adds  nothing 
to  the  support  of  the  stomach.  The  gastrophrenic  ligament,  which 
toward  the  right  passes  into  the  lesser  omentum,  and  toward  the 


20 


ANATOMY  OF  THE  STOMACH. 


left  extends  into  the  phrenosplenic  ligament,  surrounds  and  em- 
braces the  cardia.  This  portion  is  lower  than  the  fundus,  its  situation 
corresponding  to  the  upper  end  of  the  sixth  and  seventh  costal 
cartilages,  or  to  the  level  of  the  ninth  thoracic  vertebra.  This  part 
of  the  stomach  is  therefore  moved  to  the  left  of  the  middle  line, 
and  next  to  the  spinal  column,  at  about  the  level  of  the  twelfth 
thoracic  and  first  lumbar  vertebrae  ; here  it  is  fixed  to  the  lumbar 
part  of  the  diaphragm. 

The  greater  omentum  arises  from  the  large  curvature.  The 
posterior  fold  of  this  omentum  forms  the  transverse  mesocolon. 
This  is  the  reason  why  changes  of  location  in  the  greater  omentum 
(hernia  and  inflammatory  adhesions)  can  produce  traction  upon  the 
stomach.  As  the  stomach  is  really  attached  only  at  the  cardia,  and 
the  pylorus  is  adherent  to  the  posterior  abdominal  wall,  together  with 
the  descending  portion  of  the  duodenum,  the  organ  is  capable  of 
being  moved  about,  not  so  much  in  its  entirety  as  in  its  parts  (the 
great  curvature,  for  instance).  The  stomach  has  a complete  peri- 
toneal covering  which  consists  of  an  anterior  and  a posterior  layer, 
uniting  at  the  two  curvatures  of  the  stomach  to  form  the  lesser  and 
the  greater  omentum  ; between  these  two  layers  space  is  left  for 
the  blood- and  lymph-vessels  of  the  stomach. 

Muscular  Layer. — The  muscular  stratum  contains  three  kinds 
of  fibers — longitudinal,  transverse,  and  oblique.  The  longitudinal 
layer  of  muscular  fibers — a continuation  of  those  of  the  esophagus — 
presents  a denser  arrangement  at  the  lesser  curvature  than  at  the 
greater,  and  forms  the  ligamenta  pylorica  at  the  pyloric  part,  which 
are  bands  of  muscular  fibers  expanded  and  broadened  out, — not 
ligaments  in  the  real  sense  of  the  word. 

The  circular  layer  of  muscular  fibers  is  placed  internally  to  the 
longitudinal  layer,  the  fibers  of  which  it  crosses  at  right  angles. 
The  circular  fibers  run  around  the  stomach  in  a ring  or  belt-like 
manner;  at  the  pylorus  they  form  a local  thickening  of  the  muscle 
rings — the  pyloric  sphincter.  A fold  of  the  mucosa  to  the  innermost 
side  of  this  sphincter  constitutes  the  pyloric  valve.  The  longi- 
tudinal fibers  also  have  a part  in  the  formation  of  the  sphincter, 
for  while  the  superficial  layer  of  longitudinal  fibers  passes  on 
over  the  pyloric  sphincter  into  the  duodenum,  the  deeper  longi- 
tudinal fibers  enter  the  pyloric  valve,  encircling  and  grasping  the 
circular  fibers  in  a loop-like  manner  (dilator  pylori — Rudinger). 
The  cardia  has  no  special  sphincter,  but  the  oblique  fibers  cross 
and  decussate  at  the  periphery  of  this  portion.  The  sphincter 


MUCOUS  MEM B KANE. 


2 I 

pylori  is  contracted  during  digestion,  but  gas  and  liquids  can 
readily  escape  through  the  cardia.  The  oblique  fibers  are  limited 
chiefly  to  the  cardiac  end  of  the  stomach,  where  they  are  disposed 
as  a thick,  uniform  layer, some  passing  obliquely  from  left  to  right, 
others  from  right  to  left,  around  the  cardiac  orifice.  The  sub- 
mucosa, or  cellular  coat  of  the  stomach,  consists  of  a loose,  fila- 
mentous, areolar  tissue,  and  loosely  binds  the  mucosa  to  the 
muscular  layers. 

The  most  important  and  interesting  layer  is  the  mucosa,  or 
mucous  membrane  proper  of  the  stomach.  It  is  a thick  layer  with 
a smooth,  soft,  velvety  surface.  During  infancy  and  immediately 
after  death  it  is  of  a pinkish  tinge,  but  in  adult  life  and  in  old  age 
it  becomes  of  a pale  straw  or  ash-gray  color.  At  the  pylorus  it  is 
much  thicker  than  at  the  cardia.  During  the  contracted  state  of 
the  organ  it  is  thrown  into  numerous  plaits  or  rugae,  which,  for  the 
most  part,  have  a longitudinal  direction,  and  are  most  marked 
toward  the  lesser  end  of  the  stomach  and  along  the  greater  curva- 
ture ; these  folds  are  entirely  obliterated  when  the  organ  becomes 
distended. 

Structure  of  the  Mucous  Membrane. — When  examined  with 
a lens,  the  inner  surface  of  the  mucous  membrane  presents  a pecu- 
liar honeycomb  appearance,  from  being  covered  with  small,  shallow 
depressions,  or  alveoli,  of  a polygonal  or  hexagonal  form,  which 
vary  from  to  3-^-  of  an  inch  in  diameter,  and  are  separated 
by  slight  ridges.  In  the  bottom  of  the  alveoli  are  seen  the 
orifices  of  minute  tubes, — the  gastric  follicles, — which  are  situated 
perpendicularly  side  by  side  in  the  entire  substance  of  the  mucous 
membrane.  They  are  short  and  of  a simple  tubular  character 
toward  the  cardia,  but  at  the  pyloric  end  they  are  longer,  more 
thickly  set,  convoluted,  and  terminate  in  dilated  saccular  ex- 
tremities, or  are  subdivided  into  from  two  to  sixteen  tubular 
branches. 

Watney  has  pointed  out  that  these  convoluted  or  coiled  tubes 
form  the  transition  from  the  simple  tubular  follicles  to  the  convo- 
luted glands  of  Brunner,  which  lie  immediately  below  the  pylorus. 
Some  histologists  speak  of  a homogeneous  basement  membrane, 
formed  by  the  connective-tissue  framework,  lined  upon  its  free  sur- 
face by  a layer  of  cells,  which  differ  in  their  character  in  different 
parts  of  the  stomach.  The  author  could  never  confirm  the  existence 
of  such  a basement  membrane.  Toward  the  pylorus  the  tubes 
are  lined  throughout  by  columnar  or  cuboidal  epithelium  ; they 


22 


ANATOMY  OF  THE  STOMACH. 


are  termed  the  mucous  glands,  and  are  supposed  to  secrete  the 
gastric  mucus.  In  other  parts  of  the  organ  the  deep  part  of  each 
tube  is  filled  with  nucleated  cells,  the  upper  fourth  of  the  tube 
being  lined  by  columnar  epithelium  : these  are  called  the  peptic 
glands,  and  are  the  source  of  the  gastric  juice. 

Simple  follicles  are  found  in  greater  or  less  numbers  over  the 
entire  surface  of  the  mucous  membrane  ; they  are  most  numerous 
near  the  pyloric  end  of  the  stomach,  and  are  especially  distinct  in 
early  life.  The  epithelium  lining  of  the  mucous  membrane  of  the 
stomach  and  its  alveoli  is  of  the  columnar  variety. 

Usually  four  to  sixteen  gland  openings  are  found  at  the  base  of 
each  follicle.  According  to  Sappey,  there  are  5,000,000  of  these 
glands  in  the  organ,  for  which  reason  the  gastric  mucosa  may 
justly  be  considered  a continuous  gland  spread  out  upon  a flat 
surface  (Hyrtl  and  Luschka).  The  gland  tubules  are  as  long  as 
the  entire  thickness  of  the  mucosa,  and  their  sac-like  and  branched 
bases  extend  into  the  muscularis  mucosae,  the  contraction  of  which 
assists  in  the  evacuation  of  the  tubules  during  digestion.  The 
ends  of  the  tubules  extending  into  the  muscular  layer  are  usually 
branched. 

Three  Kinds  of  Cells  of  the  Peptic  Glands. — First,  the  cylin- 
drical cells  of  the  gland  duct  and  pit,  lining  one-fourth  to  one- 
third  of  the  distance  from  the  surface  of  the  mucous  membrane 
downward.  They  are  a continuation  of  the  cylindrical  epithelium 
of  the  general  internal  surface  of  the  gastric  mucous  membrane, 
apparently  secreting  mucus  only.  Secondly,  the  lightly  colored 
pyramidal  or  cuboidal  cells,  with  a granular  protoplasm  and 
spherical  nucleus.  These  cells  do  not  stain  with  anilin,  and 
were  termed  adelomorphous  cells  by  Rollet  because  they  show  no 
cell  contours  in  the  fresh  state.  Rosenheim  states  that  they  are 
almost  clear  and  transparent  during  fasting,  and  become  cloudy 
and  granular  during  digestion.  Heidenhain  designated  them  as 
the  chief  or  central  cells,  and  they  were  held  by  him  to  be  the 
sources  of  the  ferments  pepsinogen  and  rennin  zymogen. 
These  chief  or  central  cells  touch  the  lumen  of  the  duct  more 
extensively  than  the  following  variety.  The  third  kind  of  peptic 
cells  are  known  as  the  border,  parietal,  or  oxyntic  cells;  they 
rest  upon  the  connective-tissue  framework  with  much  broader 
bases  than  the  chief  or  central  cells.  For  this  very  reason  they 
participate  to  a less  degree  in  the  limitation  of  the  lumen  of  the 
duct.  They  are  generally  round  or  triangular,  finely  granular, 


PEPTIC  CELLS. 


23 


and  stain  intensely  with  anilin,  and  were  designated  by  Rollet  as 
deloniorphous  cells.  Heidenhain  supposes  them  to  be  the  sources 
of  hydrochloric  acid.  If  we  assume,  for  the  sake  of  locating 
these  various  cells,  a division  of  the  tubule  into  four  sections, 
beginning  at  the  portion  nearest  the  submucosa,  we  shall  have  ( a ) 
the  fundus  of  the  gland  tubule  ; then  ( b ) the  outer  secretory  por- 
tion ; (c)  the  inner  secretory  portion  ; and,  opening  on  the  inner 
surface  of  the  mucosa,  (d)  the  alveolus  (“  Vorraum  ”).  Then,  one 
finds  the  border,  parietal,  oxyntic,  deloniorphous,  or  anilin  cells 
most  numerous  in  the  outer  secreting  portion,  and  becoming  scarce 
in  the  fundus  or  end  portion.  A fourth  kind  of  cell,  occurring  at 
rare  intervals,  is  known  as  Nussbaum’s  cell;  its  significance  is 
unknown. 

Heidenhain  asserted  that  there  were  no  border  cells  in  the 
fundus  at  all  ; but  this  has  been  denied  by  Stohr,  Kupffer,  and  Boas. 
The  size  of  border  or  acid  cells  depends  upon  the  stage  of  diges- 
tion ; as  this  function  proceeds,  the  border  cells  increase,  and 
diminish  again  at  the  end  of  digestion.  The  chief,  central,  or  fer- 
ment cells  enlarge  also,  and  become  darker  during  digestion. 
In  a fasting  state  the  chief  cells  are  largely  in  excess.  Heiden- 
hain’s  conclusions,  that  the  chief  or  central  cells  are  producers  of 
the  digestive  ferments,  and  that  the  border  or  anilin-staining  cells 
produce  the  hydrochloric  acid,  have  been  confirmed  by  a number 
of  other  observers  (Griitzner,  von  Swiezicki,  and,  recently,  Sehr- 
wald  and  Mall). 

It  is  known  that  the  glandular  tubules  of  the  pyloric  region  con- 
tain only  chief  or  central  cells  (producing  ferments  only,  and  no 
acid),  while  the  gland  tubules  of  the  fundus  contain  both  central 
cells  and  also  border  or  acid  cells.  Heidenhain  succeeded  in  re- 
moving the  pyloric  portion  of  the  stomach  entirely  in  a number 
of  dogs,  and  uniting  the  organ  with  the  external  abdominal  wall. 
In  other  dogs  he  removed  the  fundus  entirely,  leaving  the  pyloric 
portion  intact,  and  succeeded  in  making  this  altered  stomach  with- 
out a fundus  unite  with  the  external  abdominal  wall. 

He,  therefore,  had  two  kinds  of  operated  animals  with  stomachs 
opening  on  the  abdomen.  After  this,  it  was  found  that  animals  in 
which  the  pyloric  region  was  excised  furnished  a juice  that  con- 
tained both  acid  and  pepsin  ; these  are  therefore  produced  by  the 
glands  of  the  fundus  which  contain  both  varieties  of  secretory 
cells.  In  the  animals  that  had  been  deprived  of  the  fundus  by  ex- 
cision, however,  the  only  secretory  surface  that  was  left  being  the 


24 


HISTOLOGY  OF  THE  STOMACH. 


pyloric  region,  it  was  found  that  an  alkaline  juice  was  secreted  con- 
taining only  ferments.  That  this  juice  did  contain  pepsin  was 
proved  by  its  power  of  digesting  fibrin  when  hydrochloric  acid 
was  added  to  it. 

Now,  as  the  gland  tubules  of  the  pylorus  contain  only  chief  or 
central  cells,  which  do  not  stain  with  anilin,  the  conclusion  seems 
justifiable  that  the  chief  cells  secrete  only  ferments,  and  that  there- 
fore the  border  or  anilin-staining  cells  must  secrete  the  hydrochloric 
acid. 

It  has  been  found  that  the  border  or  acid  cells — called  also  the 
oxyntic  cells — are  in  communication  with  the  central  canal  of  the 
gland  tubule  by  tiny  canaliculi — extensions  from  the  central 
lumen  of  the  gland  to,  or  into,  the  oxyntic  or  acid  cells.  These 
canaliculi  were  brought  out  with  the  silver  stain  by  Golgi. 


CHAPTER  II. 

HISTOLOGY  OF  THE  STOMACH. 

R.  R.  Bensley,  B.A  , M.B.,  has  published  a very  interesting  paper 
on  the  “ Histology  and  Physiology  of  the  Gastric  Glands,”  in  the 
“ Proceedings  of  the  Canadian  Institute,”  1896.  The  work  was 
done  in  the  biological  laboratory  of  the  University  of  Toronto. 
Mr.  Bensley  was  kind  enough  to  present  us  with  four  sketches 
illustrating  the  various  phases  of  secretion  in  the  gland  cells  of 
the  deep  ends  of  the  fundus  glands  of  the  cat’s  stomach.  We 
consider  his  results  a valuable  addition  to  the  work  of  Heidenhain, 
Ebstein,  Langley,  Sewall,  and  others.  We  have,  by  repeating  his 
methods,  assured  ourselves  that  with  staining  as  used  by  him,  it  is 
possible  to  recognize  the  precursory  stages  of  the  ferments  within 
the  structure  of  the  cells.  We  submit  the  drawings,  with  explana- 
tory text.  The  following  are  his  conclusions  : 

“ 1.  During  digestion,  a substance  similar  in  chemical  properties 
to  the  chromatin  of  the  nucleus  makes  its  appearance  in  the  outer 
clear  zone  of  the  chief  cells  of  the  fundus  glands.  This  substance, 
which  may  be  called  prozymogen,  stains  deeply  and  readily  in 
hematoxylin,  and  presents  a characteristic  fibrillated  appearance. 
During  rest  this  prozymogen  is  used  up  in  some  way,  giving  rise 
to  zymogen  granules. 


MUCOSA. 


“ 2.  The  chief  cells  of  the  neck  of  the  glands  do  not  contain  at 
any  period  of  digestion  either  zymogen  or  prozymogen,  but  are 
engaged  in  the  formation  of  a mucinoid  secretion,  which  has  a 
powerful  elective  affinity  for  indulin  and  Bordeaux  red,  and  stains 
metachromatically  in  thionin. 

“ 3.  The  pyloric  gland  cells,  likewise,  form  neither  zymogen  nor 
prozymogen,  and  are  similar  in  structure,  in  staining  properties, 
and  in  the  nature  of  their  secretion,  to  the  cells  of  the  neck  of  the 
fundus  gland. 

“ 4.  The  cells  of  the  pyloric  glands  and  of  the  neck  of  the  fundus 
glands  pass,  by  gradual  transition,  into  the  mucous  cells  of  the 
surface,  to  which  they  are  obviously  closely  allied.” 

From  Mall’s  article  on  the  anatomy  of  the  stomach  (“Johns 
Hopkins  Hospital  Reports,”  vol.  1)  we  have  quoted  the  following 
graphic  description  : 

Mucosa. — That  more  than  one  kind  of  gland  is  present  in  the 
stomach  has  been  repeatedly  noticed  (Wassman,  Frerichs,  Brinton, 
Leydig,  Kolliker),  but  a more  careful  study  of  them  was  delayed 
until  1870  (Heidenhain,  Rollet). 

There  are  two  kinds  of  glands  present  in  the  dog’s  stomach — 
the  pyloric  and  the  peptic.  The  peptic,  in  turn,  are  formed  in  great 
part  of  two  kinds  of  cells — the  border  or  oxyntic  and  the  central 
or  ferment  cells. 

A study  of  descriptions  of  Mall  and  Oppel  shows  that  in  the 
pyloric  region  the  necks  of  the  glands  are  the  longest  (0.68  mm.), 
and  that  they  diminish  in  length  throughout  the  middle  zone  (0.25 
mm.),  until  the  cardiac  portion  is  reached.  In  the  pyloric  por- 
tion, where  the  necks  of  the  glands  are  the  longest,  many  gland 
tubes  empty  into  one  outlet;  in  the  middle  zone  there  are  less,  in 
rough  about  nine,  into  each  gland  mouth  ; while  in  the  cardiac  por- 
tion each  gland  has  a special  opening — in  other  words,  there  are  no 
gland  necks.  In  the  pyloric  portion  the  glands  are  composed 
wholly  of  central  cells.  In  the  central  zone  there  are  many  border 
cells,  the  proportion  to  the  central  cells  being  as  described  by 
Heidenhain  and  his  pupils.  Throughout  the  fundus  are  but  few 
border  cells,  while  around  the  esophagus  there  is  a small  zone  in 
which  there  are  many  border  cells. 

According  to  Mall,  about  1600  gland  tubes  open  within  each 
square  centimeter  of  mucous  membrane  in  the  pyloric  portion,  in 
the  middle  zone  2500,  and  in  the  fundus  4900.  For  an  average 
stomach  there  is  an  area  of  about  28  square  cm.  in  the  pylorus,  108  in 


26 


HISTOLOGY  OF  THE  STOMACH. 


the  middle  zone,  and  120  in  the  cardiac  portion,  or  these  surfaces 
are  to  each  other  as  7 : 27  : 30.  The  estimation  carried  further 
gives  somewhat  over  1,000,000  gland  openings  in  the  stomach. 


Fig.  3. 

Sections  ok  Deep  Ends  of  Fundus  Glands  of  the  Cat  in  Different  Secretive  Phases. 

X 1000  — {Bens  ley.) 

Fig.  i. — From  a fasting  stomach.  The  chief  cells  are  filled  with  large  zymogen  granules; 
nuclei  near  the  outer  ends  of  cells.  Gentian-violet  preparation,  b.  Border  cells. 

Fig.  2.— Six  hours  after  an  abundant  meal  of  raw  flesh.  The  chief  cells  exhibit  two  zones,  the 
inner  occupied  by  large  zymogen  granules,  the  outer  by  a deeply  staining,  obscurely  fibrillar 
element,  prozymogen ; the  nuclei  lie  at  the  junction  of  the  two  zones,  b.  Border  cells,  pr.  Pro- 
zymogen. c.  Mucin  secreting  cell,  similar  to  those  found  in  the  neck  of  the  gland.  Gentian- 
violet  preparation. 

Fig.  3. — Twelve  hours  after  feeding  with  sponge  soaked  in  fat.  Preparation  stained  in  hema- 
toxylin exhibits  a deeply  stained  outer  zone  filled  with  prozymogen,  and  a clear  inner  zone  from 
which  the  granules  have  disappeared  in  course  of  preparation.  The  nuclei  are  now  much  nearer 
to  the  lumen,  b.  Border  cells,  pr.  Prozymogen. 


On  the  other  hand,  if  the  blind  tubes  opposite  the  muscularis 
mucosae  are  estimated,  the  number  exceeds  16,500,000.  In  other 
words,  each  gland  neck  subdivides  sixteen  times,  on  an  average, 


MUCOSA. 


2 7 


before  the  muscularis  mucosae  is  reached.  It  may  be  interesting 
to  note  that  for  each  gland  opening  in  the  stomach  we  have  one 
villus  in  the  intestine,  and  for  each  subdivision  there  is  one  Lieber- 
kiihn’s  crypt. 

The  observations  quoted,  as  well  as  those  of  others,  apparently 
do  not  confirm  Heidenhain’s  statement — i.  e.,  that  “ wherever  we 
have  central  cells  we  have  pepsin.”  Yet  it  seems  true  that  the 
degree  of  acidity  is  in  proportion  to  the  number  of  border  cells 
present  in  any  portion  of  the  stomach,  and  that  there  are  portions 
of  the  stomach  which  do  not  contain  border  cells,  but  yield  pepsin. 
In  general,  the  formation  of  pepsin  is  most  marked  in  those  por- 
tions of  the  stomach  which  produce  most  acid  ; and  this  ought  to 
be  the  case,  for  acid  favors  the  formation  of  pepsin  from  pepsino- 
gen (Podwyssozki,  Langley,  and  Edkins),  and  the  pepsin  seems 
more  or  less  combined  with  acid  (Schiff,  Richet).  We  must,  there- 
fore, conclude  with  Heidenhain  that  the  border  cells  play  a most 
important  part  in  the  formation  of  acid.  Between  the  glands  lie 
the  blood-vessels,  lymphatics,  some  round  cells,  and  the  reticulum. 
In  those  portions  of  the  stomach  in  which  there  is  a “ neck  zone,” 
there  is  a distinct  layer  of  reticulum  fibrils.  In  this  layer  peculiar 
spindle  cells  are  frequently  seen  which  surround  the  gland  openings 
and  appear  much  like  the  subepithelial  cells  in  the  villi  of  the 
intestine.  Under  no  condition  could  a basement  membrane  be 
isolated,  nor  does  Mall  believe  it  exists,  but  instead  there  is  a most 
beautiful  network  of  the  reticulum. 

“ Conclusions. — From  a histological  standpoint  the  mucous 
membrane  of  the  stomach  may  be  divided  into  three  zones — the 
pyloric,  with  no  border  cells;  the  middle,  with  many  border  cells; 
and  the  fundus,  with  but  few  border  cells. 

“ Digestion  of  the  different  portions  of  the  mucous  membrane  with 
weak  HCi  shows  that  the  middle  zone  digests  most  easily,  the 
fundus  less  quickly,  and  the  pyloric,  as  a rule,  not  at  all.  Assum- 
ing that  the  rapidity  of  digestion  of  the  different  portions  is  in 
proportion  to  the  quantity  of  pepsin  present,  it  makes  it  probable 
that  most  pepsin  is  formed  in  the  middle  zone.  Although  it  has 
been  proved  that  pepsin  is  formed  in  glands  which  do  not  contain 
border  cells,  in  general  it  may  be  stated  that  the  amount  of  pepsin 
formed  by  the  different  glands  is  in  proportion  to  the  number  of 
border  cells. 

“ The  degree  of  acidity  of  the  mucous  membrane  is  in  proportion 
to  the  number  of  border  cells  present.  It  is  reasonable  to  suppose 


28 


HISTOLOGY  OF  THE  STOMACH. 


that  the  formation  of  acid  in  any  portion  of  the  stomach  aids 
materially  in  the  formation  of  pepsin  in  the  same  part.  This  is 
very  essential,  because  acid  favors  the  formation  of  pepsin  from 
pepsinogen.  Since  border  cells  are  only  with  the  greatest  diffi- 
culty digested  in  acid,  we  can  not  ascribe  to  them  the  power  to 
secrete  pepsin  ; and  since  the  morphology  of  the  central  cells  varies 
during  digestion  and  rest,  and  they  are  so  easily  digested  upon  the 
addition  of  acid,  we  must  conclude  with  Heidenhain  that  the  former 
are  probably  concerned  in  the  production  of  acid  and  the  latter  in 
the  production  of  pepsin. 

“ When  the  stomach  is  forcibly  distended,  it  is  found  that  the 
dilatation  is  mostly  at  the  expense  of  the  fundus.  This  seems  also 
to  be  the  case  when  the  stomach  is  naturally  filled  with  food. 
Although  the  middle  zone  is  practically  not  stretched  when  the 
stomach  is  filled,  distention  seems  to  favor  circulation  through  this 
part  because  the  blood-vessels  are  more  easily  injected  in  a moder- 
ately distended,  than  in  an  empty,  stomach. 

“ In  the  intestine  it  is  found  that  the  longitudinal  and  circular 
muscle-fibers  are  antagonistic.  In  the  stomach  the  pyloric  valve 
is  closed,  after  the  muscle-cells  are  dead,  by  a fold  of  mucous  mem- 
brane being  thrown  into  the  lumen.  This  may  take  place  in  a 
living  stomach.  A contraction  of  the  circular  muscle  tends  to 
strengthen  this  valve,  while  a contraction  of  the  longitudinal  muscle 
tends  to  weaken  it,  because  with  the  contraction  of  the  longitudinal 
muscle  there  is  always  an  accompanying  relaxation  of  the  circular 
muscle.  Under  ordinary  circumstances  it  seems  as  though  the 
stomach  reduced  its  lumen  by  simultaneous  contraction  of  both 
longitudinal  and  circular  muscle-fibers.  What  complex  motions 
take  place  during  peristalsis  are  absolutely  unknown.  It  is,  how- 
ever, a remarkable  fact  that  a bundle  of  the  circular  fibers  (oblique 
fibers)  are  parallel  with  the  longitudinal  fibers,  which  are  increased 
in  number  in  the  middle  zone.  A solution  of  this  problem  seems 
within  the  range  of  experimentation. 

“ The  celiac  axis  supplies,  besides  the  stomach,  also  the  spleen 
and  the  liver.  With  a given  pressure  within  the  aorta,  variation  in 
the  resistance  in  the  capillaries  of  the  spleen  and  the  liver  will  have 
a marked  effect  upon  the  circulation  through  the  stomach.  The 
portion  of  the  stomach  (middle  zone)  supplied  by  the  gastric  artery 
is  to  a less  extent  under  the  control  of  these  side  influences  than  is 
that  which  is  supplied  by  arteries  arising  from  the  main  branches 
to  the  spleen  and  to  the  liver.  It  must  be  again  stated  that  there 


Three  Sections  of  Stomach-walls  Placed  Side  by  Side  to  Show  the  Positions  of 
Blood-vessels  and  Lymphatics  to  the  Different  Layers. — (F.  Mall , “ Johns 
Hopkins  Hospital  Reports Vol.  I.) 

M.  Mucosa.  M ' . Muscularis  mucosae.  S.  Submucosa.  C and  Z.  Circular  and  longitudinal 
muscles  enlarged  70  times. 


PLATE  11. 


LIBRARY 

OF  THE 

UNWERSITY  of  ILLINOIS. 


MUCOSA.  29 

are,  in  all  probability,  many  other  influences  which  play  most  im- 
portant parts  in  the  distribution  of  blood. 

“ 7.  Around  the  two  curvatures  of  the  stomach  there  is  a com- 
plete circle  of  anastomosis,  which  has  a tendency  to  equalize  the 
pressure  in  the  arteries  penetrating  the  muscle-walls.  But  the 
anastomoses  arising  therefrom  have  only  a tendency  to  make 
gradual  gradations,  and  not  an  equal  pressure  throughout.  The 
additional  set  of  anastomoses  within  the  submucosa  are,  again,  not 
sufficient  to  equalize  the  flow  throughout  the  whole  mucosa. 
After  ligating  arteries,  as  well  as  by  examining  the  mucous  mem- 
brane, during  digestion  and  rest,  it  is  found  that  no  sharp  lines 
can  be  drawn. 

“ 8.  The  blood-vessels  are  arranged  in  such  a manner  that  from 
any  portion  of  the  submucosa  about  one-fourth  of  the  blood  may 
go  to  the  muscle-coats  and  three-fourths  to  the  mucosa.  It  is 
therefore  probable  that  when  the  flow  is  poured  to  one  side  it  is 
diminished  to  the  other,  and  vice  versa.  There  is,  however,  a ten- 
dency to  equalize  this  by  the  submucous  anastomoses. 

“ 9.  Since  there  is  but  one  set  of  arteries  to  the  mucosa,  there 
must  be  but  one  sort  of  circulation,  which  may  vary  in  degree 
only.  Within  the  mucosa  the  arrangement  is  such  that  the  portion 
of  the  gland  which  is  deepest  receives  the  blood  richest  in  O.  The 
mucous  membrane,  omitting  the  muscularis  mucosae,  lies  between 
two  venous  plexuses.  Contraction  of  the  muscle-fibers  between 
the  glands  and  those  of  the  muscularis  mucosae  should  diminish 
the  volume  of  the  mucosa.  This  would  have  a tendency  to  empty 
the  glands,  as  well  as  to  press  blood  from  the  two  venous  plexuses, 
especially  the  lower.  Whether  or  not  there  is  a force  within  the 
mucosa  which  can  augment  the  circulation  seems  at  present  im- 
possible to  determine  by  experiment.  The  arrangement  of  the 
parts  is  very  suggestive. 

“ 10.  The  rich  venous  plexus  of  veins  within  the  submucosa  is 
sufficiently  large  to  hold  a considerable  quantity  of  blood.  This 
must  be  the  case  when  the  valves  within  the  veins  coming  from  the 
stomach  are  temporarily  closed.  When  the  valves  are  closed,  a 
contraction  of  the  circular  muscle  is  sufficient  to  drive  all  the  blood 
from  the  underlying  veins.  It  is  therefore  possible  that  a rhythmical 
contraction  in  any  part  of  the  stomach  may  favor  the  circulation 
through  its  walls. 

“ 1 1 . The  arrangement  of  the  lymphatics  is  much  the  same  as  that 
of  the  veins,  and  the  foregoing  consideration  (10)  applies  equally 
3 


30 


HISTOLOGY  OF  THE  STOMACH. 


well  to  them.  When  we  consider  the  resistance  to  be  overcome 
while  the  lymph  passes  through  so  many  networks  before  the  cis- 
terna  chyli  is  reached,  it  makes  it  plausible  to  state  that  the  circu- 
lation is  favored  by  muscular  contraction. 

“ 12.  Since  the  blood  which  leaves  the  stomach  must  pass 
through  the  capillaries  of  the  liver,  it  is  necessary  that  it  be  con- 
stantly under  a comparatively  high  pressure.  This  pressure  is  also 
dependent  upon  the  spleen  and  the  intestine.  If  the  pressure  is 
high,  a regurgitation  into  the  stomach  is  impossible  on  account  of 
the  presence  of  valves. 

“ 13.  In  a stomach  in  which  the  vessels  are  all  equally  distended 
the  rapidity  of  circulation  in  the  celiac  axis  would  be  263  times 
that  in  the  capillaries.  The  area  of  the  section  of  the  celiac  axis 
is  0.0592  square  cm. ; the  immediate  branches  to  the  stomach,  0.0348 
square  cm. ; to  the  spleen  and  liver,  0.0244  square  cm.  All  the 
capillaries  of  the  stomach:  mucosa,  6.4524  square  cm. ; muscle- 
coats,  2.7214  square  cm.;  total,  9.1738  square  cm.;  9.1738 
0.0348  = 263. 

“ A like  estimation  shows  that  the  rapidity  of  circulation  in  all 
the  capillaries  is  ^3  of  that  in  the  arteries  penetrating  the  muscle- 
walls ; while  if  the  capillaries  of  the  muscle-walls  are  excluded, 
the  rapidity  in  the  capillaries  of  the  mucosa  rises  to 

“ Considering  the  glands  on  an  average  0.05  cm.  long  and  0.003^ 
cm.  in  diameter,  excluding  the  necks,  the  area  of  all  the  glands 
would  be  8671  square  cm.,  or  thirty-eight  times  the  area  of  mucous 
membrane.  A like  estimation  of  the  capillaries,  considering  each 
capillary  0.04  cm.  long,  gives  for  them  a total  area  of  1718  square 
cm.,  or  7J/2  times  the  mucous  surface.  The  secreting  surface  is 
five  times  that  of  the  blood-supply.” 

Vessels  and  Nerves. — The  arteries  supplying  the  stomach  are: 
the  coronaria  ventriculi ; the  pyloric  and  right  gastro-epiploic 
branches  of  the  hepatic  ; the  left  gastro-epiploic  and  vasa  brevia 
from  the  splenic.  They  supply  the  muscular  coat,  ramify  in  the 
submucous  coat,  and  are  finally  distributed  to  the  mucous  mem- 
brane. The  arrangement  of  the  vessels  in  the  mucous  membrane 
is  somewhat  peculiar.  The  arteries  break  up  at  the  base  of  the 
gastric  tubules  into  a plexus  of  fine  capillaries  which  run  upward 
between  the  tubules,  anastomosing  with  one  another  and  ending  in 
a plexus  of  large  capillaries  which  surround  the  mouths  of  the 
tubes,  and  also  form  hexagonal  meshes  around  the  alveoli.  (See 
Plate  II.)  The  veins  arise  from  the  latter,  and  pursue  a straight 


THE  SMALL  INTESTINE.  3 I 

course  back  to  the  submucous  tissue,  between  the  tubules,  to 
terminate  in  the  splenic  and  portal  veins. 

The  lymphatics  are  abundant,  and  may  be  divided  into  a super- 
ficial and  a deep  set,  which  pass  through  the  lymphatic  glands  found 
along  the  two  curvatures.  The  nerves  are  supplied  from  the  right 
and  left  pneumogastric,  and  numerous  branches  from  the  abdomi- 
nal sympathetics.  (Solar  plexus.) 


CHAPTER  III. 

THE  SMALL  INTESTINE. 

The  small  intestine  commences  at  the  pylorus,  and  after  many 
convolutions  terminates  in  the  large  intestine.  It  measures,  on  an 
average,  about  twenty-two  feet  in  length  in  an  adult,  and  becomes 
gradually  narrower  from  its  upper  to  its  lower  end.  Its  convolu- 
tions occupy  the  middle  and  lower  parts  of  the  abdomen,  fre- 
quently descending  into  the  pelvis. 

The  small  intestine  is  divided  into  three  portions,  which  have  re- 
ceived different  names  : The  first  ten  to  twelve  inches  immediately 
succeeding  the  stomach,  and  comprising  the  widest  and  most  fixed 
part  of  the  tube,  are  called  the  duodenum.  This  part  is  further 
distinguished  by  its  close  relation  to  the  head  of  the  pancreas,  and 
by  the  absence  of  a mesentery.  The  remainder,  which  is  arbitrarily 
divided  into  an  upper  two-fifths,  called  the  jejunum,  and  a lower 
three-fifths,  called  the  ileum,  is  very  convoluted  and  movable,  being 
connected  with  the  posterior  abdominal  wall  by  a long  and  exten- 
sive fold  of  peritoneum  called  the  mesentery,  and  by  numerous 
blood-vessels  and  nerves.  Although  there  is  no  distinct  line  of  de- 
marcation between  the  jejunum  and  the  ileum,  yet  that  portion  of 
the  small  intestine  included  under  these  two  names  gradually  un- 
dergoes certain  changes  in  structure  and  appearance  from  above 
downward,  so  that  the  upper  end  of  the  jejunum  can  readily  be  dis- 
tinguished from  the  lower  end  of  the  ileum. 

Structure  of  the  Small  Intestine. — The  small  intestine,  like 
the  stomach,  is  composed  of  four  coats — viz. : the  serous  or  peri- 
toneal, the  muscular,  the  areolar,  and  the  mucous. 

The  external,  or  serous,  coat  almost  entirely  surrounds  the  intes- 


32 


THE  SMALL  INTESTINE. 


tinal  tube  in  the  whole  extent  of  jejunum  and  ileum,  leaving  only  a 
narrow  interval  behind,  where  it  passes  off  and  becomes  continuous 
with  the  two  layers  of  the  mesentery.  The  line  at  which  this  takes 
place  is  named  the  attached  or  mesenteric  border  of  the  intestine. 
The  duodenum,  on  the  other  hand,  is  but  partially  covered  by  the 
peritoneum.  The  muscular  coat  consists  of  two  layers  of  fibers — an 
outer  longitudinal,  arid  an  inner,  or  circular,  set.  The  longitudinal 
fibers  constitute  an  entire  but  comparatively  thin  layer,  and  are 
most  obvious  along  the  free  border  of  the  intestine.  The  circular 
layer  is  thicker  and  more  distinct. 

The  muscular  tunic  becomes  gradually  thinner  toward  the  lower 
part  of  the  small  intestine.  It  is  pale  in  color,  and  is  composed  of 
plain  muscular  tissue,  the  cells  of  which  are  of  considerable  length. 

The  progressive  contraction  of  these  fibers,  commencing  at  any 
part  of  the  intestine  and  advancing  in  a downward  direction,  pro- 
duces the  peculiar  vermicular,  or  peristaltic,  movement  by  which  the 
contents  are  forced  onward  through  the  canal.  In  the  narrowing 
of  the  tube  the  circular  fibers  are  mainly  concerned,  the  longitudinal 
fibers  tending  to  produce  dilatation  (Exner) ; and  those  found  along 
the  free  border  of  the  intestine  may  have  the  effect  of  straightening 
or  unfolding  its  successive  convolutions.  There  is  a gangliated 
plexus  of  nerve-fibers  and  a network  of  lymphatic  vessels  betweeen 
the  two  muscular  layers. 

The  submucous  coat  of  the  small  intestine  is  a layer  of  areolar 
tissue  of  a loose  texture,  which  is  connected  more  firmly  with  the 
mucous  than  with  the  muscular  coat.  Within  it  the  blood-vessels 
ramify  before  passing  to  the  mucous  membrane,  and  it  contains  a 
gangliated  plexus  of  nerve-fibers  and  a network  of  large  lymphatic 
vessels. 

The  internal  coat,  or  mucous  membrane,  is  characterized  by  the  * 
finely  flocculent,  or  shaggy  appearance  of  its  inner  surface,  resem- 
bling the  pile  upon  velvet.  This  appearance  is  due  to  the  surface 
being  thickly  covered  with  minute  processes,  named  villi.  It  is  one 
of  the  most  vascufar  membranes  in  the  body,  and  is  naturally  of  a 
reddish  color  in  the  upper  part  of  the  small  intestine,  but  is  paler, 
and  at  the  same  time  thinner,  toward  the  lower  end.  It  is  lined 
with  columnar  epithelium  throughout  its  whole  extent,  and,  next  to 
the  submucous  coat,  is  bounded  by  a layer  of  plain  muscular  tissue 
(muscularis  mucosae) ; between  this  and  the  epithelium  the  substance 
of  the  membrane,  apart  from  the  tubular  glands,  which  will  be  after- 
ward described,  consists  mainly  of  retiform  tissue,  which  supports 


VALVUL/E  CONNIVENTES.  33 

the  blood-vessels,  nerves,  lymphatics,  and  lacteals,  and  incloses  in  its 
meshes  numerous  lymph-corpuscles. 

Valvulse  Conniventes. — The  mucous  membrane,  in  addition  to 
small  efifaceable  folds,  or  rugae,  possesses  also  permanent  folds, 
which  can  not  be  obliterated,  even  when  the  tube  is  forcibly  dis- 
tended. These  permanent  folds  are  the  valvulae  conniventes,  or 
valves  of  Kerkring.  They  are  crescentic  projections  of  the  mucous 
membrane,  placed  transversely  to  the  axis  of  the  bowel,  and  follow- 
ing one  another  closely.  The  majority  of  the  folds  do  not  extend 
more  than  one-half  or  two-thirds  around  the  interior  of  the  tube, 
but  it  has  been  shown  by  Brooks  and  Kazzander  that  some  form 
complete  circles,  and  others  spirals.  The  spiral  forms  may  occur 
singly  or  in  groups  of  two  or  three.  They  generally  extend  a little 
more  than  once  around  the  lumen  of  the  bowel,  but  in  rare  cases 
may  go  around  two  or  three  times.  At  their  highest  point  they 
project  inward  for  about  of  an  inch.  Some  of  the  valvulae  con- 
niventes are  bifurcated  at  one  or  both  ends,  and  others  terminate 
abruptly.  Each  consists  of  a fold  of  mucous  membrane — that  is,  of 
two  layers  placed  back  to  back,  and  united  by  submucous  areolar 
tissue.  They  contain  no  part  of  the  circular  or  longitudinal  mus- 
cular coats.  Being  extensions  of  the  mucous  membrane,  they 
serve  to  increase  the  absorbent  surface  to  which  the  food  is  exposed. 

The  valvulse  conniventes  are  not  uniformly  distributed  over  the 
various  parts  of  the  small  intestine.  There  are  none  just  at  the 
commencement  of  the  duodenum  : a short  distance  from  the  pylorus 
they  begin  to  appear  ; beyond  the  point  at  which  the  bile  and  pan- 
creatic juice  are  poured  into  the  duodenum  they  are  very  large, 
regularly  crescentic  in  form,  and  placed  so  near  to  one  another  that 
the  intervals  between  them  are  not  greater  than  the  breadth  of  the 
valves  ; they  continue  thus  through  the  rest  of  the  duodenum,  and 
along  the  upper  half  of  the  jejunum.  Below  that  point  they  begin 
to  get  smaller  and  further  apart,  and,  finally,  toward  the  middle  or 
lower  end  of  the  ileum,  having  gradually  become  more  irregular 
and  distinct,  sometimes  even  acquiring  a very  oblique  direction, 
they  disappear  altogether. 

The  villi,  peculiar  to  the  small  intestine,  and  giving  to  its  inter- 
nal surface  the  velvety  appearance  already  spoken  of,  are  small  pro- 
cesses of  the  mucous  membrane,  which  are  closely  set  on  every 
part  of  the  inner  surface  over  the  valvulae  conniventes,  as  well  as 
between  them.  Their  length  varies  from  0.5  mm.  to  0.7  mm.,  or 
sometimes  more. 


34 


THE  SMALL  INTESTINE. 


They  are  largest  and  most  numerous  in  the  duodenum  and  jeju- 
num, and  become  gradually  smaller  and  fewer  in  number  in  the 
ileum.  According  to  Rauber,  they  are  short  and  leaf-shaped  in  the 
duodenum,  and  as  the  gut  is  followed  downward,  they  become 
gradually  longer  and  thinner,  so  that  they  are  tongue-shaped  in  the 
jejunum  and  filiform  in  the  ileum.  Occasionally,  two  or  three  are 
connected  at  their  bases.  In  the  upper  part  of  the  small  intestine 
there  are  from  io  to  18  villi  in  a square  millimeter,  and  in  the  ileum 
from  8 to  14  in  the  same  space.  This  would  give  about  4,000,000 
altogether  (Krause). 

A villus  consists  of  a prolongation  of  the  mucous  membrane 
proper.  It  is  covered  by  columnar  epithelium,  and  incloses  a net- 
work of  blood-vessels,  one  or  more  lymphatic  vessels  (lacteals),  and 
a few  longitudinal,  plain,  muscular  fiber-cells,  these  being  all  sup- 
ported and  held  together  by  retiform  lymphoid  tissue. 

Under  the  epithelium  is  a basement  membrane  composed  of 
flattened  cells  which,  on  the  one  hand,  are  connected  with  the 
branched  cells  of  the  retiform  tissue,  and,  on  the  other  hand,  send 
processes  between  the  epithelial  cells.  Nervous  fibrils  penetrate 
into  the  villi  from  the  plexus  of  Meissner,  and  form  arborizations 
throughout  their  whole  substance. 

Each  villus  receives,  as  a rule,  one  small  arterial  twig,  which  runs 
from  the  submucous  coat  through  the  muscularis  mucosae  to  the 
base  of  the  villus,  and  then  up  the  center  to  near  the  middle  line  of 
the  villus,  where  it  begins  to  break  up  into  a number  of  capillaries. 

These  form,  near  the  surface,  a fine  capillary  network  beneath 
the  epithelium  and  limiting  membrane,  from  which  the  blood  is 
returned,  for  the  most  part,  by  one  or  two  venules  which,  in  man, 
commence  near  the  tip  of  the  villus,  and  pass  down  to  its  base  to 
join  the  venous  plexus  of  the  mucous  membrane,  whence  the  blood 
is  conveyed  to  the  large  veins  of  the  submucosa. 

The  lacteal  lies  in  the  center  of  the  villus,  and,  in  the  smaller 
villi,  is  usually  a single  vessel  with  a closed  and  somewhat  expanded 
extremity,  and  of  considerably  larger  diameter  than  the  capillaries 
of  the  blood-vessels  around.  In  the  human  subject  there  are  never 
more  than  two  intercommunicating  lacteals  in  a single  villus. 

The  lacteals  in  the  villi  are  bounded  by  a delicate  layer  of  flat- 
tened epithelial  cells ; these  are  connected  with  the  branched  cells 
of  the  tissue  of  the  villus,  and  these  again  with  the  flattened 
cells  forming  the  basement  membrane ; from  the  latter,  pro- 
longations extend  between  the  epithelial  cells  toward  the  surface. 


THE  VILLI. 


35 


Briicke  first  discovered  the  muscular  tissue  within  the  villus,  con- 
sisting of  unstriated,  plain  fiber-cells,  disposed  longitudinally  around 
the  lacteal.  These  fibers  are  prolongations  of  the  muscularis 
mucosae. 

When  they  are  stimulated  in  animals,  a very  evident  retraction 
of  the  villus  is  observable. 

The  fiber-cells  at  the  sides  and  toward  the  end  of  the  villus  pass 
from  the  lacteal  to  be  attached  to  the  basement  membrane  in  a 
bifurcating  manner. 

Columnar  epithelial  cells  cover  not  only  the  villi,  but  also  the 
rest  of  the  surface  of  the  small  intestine,  and  extend  into  the  tubular 
glands.  There  is  never  any  continuity  between  the  extremity  that 
is  attached  to  the  basement  membrane  and  the  branched  corpuscles 
of  the  retiform  tissue  of  the  villus.  This  epithelium  separates  easily 
from  the  subjacent  tissue.  Between  the  cells  composing  it  is  a 
variable  number  of  leukocytes,  most  numerous  in  the  lower  part  of 
the  intestines  near  the  lymphoid  follicles.  Occasionally,  they  are 
seen  to  be  free  in  small  lymph-spaces  between  the  columnar  epi- 
thelial cells  and  showing  indications  of  karyokinesis.  Hardy 
declares  that  immediately  below  the  columnar  epithelium  of  the 
villi  there  is  frequently  a well-marked  layer  of  cells  that  stain 
readily  with  eosin.  Hence  he  calls  these  cells  eosinophilic. 

Among  the  ordinary  epithelial  cells  of  the  villus  are  others,  the 
outer  half  of  which  is  filled  with  mucigen,  and  at  times  beaker- 
or  cup-shaped  empty  cells  are  observed  from  which  this  has 
been  discharged  as  mucus,  the  free  end  being  ruptured;  these  are 
sometimes  called  the  goblet-cells.  The  number  of  cells  containing 
mucus  varies  much  in  different  animals  and  under  different  condi- 
tions in  the  same  animal.  There  are  comparatively  few  mucous 
cells  in  the  glands  of  the  small  intestine. 

The  epithelial  cells  are,  as  far  as  can  be  ascertained,  the  principal 
agents  in  promoting  the  absorption  of  food  materials  from  the 
interior  of  the  gut,  and  the  seat  of  the  retrograde  processes  of 
metabolism  which  the  products  of  digestion  undergo  during 
absorption.  Peptone,  when  injected  into  the  blood  of  an  animal 
by  whose  gastric  juice  it  has  been  formed,  acts  as  a poison.  It  is 
due  to  these  epithelial  cells  of  the  intestine  that  peptone  is  so 
modified  during  absorption  that  it  becomes  of  use  to  the  organism. 

Most  food  particles  can  not  be  traced  in  microscopic  specimens, 
but  fatty  or  oily  substances,  from  their  property  of  becoming 
stained  with  osmic  acid,  can  be  followed  out  to  some  extent.  The 


36 


THE  SMALL  INTESTINE. 


examination  of  such  specimens,  taken  during  digestion  of  a meal 
containing  fat,  shows  the  epithelial  cells  turbid  with  oil  droplets  in 
their  interior;  and  in  some  animals,  at  a subsequent  stage, ameboid 
cells  appear  within  the  tissue  of  the  villus  pervaded  with  similar 
but  finer  fatty  particles,  and  eventually  the  central  lacteal  becomes 
filled  with  these.  It  is  probable  that  these  ameboid  lymph-corpus- 
cles, appearing  so  abundantly  within  the  villus  and  among  the  epi- 
thelial cells  on  its  surface,  play  an  important  part  in  the  transfer- 
ence of  such  particles  from  the  epithelial  cells  in  the  lacteal ; for 
at  certain  stages  of  fat  absorption  they  contain  abundant  fatty  par- 
ticles. Recent  investigations  point  to  the  absorption  of  the  larger 
portion  of  fats  in  form  of  fatty  acids  and  soaps.  The  present  state 
of  our  knowledge  on  the  subject  of  the  emulsion  and  solution 
theories  of  fat-absorption  is,  in  the  author’s  opinion,  by  no  means 
sufficiently  matured  to  justify  a scientific  conclusion  in  favor  of 
either  hypothesis  to  the  exclusion  of  the  other.  The  large  amount 
of  lymphoid  tissue  in  the  lower  part  of  the  small  intestine  seems 
to  be  related  to  a greater  power  of  absorption  in  that  part. 

In  the  transference  of  carbon  particles  in  the  lungs,  from  the 
interior  of  the  alveoli  into  the  lymphatics,  which  at  least  in  part  is 
due  to  the  action  of  ameboid  cells,  we  have  an  analogous  process. 

Glands. — Two  kinds  of  true  secreting  glands  are  found  in  the 
intestine ; these  are  : (i)  the  glands  or  crypts  of  Lieberkiihn  and  (2) 
the  glands  of  Brunner.  In  addition  to  these,  there  are  found  also 
two  varieties  of  intestinal  lymph-follicles,  (1)  the  solitary  and  (2) 
the  agminate  glands,  the  latter  often  designated  as  Peyer’s  patches. 

Although  the  solitary  and  agminated  lymph-follicles  have  no 
ducts  opening  upon  the  inner  intestinal  surfaces,  like  Brunner’s 
and  Lieberkuhn’s  glands,  they  are  nevertheless  spoken  of  as 
glands. 

The  follicles,  crypts,  or  glands  of  Lieberkiihn  are  tubular  pits 
lined  by  columnar  epithelium,  occurring  between  the  villi.  Here 
and  there  in  these  crypts,  goblet-cells  occur  in  the  epithelium. 
They  are  present  throughout  the  large  and  small  intestine,  and 
extend  through  the  entire  depth  of  the  mucosa,  their  ends 
approaching  the  muscularis  mucosse. 

The  duodenum  possesses  an  additional  layer  of  true  secreting 
structures  in  the  glands  of  Brunner.  They  would  appear  to  rep- 
resent the  direct  continuations  and  higher  specializations  of  the 
pyloric  glands.  In  passing  from  the  stomach  into  the  intestines, 
these  tubules  undergo  repeated  division,  at  the  same  time  sinking 


THE  BLOOD-VESSELS  OF  THE  INTESTINES.  37 

deeper  into  the  mucosa,  finally  reaching  below  this  layer  to  take 
up  a position  within  the  submucosa  of  the  duodenum,  underneath 
the  overlying  layer  of  the  crypts  of  Lieberkuhn,  which  are  con- 
tained in  the  mucosa  proper.  Brunner’s  glands  belong  to  the  race- 
mose type,  and  under  the  microscope  they  consist  of  a number  of 
tubular  alveoli  connected  by  terminal  ramifications  of  the  duct 
which  penetrates  the  muscularis  mucosae,  and  opens  either  between 
the  mouths  of  the  Lieberkuhn  crypts  or  sometimes  into  their 
bases. 

The  solitary  glands  are  isolated  lymph-follicles  scattered  through 
the  entire  intestine,  most  abundant  in  the  lower  ileum.  Situated  in 
the  mucosa,  at  times  in  the  submucosa,  the  lymphoid  tissue  in  them 
is  denser  toward  the  periphery,  but  is  everywhere  so  closely 
packed  that  the  supporting  reticulum  of  connective  tissue  is 
masked. 

The  agminated  glands,  or  Peyer’s  patches,  are  large,  oval  aggre- 
gations of  lymph-follicles  held  together  by  diffuse  adenoid  tissue, 
limited  to  the  lower  two-thirds  of  the  small  intestine.  Develop- 
ment of  these  is  most  perfect  in  the  ileum ; appearing  first  within 
the  mucosa,  they  later  encroach  upon  the  submucous  tissue. 

Where  the  summits  of  these  follicles  impinge  against  the  inner 
layer  of  the  mucosa,  the  position  of  the  agminated  glands  is  indi- 
cated by  an  elevation  corresponding  to  them  on  the  mucous  sur- 
face. In  that  case  the  villi  are  frequently  pushed  aside. 

The  Blood-vessels  of  the  Intestines. — The  vessels  follow 
the  general  arrangement  of  those  in  the  stomach,  the  larger  ones 
piercing  the  serous  and  muscular  coat,  giving  off  slender  twigs  to 
supply  these  tunics,  and  when  they  enter  the  submucosa,  the 
vessels  form  a wide-meshed  network.  Many  branches  then  pass 
through  the  muscularis  mucosae,  to  be  distributed  to  the  deeper,  as 
well  as  the  superficial,  part  of  the  mucosa.  Around  the  tubular 
glands  a network  is  formed  by  narrow  capillaries,  and  just  beneath 
the  epithelium  the  capillaries  become  wider  and  encircle  the  mouths 
of  the  follicles.  From  this  superficial  capillary  network  the  veins 
arise,  and,  passing  down  between  the  follicles,  join  the  deeper 
venous  plexus,  this  in  turn  communicating  with  the  larger  veins  of 
the  submucosa. 

The  villi  have  special  additional  arteries  running  to  their  bases, 
expanding  into  capillaries,  and  then  extending  beneath  the  epithe- 
lium and  around  the  central  lacteals  as  far  as  the  ends  of  the  villi. 
These  capillaries  terminate  in  venous  stems  which  descend  almost 


38 


THE  SMALL  INTESTINE. 


perpendicularly  into  the  mucosa,  in  their  course  receiving  the 
superficial  capillaries  encircling  the  gland-ducts.  Brunner’s  glands, 
and  the  solitary  and  agminated  follicles,  are  supplied  from  the  sub- 
mucosa by  vessels  terminating  in  capillary  networks  distributed  to 
the  acini  of  the  glands  and  interior  of  the  lymph-follicles. 

The  blood-vessels  of  the  intestines,  taken  as  a whole,  constitute 
a mighty  vascular  territory  which  is  capable  of  taking  up  one-third 
of  the  total  amount  of  blood  of  the  body. 

The  arteries  are  all  branches  of  the  superior  and  inferior  mesen- 
teric arteries,  which  run  along  and  approach  the  gut  in  the  mesen- 
tery. The  intestinal  veins  form  the  principal  portion  of  the  portal 
system. 

Lymph-vessels. — The  beginning  of  the  lymph-vessels  can  be 
traced  to  the  lacteals  within  the  villi,  where  they  begin  as  tiny, 
blind  pouches  at  the  apex  of  the  villus.  In  some  broad  villi  there 
are  two  such  lymph-vessels  that  anastomose  with  each  other. 
From  here  they  run  down  in  the  septa  between  the  glands  in  the 
lymph-vessel  meshwork  over  the  muscularis  mucosae.  Here  they 
again  anastomose  with  an  outer  lymph-vessel  network  in  the 
submucosa.  Here  the  lymphatics  begin  to  be  provided  with 
valves. 

The  nerves  of  the  intestine,  like  those  of  the  stomach,  originate 
chiefly  from  the  mesenteric  plexus,  which  is  formed  by  branches 
from  the  celiac  plexus,  the  semilunar  ganglion,  and  vagus  nerve, 
consisting  of  medullated  and  non-medullated  fibers  that  begin  to 
form  an  abundant  network  under  the  peritoneum  of  the  intestine, 
then  penetrate  the  longitudinal  muscular  stratum,  and  between  this 
and  the  circular  layer  form  a peculiar  plexus  with  numerous  micro- 
scopical ganglia,  constituting  the  plexus  of  Auerbach. 

In  the  submucosa  a similar  network  of  fibers  and  ganglia  has 
been  termed  Meissner’s  plexus.  From  Meissner’s  plexus  very  fine 
fibers  are  spun  about  the  Lieberkiihn  crypts,  villi,  and  limiting 
membrane. 

Relations  of  the  Duodenum. — This  part  of  the  gut  in  the  adult 
is  horseshoe-shaped,  generally  presenting  well-marked  angles, 
which  divide  it  into  four  parts  having  four  distinct  directions;  these 
are:  (i)  The  horizontal  or  superior  part,  running  backward  from 
the  pylorus,  to  the  right,  in  contact  with  the  quadrate  lobe  of  the 
liver,  to  the  under  side  of  the  neck  of  the  gall-bladder,  where  it 
curves  sharply  downward  to  join  the  second  part.  This  first  or 
horizontal  part  is  about  two  inches  long  when  the  stomach  is 


RELATIONS  OF  THE  DUODENUM. 


39 


empty.  (2)  The  second  or  descending  portion  is  about  three  inches 
long,  and  commences  just  below  the  neck  of  the  gall-bladder  oppo- 
site the  right  side  of  the  first  lumbar  veretebra,  and  passes  down  to 
the  level  of  the  third  or  fourth  lumbar  vertebra,  where  it  turns 
sharply  inward  to  join  the  third  part.  (3)  The  third  or  transverse 
portion  is  from  two  to  three  inches  long  ; beginning  at  the  right 
of  the  third  or  fourth  lumbar  vertebra,  it  crosses  over  to  the  left 
side  with  a slight  upward  inclination,  and  ends  to  the  left  of  the 
aorta  by  curving  upward  to  join  the  terminal,  (4)  fourth,  or  ascend- 


A 


Fig.  4.— Plaster  Casts  of  Duodenum  of  Infant  and  Adult.— {From  Museum  of  Harvard 
University .) 

A.  Infant  duodenum.  B.  Adult.  V.  Valvulae  conniventes.  P.  Pylorus. 


ing,  portion,  which  is  about  two  inches  long ; it  passes  upward  to 
the  left  side  of  the  aorta,  as  high  as  the  upper  border  of  the  second 
lumbar  vertebra ; here  it  turns  abruptly  forward  to  join  the  jeju- 
num, forming  the  duodenojejunal  flexure. 

Thus  the  end  of  the  duodenum  is  brought  to  the  same  level  as 
the  beginning.  It  has  been  compared  to  a water-trap,  its  ends 
being  always  higher  than  its  middle,  which  is  thus  fitted  to  retain 
the  fluid  poured  into  it  from  the  liver,  pancreas,  and  its  own  glands, 
besides  that  which  it  receives  from  the  stomach,  at  the  same  time 


40 


THE  SMALL  INTESTINE. 


preventing  the  regurgitation  of  gases  from  the  jejunum  into  the 
pyloric  part  of  the  duodenum  and  stomach. 

Jejunum  and  Ileum. — The  upper  two-fifths  of  the  remaining 
intestine  immediately  following  the  duodenum  are  called  the 
jejunum  ; the  lower  three-fifths,  the  ileum.  Both  are  attached  to 
the  posterior  abdominal  wall  by  an  extensive  fold  of  peritoneum, 
— the  mesentery. 

The  jejunum  lies  above  and  to  the  left  of  the  ileum,  but  the  coils 
are  so  irregular  that  the  position  of  any  individual  loop  affords  but 
little  clue  to  the  part  of  the  intestine  to  which  it  belongs. 

The  large  intestine  consists  of  the  cecum,  the  colon,  and  the 
rectum.  The  colon  is  subdivided,  according  to  the  directions  it 
takes,  into  four  parts,  which  are  (i)  the  ascending,  (2)  transverse, 
(3)  descending,  and  (4)  sigmoid  colon  or  flexure. 

The  end  of  the  ileum,  which  rises  out  of  the  pelvis  to  the  right 
iliac  fossa,  is  not  inserted  into  the  beginning  of  the  large  intestine, 
but  above  the  beginning  and  at  the  side  of  it.  The  part  of  the 
large  intestine  below  this  insertion  is  a blind  pouch, — the  cecum. 
From  the  inner  and  back  part  of  the  cecum,  a little  below  the  ileo- 
colic opening,  a narrow,  round,  worm-like  process,  about  two  or 
three  inches  long,  is  given  off, — the  vermiform  appendix. 

The  cecum  continues  upward  into  the  ascending  colon,  which 
rises  up  in  front  of  the  right  kidney  to  the  edge  of  the  liver;  then 
this  same  large  intestine  passes  beneath  the  greater  curvature  of  the 
stomach,  and  horizontally  across  to  the  left  side,  as  the  transverse 
colon ; here,  at  the  lower  border  of  the  spleen,  it  turns  downward 
as  the  descending  colon. 

This  large  gut  describes  two  right-angled  curves,  the  right  and 
left  colonic  flexures  fixed  by  the  hepatocolic  and  gastrocolic  liga- 
ments respectively.  The  descending  colon  continues  into  the 
sigmoid  colon  or  flexure,  which  connects  it  with  the  rectum.  The 
rectum,  following  the  curves  of  the  sacroiliac  symphysis  and  the 
hollow  of  the  sacrum,  has  itself  two  curves : an  upper  larger  curve, 
concave  anteriorly,  and  a lower  smaller  curve,  convex  anteriorly. 

Only  the  cecum,  transverse  colon,  and  sigmoid  colon  have  a com- 
plete peritoneal  covering ; the  rest  of  the  large  gut  is  only  covered 
anteriorly.  From  the  third  sacral  vertebra  on,  the  rectum  has  no 
peritoneum.  Those  parts  having  no  complete  peritoneum,  therefore, 
have  no  mesentery,  and  are  not  very  movable.  The  longitudinal 
fibers  are  contracted,  or  narrowed  down  to  three  parallel  bands 
(Fasciae  teniae,  or  ligamenta  coli).  One  of  these  bands  runs  along 


FOOD  SUBSTANCES. 


41 


the  attachment  of  the  gastrocolic  ligament  on  the  transverse  colon 
(fascia  omentalis),  the  second  along  the  mesenteric  border,  and  the 
third  is  free. 

Running  down  into  the  rectum  these  bands  become  so  broad 
that  they  occupy  the  entire  periphery  of  the  tube.  These  longi- 
tudinal bands  being  shorter  than  the  other  layers  of  the  wall  of  the 
colon,  they  bring  about  the  characteristic  sacculation  of  the  large 
intestine.  In  the  lower  part  of  the  rectum  the  circular  muscular 
layer  becomes  thickened  to  form  the  internal  anal  sphincter  of  in- 
voluntary fibers. 

The  external  sphincter  is  composed  of  striated  voluntary  muscle- 
fibers.  The  histology  of  the  large  intestine  differs  from  that  of  the 
small  by  the  absence  of  the  villi  and  the  larger  size  of  the  crypts 
and  follicles.  Several  longitudinal  elevations  over  the  anus  are 
called  the  columns  of  Morgagni ; from  this  point  downward  the 
cylindrical  epithelium  ceases  to  exist  and  flat  pavement  epithelium 
takes  its  place. 


CHAPTER  IV. 

PHYSIOLOGY  OF  DIGESTION. 

Food  Substances. — The  simple  chemical  elements  of  the  various 
food  substances,  namely,  C,  H,  N,  S,  and  P,  are  not  assimilable  as 
such,  because  the  human  body  is  not  capable  of  constructing  higher 
compounds  from  them.  It  is  compelled  to  take  in  these  com- 
pounds in  the  form  of  proteid  or  albuminous  substances,  carbohy- 
drates, and  fats,  together  with  such  inorganic  bodies  as  water 
and  salts. 

.Even  these  food-stuffs,  which  are  essential  for  the  maintenance 
and  development  of  the  organism,  are  not  ingested  as  such,  but  are 
contained,  together  with  innutritious  materials,  in  the  various 
articles  of  diet  which  we  derive  from  the  animal  and  vegetable 
kingdoms. 

The  innutritious  admixtures  of  the  food  substances  are  not 
harmful,  but  are  important  as  stimulants  to  the  intestinal  mucosa 
and  to  the  evacuation  of  feces.  Among  these  innutritious  sub- 
stances are  classed  the  connective  tissue,  cartilages  and  tendons 
of  meat,  and  the  cellulose  of  plants. 


42 


PHYSIOLOGY  OF  DIGESTION. 


Water  plays  a most  important  role  in  the  economy  of  the  body, 
for  it  goes  to  make  up  sixty  per  cent,  of  the  total  organism.  We  lose 
about  2 y2  liters  of  water  in  twenty-four  hours,  through  insensible 
perspiration,  secretion,  and  defecation.  About  300-400  gm.  of 
water  are  formed  by  oxidations  of  food  substances  in  twenty-four 
hours;  so  we  have  a deficit  of  1500-1600  gm.,  which  must  be 
supplied  by  the  daily  consumption  of  a corresponding  amount  of 
water;  this  is  done  principally  by  the  drinking  of  water  after  we 
have  taken  in  part  of  it  by  our  foods,  or  in  the  shape  of  beverages 
(soups,  milk,  fruits,  vegetables,  potatoes,  beer,  wine,  coffee,  tea, 
etc.). 

In  mineral  substances  we  must  supply  the  daily  loss  of  sodium 
chlorid  and  other  salts,  particularly  compounds  of  iron.  These  are 
normally  introduced  in  sufficient  quantities  in  food  and  drink. 

The  chief  constituents  of  food — albuminous  bodies,  fats,  and 
carbohydrates — are  of  organic  nature.  The  proteids,  or  albuminous 
bodies,  and  the  fats,  are  derived  partly  from  the  animal  and  partly 
from  the  vegetable  kingdom.  The  carbohydrates  are  almost  exclu- 
sively derived  from  the  vegetable  kingdom.  The  former  serve  for 
the  building  up  of  the  organism,  and  the  continuance  of  life  pro- 
cesses. The  latter  are  the  prevailing  sources  of  heat  and  force;  in 
the  process  of  oxidation  they  finally  reach  the  stages  of  H2C03 
and  H20. 

In  addition  to  these,  a number  of  other  substances  occur  in  the 
food  that  are  oxidized,  and  might  serve  as  sources  of  energy  ; these 
are  the  nitrogen-free  vegetable  acids,  the  amido- acids,  and  alcohol, 
for  instance ; quantitatively,  however,  they  are  not  important. 

Other  organic  bodies  that  are  contained  in  food  materials  as 
normal  constituents,  such  as  creatin  in  meat,  glucosids,  alkaloids, 
and  ethereal  oils  in  vegetables  and  spices,  pass  through  the  body 
without  being  oxidized  or  assimilated ; they  are  not  foods,  as  they 
do  not  enter  the  metabolism  of  the  body,  nor  do  they  develop 
energy  by  chemical  transformation.  However,  a number  of  these 
are  of  importance  in  nutrition,  as  they  render  the  food  more  palat- 
able, and  stimulate  the  secretions  and  the  motility  of  the  digestive 
tract. 

It  has  been  said  that  the  elements  S,  P,  Cl,  K,  Na,  Ca,  Fe,  Mg 
are  not  food  materials,  but  it  must  not  be  understood  that  they  are 
entirely  useless.  They  are  of  some  significance  in  the  construction 
of  tissue,  although  the  organism  can  derive  no  energy  from  them, 
as  they  are  always  taken  in  a highly  oxidized  state,  and  leave  in 


CALORIC  VALUES.  43 

the  same  condition.  Nevertheless,  the  body  will  suffer  if  any  one 
of  these  elements  be  excluded  from  the  food. 

A certain  minimum  of  these  elements — the  amount  has  not  yet 
been  ascertained — is  absolutely  necessary.  Outside  of  the  sub- 
stances named,  the  food  contains,  as  previously  stated,  a number 
of  materials  that  are  not  at  all  absorbable  or  digestible,  and  leave 
the  digestive  tract  in  an  unchanged  form  ; this  is  the  slag  and 
dross  of  the  food,  and  is  taken  into  the  body  principally  with 
vegetables. 

The  normal  adult  human  organism  daily  loses  by  its  metabo- 
lism 120  gm.  of  albuminous  or  proteid  bodies,  80  gm.  fat,  400  gm. 
carbohydrates,  25  gm.  salts,  and  2 y2  liters  of  water.  Accordingly, 
a corresponding  amount  of  food-stuffs  must  be  introduced  in  the 
diet.  The  articles  of  food  contain  these  nutritious  substances  in  a 
variety  of  proportions.  The  rational  combination  of  these  sub- 
stances is  one  of  the  objects  of  dietetics.  Gilman  Thompson 
(“  Dietetics  ”)  divides  foods  into  six  groups,  as  follows  : (1)  Water  ; 
(2)  salts;  (3)  proteids  (chiefly  albuminous  and  allied  gelatins); 
(4)  starches;  (5)  sugar;  (6)  fats  and  oils. 

It  still  remains  extremely  difficult,  in  the  case  of  all  foods,  to 
trace  their  final  uses  in  the  body,  and  determine  with  any  accuracy 
what  proportions  each  furnish,  respectively,  of  energy,  repair  of 
tissue,  and  heat ; for  there  are  no  more  complex  chemical  processes 
known  than  those  of  metabolism.  Foods  have  three  kinds  of 
values:  (1)  nutrient,  (2)  heat-producing,  (3)  force-producing. 

Caloric  Values. — The  calculation  of  these  different  values  for 
each  kind  of  food  has  been  much  simplified  by  the  introduction  of 
the  conception  of  calories  into  the  doctrines  of  nutrition.  Formerly, 
investigators  said:  “ A healthy  man  needs  so  many  gm.  proteid, 
so  many  gm.  carbohydrates,  so  many  gm.  fat,”  etc.  It  proved 
inconvenient  to  reckon  with  three  magnitudes,  and  to  bring  them 
into  correct  relation  with  the  requisites  of  the  individual  organ- 
ism. 

Nowadays  we  compute  the  values  of  food-stuffs  according  to  the 
physiological  (kinetic)  energy  liberated  in  their  oxidation.  Ger- 
mans call  this  “ degree  of  energy,”  which  is  always  expressed  in 
terms  of  heat,  the  Brennwerth  (“  fuel  value  ”) — i.  e.,  the  value  of  food 
when  it  is  burned  in  the  process  of  metabolism,  for  this  is  nothing 
but  a slow  combustion.  Now,  the  unit  for  measurement  of  this 
heat  energy  of  food  is  called  a calory.  This  capacity  for  heat 
production  of  foods  is  determined  from  the  amount  of  heat  which 


44 


PHYSIOLOGY  OF  DIGESTION. 


is  liberated  when  any  particular  food-substance  is  transformed  from 
its  original  composition  when  it  entered  the  body, — by  oxidation, — 
into  those  chemical  combinations  in  which  it  leaves  the  organism. 
The  unit  for  measurement,  or  the  calory,  signifies  the  amount  of 
heat  which  is  necessary  to  raise  one  kilogram  of  water  i°  C. 


I gm.  of  albumin  furnishes 4.1  calories. 

I “ carbohydrate  furnishes 4.1  “ 

I “fat  “ 9.3 

1 “ alcohol  “ 7 “ 


Instead  of  saying  a man  requires  100  gm.  albumin,  100  gm.  fat, 
and  400  gm.  carbohydrates,  one  now  expresses  this  in  calories, 


thus  : A man  requires 

100  gm.  albumin  X 4-L 410  calories. 

100  gm.  fats  X 9-3. 93° 

400  gm.  carbohydrates  X 41* 1640  “ 

Total, 2980  “ 


For  every  kilogram  of  body-weight,  an  adult  requires,  when  at 
rest,  a food-supply  of  30  to  34  calories:  during  light  occupation,  a 
food-supply  of  34  to  40  calories;  during  medium  occupation,  a 
food-supply  of  40  to  45  calories  ; during  hard  work,  a food-supply 
of  45  to  60  calories. 

In  very  obese  persons  the  requirements  for  food  are  less  than 
the  quantities  stated  by  one-quarter  to  one-third.  If  the  above 
calculations  of  the  requisite  number  of  calories  per  kilogram 
weight  of  any  person  are  correct,  and  the  supply  maintained  accord- 
ingly, the  individual  will  maintain  his  weight.  If  the  supply  of 
calories  is  greater,  he  will  gain  weight;  if  the  supply  is  less,  he 
will  lose  weight. 

In  a condensed  statement  of  facts  like  the  present,  it  will  be  ex- 
pedient to  pass  over  the  physiology  of  hunger,  appetite,  and  thirst, 
which  will  be  considered  in  the  clinical  part  of  this  work  (bu- 
limia, anorexia,  etc.),  and  proceed  at  once  to  the  study  of  digestion. 

Ptyalin  Digestion. — Digestion  really  begins  in  the  mouth, 
where  the  food  is  chewed  into  small  bits  and  mixed  with  the  saliva, 
which  mechanically  facilitates  the  mastication  and  deglutition. 
Chemical  transformation  also  begins  here,  for  the  diastasic  ferment 
of  saliva — ptyalin — transforms  a small  portion  of  the  starchy  foods 
into  maltose  and  dextrose. 

Ptyalin  can  produce  this  transformation  of  starchy  foods  only  in 
an  alkaline  medium;  accordingly  the  action  ceases  in  the  stomach; 


DIGESTION  OF  STARCHES. 


45 


but  not  immediately,  however,  as  the  conversion  of  starches  into 
sugar  goes  on  until  the  degree  of  acidity  reaches  I : 1000.  As  the 
ptyalin  ferment  becomes  inactive  in  this  acidity,  the  question  arises, 
whether  its  activity  is  permanently  destroyed  by  an  acidity  of 
I : iooo,  or  only  temporarily,  and  whether  it  can  resume  its  invert- 
ing power  when  the  acid  is  neutralized.  Boas,  who  attempted  a 
solution  of  this,  came  to  the  conclusion  that  subsequent  alkalini- 
zation,  or  diminution  of  the  acid,  causes  the  ptyalin  to  act  again, 
so  that  in  later  stages  of  digestion,  when  the  acid  production 
ceases,  the  conversion  of  starch  into  grape  sugar  by  ptyalin  may 
be  resumed,  but  the  ferment  never  becomes  as  active  as  before. 

The  existence  of  appetite  is  to  a degree  dependent  upon  the 
proper  functioning  of  the  salivary  glands. 

Digestion  of  Starches. — In  order  to  understand  the  various 
stages  of  starch  conversion,  it  is  essential  to  study  the  digestion 
of  starch  by  ptyalin  in  the  laboratory.  There  are  recognized 
four  stages  of  starch  conversion,  each  distinct  from  the  other, 
until  dextrose  is  reached. 

1.  ( a ) This  is  common  starch,  representing  a glue-like,  muci- 
laginous jelly,  not  a clear  solution,  giving  a dark-blue  color  with 
iodin  in  iodid  of  potassium  solution.  The  next  stage  shows  the 
first  action  of  ptyalin. 

( b ) Amidulin  or  Amylodextrin. — This  still  gives  a distinctly  blue 
color,  though  not  so  deep  as  No.  I ( a ),  with  Lugol’s  solution  ; 
but  amylodextrin  is  a soluble  starch,  and  represents  a real  solution. 

2.  (a)  Ery  thro  dextrin. — Gradually,  as  the  inversion  progresses,  the 
color  produced  by  the  iodin  solution  becomes  violet-blue,  violet, 
red  violet,  red,  or  mahogany  brown ; this  modification  is  called 
erythrodextrin. 

(h)  Achroodextrin. — With  continued  action  of  the  ptyalin,  a sub- 
stance is  reached  which  gives  no  color  with  iodin ; this  is  called 
achroodextrin.  Amidulin  is  precipitated  by  tannic  acid  and 
alcohol,  but  erythrodextrin  and  achroodextrin  are  precipitated  by 
alcohol  and  ether,  not  by  tannic  acid.  These  two  dextrins  do  not 
reduce  Fehling’s  solution,  and  do  not  ferment  with  yeast. 

3.  Maltose. — Soluble  in  alcohol,  insoluble  in  ether ; reduces 
Fehling’s  solution,  but  not  Barfoed’s  reagent  (a  four  per  cent, 
solution  of  cupric  acetate  to  which  one  per  cent,  acetic  acid  is 
added)  ; does  not  ferment  with  yeast. 

4.  Dextrose. — Insoluble  in  alcohol  and  ether;  reduces  Fehling’s 
as  well  as  Barfoed’s  solution  ; ferments  readily  with  yeast. 

4 


46 


PHYSIOLOGY  OF  DIGESTION. 


It  is  important  to  familiarize  one’s  self  with  these  reactions,  as  it 
often  becomes  necessary  to  determine  the  degree  of  starch  conver- 
sion in  cases  of  hyperacidity  or  supersecretion. 

It  was  formerly  thought  that  the  starch  was  first  converted 
to  dextrin,  and  this  in  turn  was  converted  to  sugar.  According 
to  Professor  W.  H.  Howell  (“Amer.  Textbook  of  Physiology”), 
the  starch  molecule,  which  is  quite  complex,  consisting  of  some 
multiple  of  C6H10O5, — possibly  (C6H10O5)2O, — first  takes  up  water, 
thereby  becomes  soluble  (soluble  starch,  amylodextrin),  and  then 
splits  with  the  formation  of  dextrin  and  maltose,  and  that  the 
dextrin  again  undergoes  the  same  hydrolytic  process  and  may 
continue  under  favorable  conditions  until  only  maltose  is  present. 
The  difficulty  at  present  is  in  isolating  the  different  forms  of 
dextrin  that  are  produced.  It  is  usually  said  that  at  least  two 
forms  occur,  one  of  which  gives  a red  color  with  iodin,  and  is 
known  as  erythrodextrin,  while  the  other  gives  no  color  reaction 
with  iodin,  and  is  termed  achroodextrin.  It  is  pretty  certain, 
however,  that  there  are  several  forms  of  achroodextrin,  and, 
according  to  some  observers  also,  erythrodextrin  is  really  a mixtuie 
of  dextrins  with  maltose  in  varying  proportions.  In  accordance 
with  the  general  outline  of  the  process  given  above,  Neumeister 
proposes  the  following  schema,  which  is  useful  because  it  gives  a 
clear  representation  of  one  theory,  but  which  must  not  be  con- 
sidered as  satisfactorily  demonstrated: 


Maltose. 


Starch — Solu- 
ble Starch. 
Amylodex- 
trin. 

/ Ery  thra- 

y  Maltose. 

r Maltose. 

ll  dextrin. 

I Achroo- 

| 

f Maltose. 

f dextrin.  a 

J Achroo-  o 
L dextrin.  1 

) 

) Achroo- 
l dextrin. 

(Malto- 

dextrin.) 

^ Maltose. 
( Maltose. 


Von  Mering  and  Ewald  have  shown  that  in  the  transformation 
of  starch  into  sugar  by  ptyalin,  the  greater  portion  is  converted 
into  maltose — only  a small  portion  into  dextrose.  But  the  maltose 
formed  in  the  stomach  is  changed  to  dextrose  in  the  intestine.  If 
the  amylaceous  transformation  proceeds  normally  in  the  mouth 
and  stomach,  after  a time — within  an  hour,  at  least — so  much  starch 
has  been  changed  into  achroodextrin,  maltose,  and  dextrose,  that 


GASTRIC  JUICE. 


47 


the  addition  of  small  quantities  of  Lugol’s  solution  to  the  filtered 
stomach  contents  no  longer  produce  any  changes  in  color.  The 
occurrence  of  a purple  (erythrodextrin)  or  a blue  color  (starch) 
shows  that  the  starch  transformation  has  been  incomplete.  This 
may  be  due  either  to  a deficiency  of  ptyalin  or  to  a rapidly 
increasing  acidity  or  hyperacidity  of  the  stomach. 

Ewald  states  that,  although  he  tested  a large  number  of  patients 
for  the  fermentative  power  of  saliva,  he  never  found  a saliva  that 
could  not  convert  starch  into  sugar.  This,  too,  when  he  tested  the 
salivary  secretion  of  patients  with  dental  caries,  angina,  diphtheria, 
and  carcinoma  of  the  tongue. 

From  the  above  it  is  evident  that  there  must  be  two  stages  of 
gastric  digestion,  (i)  an  amylolytic  and  (2)  a proteolytic.  Having 
satisfied  ourselves  as  regards  the  fate  of  the  starches,  let  us  pro- 
ceed to  study  proteolytic  digestion,  or  conversion  of  proteids, 
gelatins,  fibrins,  elastin,  etc. 

Gastric  Juice. — Hydrochloric  Acid. — The  secretion  of  the 
stomach  is  a complex  fluid,  clear,  colorless,  and  of  acid  reaction; 
it  has  only  one-half  per  cent,  of  solid  ingredients.  The  amount 
secreted  in  twenty-four  hours  is  about  1600  gm.  Its  chief  con- 
stituent is  hydrochloric  acid,  which  it  contains  in  the  amount  of  0.1 
to  0.22  per  cent,  (one  to  two  per  thousand).  This  degree  of  acidity 
is  not  reached  at  once,  but  gradually;  at  the  beginning  and  end  of 
stomach  digestion  the  percentage  of  HC1  is  considerably  less. 
Besides  the  HC1,  gastric  juice  contains  two  unorganized  ferments, 
pepsin  and  rennin  (or  chymosin). 

Hydrochloric  acid  acts  in  six  different  ways,  all  of  which  are  of 
great  significance  for  the  normal  progress  of  digestion. 

1.  HC1  acts  as  an  antizymotic  or  antiseptic,  destroying  patho- 
genic organisms  and  preventing  abnormal  fermentations.  This 
antibacterial  effect  extends  even  into  the  duodenum. 

2.  HC1  has  the  power  to  convert  the  proenzymes  of  the  gastric 
glands  (pepsinogen  and  rennin  zymogen)  into  active  ferments  in  a 
very  short  time  (according  to  Langley,  in  one  minute). 

3.  This  gastric  acid  possesses  a certain  regulating  influence  on 
the  progress  of  peristalsis. 

4.  HC1  transforms,  with  the  aid  of  pepsin,  albuminous  bodies  into 
peptones,  gelatin  into  gelatin  peptone,  elastin  into  elastin  peptone. 
But  in  reality  the  pepsin  is  the  main  or  chief  agent  in  these  trans- 
formations, as  the  HC1  can  be  effectively  substituted  by  nitric, 
phosphoric,  oxalic,  sulphuric,  lactic,  and  butyric  acids. 


48 


PHYSIOLOGY  OF  DIGESTION. 


5.  By  HC1  cane  sugar  is  changed  to  invert  sugar  (dextrose 
and  levulose).  This  property  is  also  ascribed  to  a number  of  bac- 
teria that  can  invert  cane-sugar,  although  after  a longer  time. 

6.  HC1,  finally,  is  instrumental  in  bringing  into  solution  the 
soluble  calcium  and  magnesium  salts,  introduced  in  the  food. 

Concerning  the  origin  and  derivation  of  the  hydrochloric  acid, 
we  unfortunately  have  nothing  but  speculation.  No  free  acid  oc- 
curring in  the  blood  or  lymph,  it  is  rational  to  conclude  that  it  is 
produced  in  the  secreting  (oxyntic)  cells  of  the  gland-ducts.  It 
seems  probable  that  the  acid  is  derived  from  the  neutral  chlorids  of 
the  blood,  which  are  in  some  way  decomposed,  the  chlorin  uniting 
with  hydrogen  to  form  HC1.  The  acid  is  secreted  at  the  gastric 
mucosa,  while  the  base  remains  behind,  and  probably  passes  back 
into  the  blood.  This,  in  a way,  explains  the  increased  alkalinity  of 
the  blood  and  the  decrease  of  acidity  of  the  urine  after  meals,  the 
return  of  basic  substances  into  the  circulation  naturally  having  such 
an  effect.  According  to  Heidenhain,  a free  organic  acid  is  secreted 
by  the  cells  (oxyntic),  which  then  decomposes  the  chlorids.  Ac- 
cording to  Maly,  the  HC1  is  the  result  of  a reaction  between  the 
phosphates  and  chlorids  of  the  blood,  as  expressed  in  the  following 
two  equations  : 

NaH2P04  -f  NaCl  = Na2HP04  + HC1  or 
3CaCl2  -f-  2Na2HP04=  Ca3(POJ2  + 4NaCl  + 2HCI. 

What  is  known  thus  far  of  the  specific  action  of  living  cells  en- 
forces the  impression  here,  that,  as  in  other  chemical  processes  not 
yet  understood,  vital  phenomena  are  difficult  to  express  in  chemical 
formulas. 

The  gastric  secretion  is  dependent  upon  innervation  through  the 
vagi.  When  the  vagi  are  cut  through  in  dogs  (the  right  one  in 
such  a manner  as  to  leave  the  inferior  laryngeal  and  the  cardiac 
rami  intact — i.  e.y  below  the  point  at  which  these  nerves  are  given 
off,  so  as  to  preserve  the  sensibility  and  motility  of  the  larynx 
and  the  cardiac  innervation),  the  secretion  of  gastric  juice  ceases 
(J.  P.  Pawlow,  “ Die  Arbeit  der  Verdauungsdrusen  ” [original  in 
Russian],  1898,  p.  72). 


PEPSINOGEN  AND  PEPSIN. 


49 


CHAPTER  V. 

PEPSINOGEN  AND  PEPSIN.— RENNIN  ZYMOGEN  AND 
RENNIN.— INTESTINAL  DIGESTION.— 
DUODENAL  INTUBATION. 

It  should  not  be  understood  that  all  combinations  of  the  gastric 
juice  with  albumins  are  at  once  peptones;  like  the  starches,  the 
proteids  reach  their  end  stage  of  gastric  digestion  by  a series  of 
distinct  intermediate  stages.  These  are  (i)  proteid,  (2)  acid 
albumin  or  syntonin,  (3)  propeptone  or  hemialbumose,  and  (4) 
peptone.  Besides  forming  peptones  out  of  albumins,  pepsin  de- 
prives gelatin  of  its  property  to  coagulate,  or  rather  to  gelatinize, 
and  forms  gelatin  peptones  out  of  it.  Peptones  are  derived  from 
egg,  serum,  and  plant  albumins,  gelatin,  meat,  fibrin,  casein,  etc. 

The  steps  in  peptic  digestion  may  be  made  more  intelligible  by 
the  following  schema,  modified  from  that  of  Neumeister  (“  Lehr- 
buch  d.  physiol.  Chemie,”  1893,  p.  187) : 

Proteid 

Syntonin 


Primary  proteoses, Protoproteose  Heteroproteose. 

Secondary  proteoses, Deuteroproteose  Deuteroproteose. 

Amphopeptones, Peptone  Peptone. 


No  other  mineral  acid  gives  so  good  results  with  pepsin  as 
HC1,  which  can  form  pepsin  from  pepsinogen  in  the  shortest  time. 
It  is  useful  to  be  able  to  test  for  propeptone  formation.  In  normal 
digestion,  one  hour  after  the  test-breakfast,  propeptone  is  present 
only  in  traces,  or  usually  is  not  to  be  detected  at  all ; but  in  abnor- 
mally slow  digestion  it  is  still  abundant  at  that  period. 

The  most  expedient  method,  up  to  present  date,  is  by  means  of 
the  biuret  reaction.  In  this  reaction  a dilute  solution  of  cupric 


PEPSINOGEN  AND  PEPSIN. 


50 

sulphate  is  added  to  stomach  contents  in  the  cold,  and  a few  drops 
of  potassium  hydroxid  added  sufficient  to  make  the  solution  alka- 
line ; an  intense  red  color  results.  Cupric  sulphate  and  KOH, 
added  to  ordinary  albumin  and  syntonin,  without  warming,  pro- 
duces a bluish  violet,  which  must  be  distinguished  from  the  purple- 
red  of  biuret. 

The  more  marked  the  propeptone  reactions  are,  the  less  the  pep- 
tone which  has  been  formed  and  eventually  removed  from  the 
stomach.  We  can  approximately  estimate  the  amount  of  the  pep- 
tone by  the  intensity  of  the  biuret  reaction  if  we  always  use  the 
same  quantities  of  stomach  contents,  caustic  potash,  and  cupric  sul- 
phate, and  compare  it  with  the  reaction  given  with  a peptone  solu- 
tion of  known  strength.  One  hour  after  an  Ewald  test-breakfast, 
given  to  a person  with  normal  digestion,  propeptone  is  either  not 
found  at  all  or  only  in  traces ; but  in  abnormally  weak  or  slow 
digestion,  propeptone  is  still  abundant  at  that  period.  Peptone 
gives  the  same  pink,  purple-red  color  with  the  biuret  reaction  as 
propeptone.  In  estimating  the  rate  of  proteolysis  in  the  stomach, 
the  biuret  reaction  will  not  permit  us  to  distinguish  between  these 
two  bodies ; the  only  differentiation  possible  is  by  precipitation  of 
the  propeptone  in  the  following  manner : The  stomach  filtrate  is 
carefully  neutralized,  an  equal  quantity  of  common  salt  solution  is 
added,  and  then  a few  drops  of  concentrated  acetic  acid.  A pre- 
cipitate will  be  propeptone,  which  can  be  filtered  off  and  weighed ; 
any  red  biuret  reaction  after  this  separation  must  be  due  to 
peptone. 

In  order  to  determine,  in  a given  specimen  of  stomach  contents, 
whether  the  pepsin  or  HC1  is  present  in  too  great  or  too  small  a 
quantity,  one  proceeds  in  the  following  manner : 

Pour  10  c.c.  filtered  stomach  contents  into  four  test-tubes  and 
number  them  Nos.  1,  2,  3,4.  To  No.  1,  nothing  further  is  added ; to 
No.  2,  enough  HC1  to  make  a solution  of  2 to  3 per  thousand 
(this  can  be  accomplished  by  adding  one  or  two  drops  of  officinal 
HC1,  U.  S.  Pharm.,to  10  c.c.  filtrate) ; to  No.  3,  0.2  to  0.5  gm.  (gr. 
iij  to  gr.  vij)  of  pure  pepsin  is  added,  and  to  No.  4 both  HC1  and 
pepsin  are  supplied. 

A small  disc  of  egg-albumen  (which  is  prepared  by  cutting 
boiled  egg-albumen  into  lamellae  of  uniform  thickness  with  a micro- 
tome and  punching  out  equal  circles  by  a cork-borer)  is  added  to 
each  test-tube,  and  they  are  then  put  in  the  incubator  at  ioo°  F. 
The  rate  at  which  the  albumin  is  dissolved  will  tell  us  whether 


RENNIN. 


51 


the  filtrate  was  perfect  as  regards  the  requisite  amount  of  pepsin 
and  HC1,  whether  pepsin  alone,  or  HC1  only,  or,  finally,  whether 
both  were  necessary.  In  this  way  we  can  discover  which  factor  is 
at  fault.  In  the  human  stomach  the  formation  of  peptone  remains 
at  a certain  percentage  by  the  removal  or  absorption  of  peptones 
over  that  amount,  and  also  it  would  seem  by  an  inhibiting  influence 
which  a certain  percentage  of  peptone  has  over  the  proteolytic  pro- 
cess in  retarding  or  suspending  it.  As  this  can  not  be  imitated  in 
a test-tube, — i.  e.,  the  absorption  of  ready-formed  peptones, — a seem- 
ingly delayed  digestive  process  of  egg-albumen  discs  in  the  test- 
tubes  may  in  reality  be  due  to  a very  active  stomach  filtrate.  The 
amount  of  HC1  and  the  amount  of  pepsin  must  be  in  definite 
relation  to  each  other.  Excess  of  HCl  is  as  much  of  a check  as 
insufficiency  of  this  acid. 

Rennin,  chymosin,  or  pexin,  the  second  gastric  ferment,  pro- 
duces a light,  not  very  cohesive,  coagulation  of  milk.  This  coagu- 
lation is  a characteristic  cake  of  casein  floating  in  clear  serum,  more 
dense,  not  lumpy,  more  cohesive  coagulation,  than  that  produced 
by  acids.  This  ferment  is  a constant  constituent  of  the  stomach 
contents,  just  as  pepsin  and  pepsinogen.  With  a complete  absence 
of  the  rennin  and  its  proenzyme,  one  can  with  certainty  conclude 
that  the  case  is  one  of  atrophy  of  the  gastric  mucosa. 

The  demonstration  of  rennin  ferment  is  carried  out  in  the  fol- 
lowing manner:  Ten  c.c.  of  raw,  unboiled  milk  are  placed  in  the 
incubator  with  2.5  drops  of  stomach  filtrate.  If  rennin  is  present, 
the  characteristic  milk  coagulation  will  occur  in  a variable  time 
(one  minute  to  several  hours,  according  to  the  quantity  of  fer- 
ment). * 

Occasionally,  rennin,  the  perfect  ferment,  is  not  contained  in  the 
stomach  contents,  while  at  the  same  time  rennin  zymogen  (pexin- 
ogen  chymosinogen)  is  present.  This  is  demonstrated,  according 
to  Hammarsten,  by  adding  to  the  mixture  just  described  2 c.c. 
of  a concentrated  solution  of  calcium  chlorid,  CaCl2. 

If  a rennin  coagulum  occurs,  it  follows  that  rennin  zymogen  is 
present,  but  not  the  perfect  ferment.  For  these  tests,  raw  milk 
only  can  be  used,  as  it  coagulates  ten  times  as  rapidly  as  boiled 
milk.  Jaworski  has  pointed  out  that  in  cases  where  tests  for  rennin 


* The  presence  of  peptone  delays  the  clotting  of  milk  by  chymosin  (E.  Gley,  “ Compt. 
Rend.,”  1896,  591.  A.  Edmunds,  “ Journ.  Physiol.,”  xix,  474,  1896.  F.  S.  Locke, 
“ Journ.  Experim.  Med.,”  vol.  II,  p.  493). 


52 


INTESTINAL  DIGESTION. 


and  rennin  zymogen  are  both  negative,  it  is  advisable  to  try  pour- 
ing a 0.3  per  cent,  to  0.6  per  cent,  solution  of  hydrochloric  acid 
into  the  stomach,  to  see  whether  this  HC1  may  not  be  able  to 
awaken  a secretion  of  rennin  ; this  should  especially  be  done  before 
making  the  diagnosis  of  complete  atrophy  of  the  mucosa.* 

The  Physiology  of  Intestinal  Digestion. — Our  knowledge  of 
the  digestive  processes  in  the  intestine  is,  from  a physiological  as 
well  as  from  a pathological  point  of  view,  defective;  at  times,  con- 
tradictory. Concerning  gastric  digestion  we  are  much  better  in- 
structed, because  here  the  processes  are  simpler,  and  material  for 
investigation  can  be  more  easily  obtained.  The  stomach-tube 
supplies  us  without  difficulty  with  gastric  contents,  but  hitherto  all 
intestinal  contents  of  human  beings  have  been  obtained  from  rare 
cases  of  intestinal  fistulae,  for  the  feces  give  no  constant  and  reliable 
information  of  the  digestive  actions  in  the  smaller  intestine. 

The  earliest  investigations  of  intestinal  contents  were  made  in 
1662  by  Regnier  de  Graaf,  who  made  experimental  fistulae  into  the 
intestinal  canal  of  animals.  It  is  a curious  historical  fact  that  this 
intestinal  experiment  antedated  the  first  investigations  of  stomach 
contents  which  were  carried  on  in  1752  by  Reaumur.  So  up  to 
the  present  time  there  was  no  prospect  of  getting  a better  insight 
into  the  physiology  of  intestinal  digestion  until  a method  for  intu- 
bating the  duodenum  in  the  living  human  subject  was  devised  by 
the  author. 

This  method,  which  is  described  in  the  “ Johns  Hopkins  Hospital 
Medical  Bulletin”  for  April,  1895,  and  also  in  Boas’  “Archives  for 
Digestive  Diseases,”  volume  11,  page  85,  consists,  in  the  first  place, 
of  the  introduction  of  a thin,  elastic  rubber  bag  into  the  stomach. 
This  bag,  when  folded  over  a tube  which  runs  through  it,  does  not 
occupy  as  much  space  as  an  ordinary  stomach-tube,  and  has  the 
exact  shape  of  the  human  stomach  when  it  is  distended  by  blow- 
ing it  up  within  that  organ,  to  which  it  fits  itself  exactly, — and  is 
closely  applied  to  the  gastric  walls. 

The  intragastric  bag  is  distended  by  the  pressure  apparatus 
shown  in  figure  6.  The  graduated  bottle  ( A ) is  full  of  water  and 
elevated  above  the  bottle  (A),  which  is  empty  and  also  graduated. 

The  stomach-shaped  bag  ( C ),  when  it  reaches  the  stomach,  is 


* The  word  “pexine”  for  this  ferment,  while  etymologically  and  historically  pre- 
ferable, has  the  serious  disadvantage  of  sounding  very  much  like  the  word  “pepsin,” 
when  rapidly  spoken.  The  word  “ chymosin  ” avoids  this  possible  confusion. 


PHYSIOLOGY  OF  INTESTINAL  DIGESTION. 


53 


connected  with  the  lower  empty  bottle,  B.  Then  the  stop-cock 
connecting  A with  B is  opened,  and  the  water  runs  from  A into  B , 
displacing  the  air  in  B}  which  distends  the  bag  C,  within  the 
stomach,  filling  it  entirely.  As  is  observable  on  this  bag,  a guide 
is  contained  in  it,  running  along  the  dotted  line  parallel  to  the  lesser 
curvature.  In  this  guide  the  duodenal  tube  is  inserted,  lubricated 
with  oil  before  the  bag  is  pushed  into  the  stomach.  This  tube  is 
provided  with  very  thick  walls,  by  virtue  of  which  it  is  not  easily 
kinked  or  bent  upon  itself. 


Fig.  5.— Apparatus  for  Obtaining  Intestinal  Contents. 


The  relation  of  the  thickness  of  the  walls  to  the  diameter  of  the 
lumen  is  shown  in  the  cross-section  of  figure  5.  When  the  intra- 
gastric  bag  is  distended,  it  fills  the  stomach  entirely.  The  duo- 
denal tube  lies  in  its  sheath  or  guide,  and  on  being  pushed  onward 
from  the  mouth,  it  is  not  possible  for  it  to  go  anywhere  else  except 
through  the  pylorus  into  the  duodenum.  In  the  illustrations  it  can 
be  seen  that  the  bag  is  not  distended  by  the  duodenal  tube,  but  a 
separate,  very  small  tube  runs  down  the  esophagus,  ending  in  the 
bag,  serving  the  purpose  of  its  distention.  Both  tubes  together  do 
not  occupy  as  much  space  as  an  ordinary  stomach-tube. 


54 


DUODENAL  INTUBATION. 


A description  of  this  method  is  considered  essential  because  it 
seems  to  be  destined  to  bring  our  knowledge  of  the  physiology  and 
pathology  of  the  intestines  upon  a basis  of  ascertained  facts ; 
we  can  at  any  time  thereby  obtain  the  contents  of  the  intestine, 
and  the  gut  may  in  any  of  its  parts  be  reached  with  safety. 

After  known  test-meals,  it  is  possible,  after  they  have  passed  from 
the  stomach  into  the  duodenum,  to  draw  out  samples  from  this 
part  and  subject  them  to  analysis.  By  alternately  distending  any 
part  with  air  or  water  we  will  be  enabled  to  locate  the  part  by  the 


Fig.  6.— Pressure  Bottles  for  Distending  the  Intragastric  Bag  during  Duodenal 
Intubation. 

percussion  sound  on  the  outside  of  the  abdomen,  and  the  distance 
it  is  located  from  the  mouth  can  be  seen  from  the  length  of  tube 
introduced. 

Small  electric  lamps  may  be  introduced  into  the  duodenum  as 
they  are  into  the  stomach,  and  the  location  and  condition  recog- 
nized by  electrodiaphany. 

Hitherto,  in  all  experiments  on  this  subject  it  has  been  impossible 
to  obtain  either  the  pancreatic  or  biliary  secretion  in  a pure  con- 
dition; this  is  due  to  the  fact  that  both  the  pancreatic  and  the 
common  gall-duct  empty  into  the  descending  portion  of  the  duo- 
denum very  near  each  other. 


THE  PANCREAS. 


55 


In  May,  1897,  we  had  under  observation  a female  patient  who 
had  suffered  repeated  attacks  of  biliary  colic.  At  times  she  passed 
small  stones  without  giving  her  much  pain — at  least  they  were 
found  in  the  stools  without  having  given  her  any  colic.  She 
was  willing  to  undergo  an  operation  to  be  relieved.  Through  the 
comparatively  thin  abdominal  walls  we  were  able  to  feel  numer- 
ous stones  in  the  gall-bladder.  She  consented  to  an  attempt 
at  intubation  of  the  duodenum  to  determine  whether  there  was 
any  bile  secreted.  The  duodenum  was  entered  without  difficulty, 
and  cleansed  by  running  in  and  aspirating  out  distilled  warm 
water.  Twelve  hours  afterward,  no  food  having  been  taken 
in  the  mean  while,  the  duodenum  was  again  intubated  accord- 
ing to  our  method,  and  washed  with  100  c.c.  of  warm  distilled 
water. 

On  being  aspirated,  the  water  was  still  clear,  but  viscid  and 
sticky,  similar  to  a solution  of  egg-albumen.  It  contained  no 
bile-pigments  nor  cholesterin,  and  was  free  from  taurocholates  and 
glycocholates.  It  was  colorless  and  odorless,  and  seemed  very 
rich  in  some  form  of  albumin.  That  it  was  a solution  of  pancreatic 
juice  was  proved  by  its  digesting  fibrin  and  serum-albumin. 

The  juice  obtained  in  this  manner  digested  from  eighty-five  to 
ninety-five  per  cent,  of  Merck’s  dried  serum-albumin  in  the  diges- 
torium  at  ioo°  F.  in  two  hours.  The  amylolytic  and  fat-decompos- 
ing property  of  the  juice  was  determined  in  a similar  manner.  One 
is  therefore  justified  in  concluding  that  in  this  case  the  pancreatic 
juice  was  obtained  almost  pure,  as  there  were  no  bile  elements  con- 
tained in  it,  the  bile  being  prevented  from  entering  the  duodenum  by 
a calculus  or  catarrhal  occlusion  in  the  common  duct.  As  there  are 
also  pancreatic  calculi,  or  occlusions  of  the  duct  by  neoplasm  or 
catarrhal  swelling,  it  is  conceivable  that  we  may  yet  be  able  to 
obtain  the  bile  in  a pure  condition,  and  free  from  pancreatic  juice, 
from  the  human  subject,  without  operation. 

The  secretions  of  Brunner’s  and  Lieberkiihn’s  glands  will,  how- 
ever, always  constitute  an  admixture  of  these  juices. 

The  Pancreas  : its  Secretion  and  Pancreatic  Digestion. — 
In  1846  Claude  Bernard  made  the  first  scientific  and  fundamental 
investigation  concerning  the  pancreatic  secretion.  Later  on 
Kuhne,  Bidder  and  Schmidt,  Corvisart,  Heidenhain,  and  others 
amplified  these  results. 

Its  secretion,  as  Bernard  first  observed,  is  dependent  upon 
digestion,  and  is  a clear,  colorless,  and  odorless  fluid,  very  alkaline, 


56 


THE  PANCREAS. 


and  so  rich  in  albumin  that  it  solidifies  on  boiling.  Zawardsky  had 
opportunity  of  analyzing  the  normal  human  pancreatic  secretion  in 
a case  of  pancreatic  fistula,  which  remained  behind  after  removal  of 
a tumor.  According  to  his  analysis  it  contained  86.4  per  cent, 
water,  13.25  organic  substances;  among  the  latter  are  9.2  proteid 
bodies  and  0.83  extractive  substances,  soluble  in  alcohol ; lastly, 
0.34  per  cent,  salts. 

The  chyme  which  passes  into  the  duodenum  from  the  stomach 
comes  under  the  influence  of  formed  or  organized  and  unformed 
or  unorganized  ferments.  The  formed  or  organized  ferments  are 
represented  by  bacteria,  which  bring  about  carbohydrate  fermenta- 
tion, mostly  in  upper  bowel,  and  proteid  putrefaction,  mostly  in 
lower  bowel. 

The  unorganized  ferments  are  contained  in  the  pancreatic  secre- 
tion, the  bile,  and  in  the  succus  entericus.  The  most  important 
constituents  of  the  pancreas  are  three  ferments  or  enzymes:  (1) 
an  amylolytic,  (2)  a preteolytic,  and  (3)  a fat-splitting  ferment 
(adipolytic). 

According  to  W.  G.  Halliburton  and  T.  G.  Burton  (“Journal  of 
Physiology,”  vol.  xx,  p.  106),  pancreatic  juice  possesses  a milk- 
precipitating  substance,  causing  at  350  to  450  C.  a granular  precip- 
itate in  milk,  but  there  is  no  solidification  until  the  milk  cools,  when 
it  sets  to  a coherent  curd.  On  warming,  the  curd  is  broken  up, 
and  the  milk  resumes  its  granular  fluidity.  The  granular  precip- 
itate produced  by  pancreatic  juice  seems,  according  to  these 
observers,  to  be  intermediate  between  casein  and  caseinogen. 

The  amylolytic  or  pancreas  diastase  is  very  similar  to  ptyalin  in 
its  action,  and  changes  boiled  starch  into  maltose  exceedingly 
rapidly  at  body  temperature.  In  addition,  small  quantities  of  dex- 
trin and  grape  sugar  are  formed  ; one  gm.  of  pancreatic  juice  from 
a dog  will  invert  3.6  gm.  starch  into  sugar.  Cane  sugar  and  inulin 
are  not  affected  by  it.  According  to  Zweifel,  this  ferment  is  absent 
in  the  pancreas  of  new-born  children. 

The  fat-splitting  ferment  of  the  pancreas  (also  called  steapsin), 
which  thus  far  has  not  been  obtained  in  a pure  state,  breaks  up 
neutral  fats  into  fatty  acids  and  glycerin.*  This  process  occurs  very 


* The  form  in  which  the  fats  are  ultimately  absorbed  from  the  intestine  is  still  a matter 
of  hypothesis  (Schafer’s  “ Textbook  of  Physiology,”  vol.  I,  article  on  Fat  Absorption). 
The  emulsion  theory — i.e. , absorption  as  natural  fat — and  the  solution  theory — i.e. , absorp- 
tion as  fatty  acids  and  soaps — are  both  advocated  by  physiologists  of  prominence,  so  that 
no  exact  scientific  conclusion  in  favor  of  either  view  is  as  yet  possible. 


THE  PANCREAS. 


57 


slowly,  however.  Berthelot  found  that  fifteen  grams  of  pancreatic 
secretion  of  the  dog  required  at  least  twenty-four  hours  to  break  up 
two  decigrams  of  monobutyrin  completely  into  butyric  acid  and 
glycerin.  The  fatty  acids  formed  during  this  transformation  com- 
bine with  alkalies  in  the  intestine  to  form  soaps,  which,  by  emulsi- 
fying other  fats,  assist  greatly  in  their  absorption.  In  the  laboratory 
it  always  requires  powerful  mechanical  action  to  effect  an  emulsion 
of  fats ; not  so  in  the  intestine,  where  it  is  evidently  accomplished 
with  great  facility.  That  this  must  greatly  assist  in  fat  resorption 
is  evident  from  the  frequent  observation  that  after  disease  of 
the  pancreas  the  feces  become  very  rich  in  fat,  which  may  be 
present  in  so  large  an  amount  as  to  congeal  on  the  surface  of  the 
stool. 

The  proteolytic  ferment  of  the  pancreas  has  been  called  trypsin 
by  Kuhne.  Digesting  boiled  blood-fibrin  with  pancreatic  juice,  he 
found  that  it  did  not  swell  up,  but  that  it  became  very  fragile,  and 
finally  liquefied.  As  we  take  in  all  of  our  albumin  in  a boiled  or 
roasted  state,  which  becomes  peptone  in  the  stomach  and  not  solu- 
ble albumin,  the  question  has  arisen  : Whence  do  we  derive  our 
soluble  native  albumin  ? This  is  obtained  from  pancreatic  trypsin 
digestion  of  boiled  albuminous  bodies,  which  changes  them  to 
albumin  soluble  in  water,  or  at  least  in  a weak  saline  solution,  from 
which  they  can  be  precipitated  by  heat.  The  proteolytic  action  of 
trypsin  takes  place  best  in  an  alkaline  or  neutral  medium,  though  it 
is  still  active  in  faintly  acid  media. 

Among  the  bodies  formed  from  albumins  and  proteids  under  the 
influence  of  trypsin  are  a globulin  that  is  insoluble  in  water,  hemi- 
peptone  and  antipeptone,  leucin,  tyrosin,  and  asparaginic  acid.  Indol, 
which  is  found  in  the  jejunum,  is  a product  of  bacterial  action  on 
albumins.  A chromogenic  body  has  been  described  by  Tiedemann 
and  Gmelin  which  has  received  the  name  tryptophan  ; it  is  a result 
of  advanced  albumin  decomposition.  Trypsin,  then,  to  sum  up, 
changes  proteids  to  peptones  and  soluble  albumins,  casein  to 
casein  peptones,  gelatin  to  gelatoses  and  gelatin  peptone,  and  elastin 
to  elastoses  and  elastin  peptones. 

In  animals  that  have  been  deprived  of  their  pancreas  by  oper- 
ation, only  forty-four  per  cent,  of  proteid,  fifty-seven  per  cent,  to 
seventy  per  cent,  of  carbohydrates,  and  no  fats  at  all,  were 
absorbed,  although  four-fifths  of  the  fats  was  split  up  into  fatty  acid 
and  glycerin. 


53 


THE  PANCREAS. 


The  processes  of  tryptic  digestion  are  briefly  represented  in  the 
following  schema,  according  to  Neumeister: 

Proteid 

Deutero Albumose 

Amphopeptone 


Antipeptone  Hemipeptone 


Leucin  Tyrosin  Aspartic  acid  Tryptophan 


Trypsin  produces  peptone  from  proteids  more  readily  than  does 
pepsin.  On  account  of  certain  differences,  chiefly  recognizable  in 
dialysis,  between  the  end-products  of  peptic  digestion  or  peptones 
and  those  of  tryptic  digestion,  the  name  of  tryptones  is  used  by 
the  author  in  reference  to  the  latter. 

The  principal  secretory  nerve  of  the  pancreas  is  the  vagus  (Paw- 
low,  /.  c.}  p.  73). 

The  gastric  chyme  by  virtue  of  its  contained  HC1  stimulates  the 
pancreatic  secretion  reflexly  by  acting  on  the  duodenal  mucosa. 
Starch  is  no  exciter  of  pancreatic  secretion,  but  it  augments  the 
amount  of  amylopsin  contained  in  it.  Fat  is  a marked  stimulant 
to  pancreatic  secretion  and  augments  its  amount  of  steapsin. 
Solutions  of  alkaline  and  neutral  salts  inhibit  the  action  of  the 
pancreas.  The  physiological  excitants  of  the  gastric  secretion  are 
the  extractives  (bouillon),  while  acids,  fats,  and  even  water  are  the 
physiological  stimulants  to  pancreatic  secretion. 


CHAPTER  VI. 


THE  BILE.— THE  SUCCUS  ENTERICUS.— INTESTINAL 
FERMENTATION.— PUTREFACTION.— FORMED 
OR  ORGANIZED  FERMENTS. 

It  is  known  at  present  that  the  bile  exerts  no  chemical  effects 
upon  the  food  materials  ; nevertheless,  its  presence  in  the  duodenal 
chyme  is  significant  on  account  of  its  alkaline  reaction  and  its 
effect  on  the  mucous  membrane.  The  most  important  function  of 
the  bile  is  the  excretion  of  metabolic  products  that  can  not  be 
utilized  in  the  organism. 

The  contents  of  the  gall-bladder  represent  a concentrated  secre- 
tion ; therefore  our  knowledge  of  the  physiological  action  of  the  bile 
depends  upon  the  discharge  of  biliary  fistulae.  The  bile  is  a golden 
yellow,  at  times  olive-brown,  secretion  ; it  is  never  of  a green  color, 
but  generally  very  mucoid  and  stringy.  Its  alkaline  reaction  is 
due  mainly  to  carbonates  and  phosphates.  The  quantity  poured 
into  the  intestine  is  largest  in  the  first  hour  after  food  is  taken. 

Albumins  increase,  fats  diminish,  this  quantity,  while  sugar  and 
carbohydrates  appear  to  exert  no  influence  (Voit).  The  quantity 
secreted  in  twenty-four  hours  averages  from  500  to  600  c.c. 
(Ranke,  Wittich,  Hammarsten).  According  to  Phaff  and  Balch 
(“  Journ.  Experim.  Med.,”  vol.  11,  p.  59),  the  daily  quantity  was 
514.3  c.c.,  and  the  greatest  quantity  may  be  secreted  at  any  time  of 
the  day,  and  stands  in  no  definite  relation  to  any  meal.  The  quan- 
titative analyses  of  Hammarsten  have  given  the  following  results  : 


Solid  materials, 1.62  to  3.52 

Water, 96.47  “ 98.37 

Mucin  and  coloring  matter, o.  27  “ 0.91 

Compounds  of  bile-acids  and  alkalies, 0.26  “ 1.82 

Taurocholate, 0.052  “ 0.203 

Glycocholate, 0.204  “ 1.61 

Fatty  acids, 0.024“  0.136 

Cholesterin, 0.048“  0.16 

Lecithin, ....  0.048  “ 0.065 

Fat, 0.061  “ 0.095 

Soluble  salts, 0.676“  0.887 

Insoluble  salts,  0.02  “ 0.049 


At  times  a diastatic  ferment  is  present  in  the  bile  ; it  is  not  a 
specific  constituent  (Neumeister),  but  appears  in  the  bile  like  the 


6o 


BILE  AND  THE  SUCCUS  ENTERICUS. 


diastatic  ferment  which  appears  in  the  urine  ; it  seems  to  be  identi- 
cal with  the  ptyalin  zymogen  of  the  pancreatic  juice. 

When  the  bile  is  prevented  from  entering  the  intestine,  albu- 
mins, gelatins,  and  carbohydrates  are  absorbed  in  a normal  manner 
(Voit  and  J.  Munk),  but  the  digestion  of  fats  is  very  seriously 
interfered  with ; a normal  animal  resorbs  99  per  cent,  of  fats,  if 
not  more  than  150  to  200  grs.  are  given — i.  e.,  only  one  per  cent, 
appears  in  the  feces,  but  on  producing  an  experimental  fistula 
conducting  the  bile  outward,  60  per  cent,  of  the  fats  are  not  util- 
ized (Voit).  The  subjoined  is  a synopsis  of  the  uses  and  functions 
of  the  bile  : 

1.  Fats  are  brought  into  a fine,  permanent  emulsion  by  bile,  just 
as  by  pancreatic  juice. 

2.  Bile  assists  the  fat-splitting  effect  of  pancreatic  juice  (Nencki). 
Without  bile,  only  61  per  cent,  of  tribenzoicin  were  decomposed  by 
pancreatic  juice  ; with  bile,  the  total  amount. 

3.  By  its  alkalinity  it  accomplishes  the  formation  of  soaps. 

4.  Bile  dissolves  fats  in  minute  quantities. 

5.  Bile  dissolves  the  saponified  alkaline  bases  which  are  insolu- 
ble in  the  juices  of  the  intestines. 

6.  Animal  membranes  moistened  with  bile  are  more  permeable 
to  emulsified  fats  than  membranes  moistened  with  water  (von 
Wisting,  Heidenhain). 

7.  Bile  is  a stimulant  to  the  intestinal  epithelial  cells,  incites  their 
proper  functioning  and  maintains  it  (Rohmann). 

8.  It  is  claimed  that  albuminous  bodies  and  pepsin,  dissolved  in 
the  chyme,  are  precipitated  as  a resinous,  sticky  deposit,  which 
adheres  better  to  the  duodenal  wall,  and  effects  a better  utilization 
of  the  albuminates  thereby. 

9.  An  inhibitory  influence  over  putrefaction  is  ascribed  to  bile 
(Maly  and  Emmerich). 

10.  An  influence  favoring  an  increase  of  the  peristalsis  of  the 
intestine  (Rohmann). 

The  Succus  Entericus. — The  succus  entericus  is  a secretion  of 
the  crypts  of  Lieberkuhn,  and  was  first  studied  in  man  by  Demant 
after  a herniotomy.  This  secretion  has  the  color  of  light  Rhine 
wine,  and  is  very  strongly  alkaline,  owing  to  the  presence  of  1.5 
per  cent,  carbonate  of  sodium.  The  principal  constituents  are 
albumins  and  mucin.  It  contains  also  ptyalin  and  an  inverting 
ferment,  but  has  no  effect  on  albumins  and  fats ; its  purpose  seems 
to  be  that  of  a neutralizer  of  the  acids  originating  from  fermenta- 


THE  FORMED  OR  ORGANIZED  FERMENTS. 


6l 


tion  of  carbohydrates;  its  excess  of  mucin  may  be  instrumental  for 
the  onward  movement  of  the  bowel  contents. 

The  Formed  or  Organized  Ferments  (Bacteria). — Proteids, 
carbohydrates,  and  fats  are  subject  to  decomposition  in  the  intes- 
tines by  bacteria.  Fats  are  not  decomposed  to  any  considerable 
extent  in  the  lower  intestinal  sections  (Nencki  and  Blank),  but  a 
small  fraction  is  split  up  into  glycerin  and  fatty  acids. 

A greater  interest  attaches  itself  to  the  fermentation  of  carbo- 
hydrates, which  occur  principally  in  the  upper  small  intestine  and 
leads  to  the  formation  of  acetic,  lactic,  butyric,  and  carbonic  acids, 
alcohols,  and  hydrogen.  It  is  not  known  how  much  of  the  carbo- 
hydrates is  decomposed  in  this  manner. 

The  putrefaction  of  proteids,  caused  by  certain  bacteria  of  the 
lower  bowel,  occurs  chiefly  in  an  alkaline  medium.  The  first  prod- 
ucts of  this  putrefaction  are  the  identical  bodies  which  are  formed 
during  pancreatic  digestion — viz. : albumoses,  peptone,  amido-acids, 
and  ammonia.  But  then  the  putrefaction  goes  still  further;  tyrosin 
is  formed,  and  from  this,  through  a series  of  complex  oxyacids,  the 
product  phenol  (carbolic  acid)  is  reached,  which  may  yield  phenyl- 
propionic  and  phenylacetic  acids.  A second  variety  of  aromatic 
substances,  not  derived  from  tyrosin,  is  represented  by  indol,  skatol, 
and  skatol  carbonic  acid ; finally,  leucin  and  ammonia  salts  of  ca- 
pronic,  valerianic,  and  butyric  acids.  The  gases  formed  are  car- 
bonic acid  gas,  hydrogen,  hydrogen  sulphid,  and  methyl-mercaptan. 
As  bacteria  can  produce  peptone,  it  might  be  presumed  that  such 
product  may  be  useful  to  the  organism.  This  peptone  is  not  made 
for  philanthropic  purposes — it  is  simply  one  intermediate,  probably 
unavoidable  stage  in  a long  chain  of  decompositions. 

We  can  not  measure  the  intensity  of  carbohydrate  fermentation, 
but  the  aromatic  end-products  of  proteid  putrefaction  can  be 
approximately  estimated  by  determination  of  the  amounts  of  com- 
bined and  ethereal  sulphates  occurring  in  the  urine. 

The  number  of  bacteria  increases  from  the  duodenum  down- 
ward until  they  become  enormously  profuse  in  the  colon.  They 
also  differ  qualitatively.  In  the  small  intestine,  Gessner  found  a 
prevalence  of  the  bacterium  lactis  aerogenes  and  streptococcus 
pyogenes  ; the  colon  bacillus  was  present,  but  insignificant  in  num- 
bers. In  the  colon,  however,  the  reverse  was  the  case.  It  was 
formerly  an  accepted  view,  principally  defended  by  Pasteur,  that 
the  intestinal  bacteria  were  absolutely  indispensable  for  digestion, 
and,  therefore,  for  the  nutrition  of  the  individual.  From  this  view 
5 


62 


BACTERIA  NOT  ESSENTIAL  TO  DIGESTION. 


we  have  returned  to  what  seems  a more  logical  belief,  based  on 
observations  of  Escherich,  who  held  that  bacteria  contributed  very 
little  to  the  digestion  of  the  infant,  as  they  do  not  affect  casein  and 
fats,  but  only  sugar  of  milk,  turning  it  into  lactic  and  carbonic 
acids  and  hydrogen.* 

Macfadyen,  Nencki,  and  Sieber  arrived  at  a similar  conclusion 
in  their  now  classical  observations  on  adults  (“  Archiv  fur  exp. 
Pathologie,”  Bd.  xxviii,  1891).  One  of  their  objects  of  study  was 
a female  with  a fistula  that  opened  the  small  intestine  on  the  exter- 
nal abdominal  wall,  just  at  the  end  of  the  ileum.  The  entire  colon 
was  therefore  excluded  from  the  digestive  act.  As  nearly  all  pro- 
teid  putrefaction  occurs  in  the  colon,  this  case  presented  a chance 
to  study  the  condition  of  absence  of  products  of  albuminous  putre- 
faction and  its  effects. 

It  was  found  that  bacteria  are  not  at  all  essential  to  digestion, 
as  their  patient  was  very  healthy  without  proteid  putrefaction. 
They  declare  that  the  bacterial  fermentation  of  carbohydrates  in 
the  small  bowel  is  detrimental,  rather  than  advantageous  ; inasmuch 
as  the  bacteria  live  at  the  expense  of  the  ingested  carbohydrates, 
a corresponding  amount  of  food  is  lost  to  the  organism. 

Our  knowledge  of  the  bacterial  activity  in  the  intestines,  though 
much  enriched  by  valuable  researches  in  the  last  decad,  is,  accord- 
ing to  our  opinion,  in  its  infancy.  So,  also,  our  knowledge  of  the 
pathogenic  significance  of  intestinal  bacteria.  There  is,  undoubt- 
edly, a kind  of  interaction  and  correlation  between  digestive 
ferments  and  juices  on  the  one  hand,  and  bacteria  on  the  other,  or 
even  between  bacteria  and  bacteria,  or  between  the  products  of 
bacterial  metabolism.  For  instance,  Metschnikoff  has  demonstrated 
that  the  multiplication  of  the  cholera  vibrio  is  much  advanced  by 
the  presence  of  torulae  and  sarcinae  in  the  intestines. 

It  is  conceivable  that  bacteria  wage  war  upon  one  another,  as  well 
as  upon  the  cells  of  our  tissue,  and  that  we  are  benefited  by  this 
mutual  self-destruction  of  our  parasitic  inhabitants.  It  is  con- 
ceivable, also,  that  they  fall  a prey  to  the  poisonous  metabolic 
products  of  their  own  or  other  species  of  bacteria.  Certain  very 
decomposable  food,  as  cheese  that  was  rich  in  germs,  has  been 
found  by  competent  observers  to  reduce  the  amount  of  indican 


* The  work  of  Nuttal  and  Thierfelder  shows  that  guinea-pigs  can  live  on  absolutely 
sterile  food,  the  excrement  of  the  animals  being  sterile  also  while  they  were  under  the 
control  of  the  experimenters. 


HYDROCHLORIC  ACID  NOT  ABSOLUTELY  ANTISEPTIC.  63 

and  of  the  ethereal  sulphates  in  the  urine,  which  indicates  a reduced 
putrefaction  (see  A.  Lockhart  Gillespie,  “ Edinburgh  Medical 
Journal/’  November,  1898,  p.  428). 

The  human  stomach  must  not  be  regarded  as  an  organ  that  can 
absolutely  sterilize  all  food.  The  spores,  being  more  resistant  to 
HC1  than  the  fully  developed  bacteria  themselves,  pass  through 
the  stomach  uninjured.  Miller  assumes  that  at  the  height  of 
digestion  only,  when  the  amount  of  HC1  is  greatest,  the  less 
resistant  bacteria  are  killed.  Bunge,  some  years  ago,  announced 
that  the  principal  object  of  the  HC1  was  one  of  sterilization.  It  is 
undeniable,  from  recent  investigations,  that  the  human  stomach  is 
at  no  time  free  from  germs.  Captain  and  Morau  found  them  at  the 
height  of  digestion.  Abelous  found  them  in  his  own  stomach 
when  it  was  perfectly  empty.  Miller  (University  of  Berlin)  demon- 
strated that  the  mouth  contains  large  quantities  of  microbes  ; in  one 
unclean  individual  he  estimated  the  numbers  of  mouth  bacteria  at 
1,140,000,000.  Of  twenty-five  different  varieties  occurring  in  the 
mouth,  this  observer  was  able  to  demonstrate  twelve  of  the  same 
in  the  feces.  Nevertheless,  the  mouth  bacteria,  according  to 
Lucksdorff,  constitute  only  three  per  cent.,  while  those  entering 
through  the  food  constitute  ninety-seven  per  cent,  of  the  bacteria 
of  the  intestine.  There  is  no  autochthonous  vegetation  of  bacteria 
in  the  intestine  ; they  are  all  introduced  from  the  mouth,  or  in  the 
food,  or  reach  thereby  way  of  the  circulation.  (By  autochthonous 
bacteria  are  meant  such  as  are  originally  developed  at  the  place 
where  they  are  found.) 

From  observations  made  up  to  the  present  time  it  seems  prob- 
able that  catarrhal  and  other  inflammatory  diseases  of  the  intestinal 
mucosa  are  not  produced  by  specific,  constantly  recurring  microbes, 
but  that  many  kinds  of  bacteria  are  capable  of  producing  these  dis- 
eases under  conditions  which  are  thus  far  not  perfectly  understood. 

It  appears,  furthermore,  that  the  same  bacterium  may  at  one 
time  be  perfectly  harmless,  or  it  may  cause  a light,  trivial  affec- 
tion, or  at  other  times  a very  serious  disturbance.  This  is  the 
case  with  the  bacterium  coli  communis,  which  is  tolerated  without 
detriment  by  the  majority  of  mankind;  but  occasionally  it  is 
demonstrated  as  the  producer  of  colitis,  dysentery,  and  cholera 
nostras. 

The  manifold  forms  of  the  catarrhal  inflammations  are  explicable 
by  the  fact  that  the  intestinal  flora  is  also  very  manifold.  These 
same  bacteria  are  factors  in  the  etiology  of  diseases  of  the  perito- 


64 


INTESTINAL  AUTO-INTOXICATION. 


neum,  and  of  all  organs  that  are  in  connection  with  the  intestines. 
Even  remote  organs,  not  in  anatomical  connection  with  the  bowel, 
are  not  safe  from  their  invasion. 

They  are  known  to  gain  entrance  into  the  blood  and  lymphatic 
channels  through  losses  of  substance  in  the  intestinal  mucosa.  The 
experiments  of  Posner  and  Lewin  have  taught  us  that  even  without 
such  portals  of  entry  they  seem  to  be  able  to  pass  through  the 
bowel-wall  in  masses,  and  threaten  the  organism.  Hans  Hensen 
(“  Zeitschr.  f.  Biol.,”  Bd.  xxxv,  p.  1 10)  has  shown  that  bacteria 
can  penetrate  natural  and  artificial  membranes  that  allow  diffusion. 
There  are  fine  canals,  passable  for  bacteria,  that  can  not  be  demon- 
strated by  the  hemoglobin  test.  Great  harm  can  be  done  to  the 
general  organism,  and  to  special  organs  in  particular,  not  only  from 
this  invasion,  but  also  from  absorption  of  the  soluble  products  of 
bacterial  metabolism  and  of  food  decomposition. 

This  condition  of  self-poisoning  from  toxic  substances  in  the 
individual’s  own  intestinal  canal  is  spoken  of  as  intestinal  auto- 
intoxication. Not  all  auto-intoxications  are  of  intestinal  origin ; 
diabetes  mellitus,  for  instance,  is  an  auto-intoxication  by  grape 
sugar,  which  is  in  this  case  a product  of  disturbed  metabolism,  and 
does  not  originate  from  the  digestive  canal. 

The  dangers  which  threaten  the  general  organism  from  the  intes- 
tinal bacteria  have  given  rise  to  many  efforts  to  sterilize  the  digestive 
tract  by  means  of  so-called  antiseptics.  Most  of  the  agents  used 
for  this  purpose — calomel,  salol,  naphthalin,  beta-naphthol,  bis- 
muth, creosote,  bismuth  salicylate — are  themselves  toxic,  and  in 
doses  sufficiently  large  to  reduce  the  number  of  bacteria  to  any 
considerable  extent,  are  harmful  to  the  body.  The  putrefaction  of 
proteids,  as  measured  by  the  relation  between  the  amounts  of  the 
combined  and  ethereal  sulphates  in  the  urine,  can  only  be  tempor- 
arily diminished  by  this  method. 

Intestinal  disinfection  is  therefore  an  unsolved  problem.  Efforts 
in  this  direction  should  still  be  encouraged,  because  we  may  be  able 
thereby  to  attenuate  the  pathogenic  inhabitants  of  our  intestines  and 
render  them  less  virulent.  The  best  disinfectant  of  the  human  in- 
testine is  its  normal  action,  and  the  best  way  to  control  putrefaction 
is  by  the  selection  of  adapted,  appropriate  diet,  by  fresh  air,  moderate 
exercise,  good  sleep,  pure  water,  and  by  the  avoidance  of  overeating 
and  overdrinking  (Hemmeter,  “ On  Intestinal  Putrefaction  and 
Albuminuria/’  “ Maryland  Medical  Journal,”  July  24  and  31,  and 
August  7,  1897). 


EFFECTS  OF  THE  ACTION  OF  SOME  DIGESTIVE  SECRETIONS.  65 


CHAPTER  VII. 

EFFECTS  OF  THE  ACTION  OF  THE  SEVERAL  DIGESTIVE 
SECRETIONS.— METHODS  FOR  TESTING  THE 
MOTOR  FUNCTIONS  OF  THE  STOMACH. 

When  the  gastric  chyme  enteis  the  duodenum,  the  albuminoid 
and  proteid  foods  appear  partly  as  syntonin,  albumoses,  and  pep- 
tones, and  partly  unchanged.  The  carbohydrates  appear  either  as 
erythrodextrin,  achroodextrin,  or  maltoses,  and  partly  unchanged. 
The  fats  are  unchanged  ; rarely  are  they  found  split  up,  so  that 
one  can  detect  traces  of  fatty  acids. 

Water,  according  to  the  interesting  investigations  of  von  Mering, 
is  absorbed  only  in  very  small  quantities  from  the  stomach.  It  ap- 
pears that  fully  ninety  per  cent,  of  all  water  taken  into  the  stomach 
is  passed  into  the  duodenum;  alcohol,  and  whatever  is  in  solution 
in  it,  is  absorbed  readily.  Grape-,  milk-,  and  cane-sugar,  also  mal- 
tose, are  absorbed  in  moderate  amounts  when  they  are  in  aqueous 
solution.  When  they  are  in  alcoholic  solution,  larger  amounts  are 
absorbed.  Dextrin  and  peptone  are  also  taken  up  from  the 
stomach,  but  in  smaller  quantities  than  sugar.  The  amount  of  the 
substances  resorbed  increases  with  the  concentration  of  the  solu- 
tion. Simultaneously  with  this  resorption,  a more  or  less  active 
secretion  of  water  occurs  into  the  stomach.  This  secretion  in- 
creases or  diminishes  as  the  quantity  of  substances  resorbed  or 
taken  up  increases  or  diminishes. 

Secretion  of  water  occurs  even  when  no  HC1  is  demonstrable  in 
the  normal  stomach.  The  chyme,  then,  as  it  enters  the  duodenum, 
still  contains  all  of  its  water,  but  is  minus  some  of  the  peptones, 
dextrins,  sugars,  and  alcohols.  It  is  more  or  less  acid  from  free  HC1. 
When  the  bile  acts  on  this  acid  chyme,  a resinous,  flocculent  pre- 
cipitate is  deposited  from  it  on  the  walls  of  the  duodenum  ; at  the 
same  time  a finely  granular  cloudiness  occurs.  The  resinous  deposit 
consists  of  bile-acids  and  syntonin  (Hammarsten),  and  the  granu- 
lar opacity  is  due  also  to  bile  acids  and  small  amounts  of  peptone. 

Excess  of  bile  may  redissolve  these  precipitates  so  that  they  can 
not  at  times  be  found  in  animals  killed  at  the  height  of  digestion. 
The  digestion  by  pepsin  is  checked  by  the  complete  neutralization 
of  HC1  by  pancreatic  juice,  bile,  and  succus  entericus.  If  any  pre- 


66 


INTERACTION  OF  DUODENAL  SECRETIONS. 


cipitation  occurs  as  stated,  pepsin  is  also  thrown  down  and  resorbed 
again  or  digested  by  trypsin.  The  bile  does  not  disturb  the  pro- 
teolytic power  of  pancreatic  juice  (Claude  Bernard).  Boas  and  the 
author  have  shown  that  the  clear  duodenal  chyme  will  digest  81 
per  cent,  of  serum-albumin  in  three  hours ; at  40°  C.  its  alkalinity 
was  0.8  per  cent.,  Na2Co3.  It  was  also  shown  that  this  duodenal 
chyme  converted  25  per  cent,  of  starch  into  maltose,  and  that  it 
produced  12.1  per  cent,  fatty  acids  from  neutral  olive  oil  in  three 
hours.  Boas  obtained  his  mixture  of  bile,  pancreatic  juice,  and 
succus  entericus  from  a patient  who  had  most  probably  a duodenal 
stenosis  and  who  vomited  this  chyme  frequently.  In  the  author’s 
experiments  the  duodenal  secretions  were  obtained  by  his  method 
of  intubation  of  the  duodenum.  The  contents  of  the  duodenum 
are  acid,  even  in  cases  where  no  HC1  is  secreted  in  the  stomach. 

It  was  found  in  these  experiments  that  the  duodenal  juices,  when 
filtered,  digested  85  per  cent,  to  95  per  cent,  of  Merck’s  dried  serum- 
albumin  in  three  hours  at  40°  C.  The  author’s  results  with  starch 
conversion  show  that  the  filtered  duodenal  juices  will  digest  42  per 
cent,  of  starches,  or  rather  convert  them  into  maltose,  which  is  con- 
siderably in  excess  of  the  figures  obtained  by  Boas.  The  fat- 
splitting effect  observed  by  us  in  this  juice  was  nearer  the 
result  of  Boas,  for  we  found  that  15.3  per  cent,  of  fatty  acids  were 
obtained  from  neutral  olive  oil.  In  a case  of  biliary  calculi,  we  have 
been  able  to  obtain  the  pancreatic  juice  free  from  bile,  as  the  bile- 
ducts  must  have  been  stenosed  either  by  a small  calculus  or  a bit 
of  thickened  bile  and  mucus  mixed. 

The  fat-splitting  effect  of  pancreatic  juice  is  improved  by  the 
presence  of  bile,  as  is  also  the  amylolytic  action  of  amylopsin. 

Demonstration. — The  action  of  pancreatic  juice  obtained  from  a 
dog  on  neutral  olive  oil  and  on  a solution  of  starch  should  be 
studied  both  with  and  without  bile.  Pancreatic  juice  plus  bile  will 
split  up  more  fat  and  convert  more  starch  into  maltose  than 
without  bile  (Martin  and  Williams). 

The  effect  of  trypsin  on  pepsin  is  not  definitely  known,  but  it  is 
probable  that  pepsin,  being  closely  allied  to  proteids,  is  disintegrated 
by  trypsin ; but  in  an  acid  solution  pepsin  checks  the  action  of  trypsin 
(Kuhne,  Langley,  Ewald,  and  Baginsky).  According  to  Baginsky, 
rennin  is  destroyed  by  a neutral  solution  at  room  temperature. 
The  ferment  action  of  bacteria  in  the  small  intestine  is  limited 
to  the  carbohydrates.  Discharges  of  food  from  fistulae  of  the  small 
intestine  show  no  fetid  decomposition  of  albuminoids  (Ewald  and 


NATURE  OF  CONTENTS  OF  ILEUM  AND  COLON. 


67 


Nencki).  The  absence  of  proteid  putrefaction  in  the  small  intestine 
is  probably  due  to  the  rapid  downward  movement  of  the  food  mass 
in  this  portion  of  the  bowel  and  to  its  acid  condition. 

Carbohydrate  fermentation  yields  mainly  lactic  acid,  ethyl 
alcohol,  carbon  dioxid,  and  hydrogen.  Macfadyen,  Nencki,  and 
Sieber  found  the  chyme  that  passed  over  into  the  large  intestine 
(the  cecum)  from  the  ileum  to  be  550  gm.,  with  4.9  per  cent,  solid 
residue  in  case  the  chyme  was  of  a very  thin  consistence  ; and  232 
gm.,  with  1 1.23  per  cent,  solid  residue,  if  the  chyme  was  very  con- 
densed. Both  of  these  figures  are  the  amounts  passing  in  twenty- 
four  hours.  The  shortest  time  in  which  food  passed  into  the  cecum 
after  it  was  swallowed  was  two  hours  ; the  longest  period,  five  and 
a quarter  hours. 

The  reaction  expressed  in  acetic  acid  was  equal  to  one  per 
thousand;  the  acidity  is  considered  to  be  due  to  newly  formed 
acetic  acid,  as  the  lactic  acid  and  the  HC1  are  neutralized  by  the 
succus  entericus.  This  chyme  contained  one  per  cent,  albumin  ; also 
peptone,  mucin,  dextrin,  sugar,  lactic  acid,  sarcolactic  acid,  and 
traces  of  fatty  acids  ; it  contained  no  leucin,  tyrosin,  urobilin,  or 
ammonia.  The  characteristic  products  of  albuminoid  decomposi- 
tion were  absent. 

Jaworski’s  investigation  on  the  contents  of  the  large  intestine, 
which  were  discharged  from  a fistula  in  the  ascending  colon,  showed 
that  the  daily  fecal  discharge  of  150  to  200  grs.  was  decidedly 
alkaline,  and  contained  the  products  of  proteid  and  albuminoid 
decompositions,  viz. : urobilin,  skatol,  phenol,  oxyacids,  ammonia, 
leucin,  cadaverin,  ethyl  and  butyl  alcohol,  sulphuretted  hydrogen, 
and  methyl-mercaptan. 

In  view  of  the  fact  that  the  putrefaction  of  albuminoids  and  pro- 
teids  occurs  mainly  in  the  colon,  it  is  of  interest  to  know  how  much 
of  this  class  of  food  substances  is  left  for  the  colon,  and  how  much 
is  digested  in  the  small  intestine.  Nencki  found  that  when  the  food 
contained  70.74  gm.  albumin,  which  represent  10.602  gm.  nitrogen, 
the  amount  of  solid  material  discharged  from  a colon  fistula  in 
twenty-four  hours  was  26.5  gm.,  with  1.61  gm.  nitrogen,  which 
represented  10.06  gm.  albumin.  From  this  it  is  evident  that  14.25 
per  cent.,  or,  in  other  terms,  only  one-seventh  of  the  total  albumin, 
is  left  for  digestion  in  the  colon,  and  that  85.75  Per  cent,  is  re- 
sorbed from  the  stomach  and  small  intestine. 

The  intensity  of  putrefaction  in  the  colon  depends  upon  four 
factors  : (1)  The  amount  of  decomposable  albuminoid  materials  in- 


ULTIMATE  FATE  OF  DIGESTIVE  FERMENTS. 


gested ; (2)  the  duration  of  their  retention  in  the  colon  ; (3)  the 
vigor  and  tonicity  of  the  intestinal  peristalsis ; and  lastly  (4)  the 
chemical  reaction  ; for  a very  strong  acid  reaction,  due  to  free 
acids,  inhibits  putrefaction. 

Bile  assists  in  this  inhibition.  Hirschler  has  demonstrated  that 
carbohydrates  suppress  putrefaction  considerably ; this  is  due  to 
the  lactic,  butyric,  acetic,  and  carbonic  acids  caused  by  their  fer- 
mentation. Albumin  and  peptone  are  absent  from  the  contents  of 
the  rectum  (feces),  but  are  present  in  typhoid  fever  (von  Jaksch). 
Peptone  is  found  in  all  diseases  that  may  produce  pus  in  the  evacua- 
tions— for  instance,  dysentery,  tuberculous  intestinal  ulcers,  per- 
foration, peritonitis,  hepatic  cirrhosis,  and  carcinoma. 

A very  important  inquiry  is  that  into  the  ultimate  fate  of  the 
digestive  ferments  : Do  they  pass  through  the  entire  intestinal 
tract?  are  they  absorbed  or  are  they  decomposed?  or  do  they 
appear  in  their  active  form  in  the  feces  ? This  question  is  a very  dif- 
ficult one  to  solve,  as  our  only  method  of  detecting  pepsin,  chymosin, 
trypsin,  and  ptyalin  is  by  their  digestive  activity.  In  all  experi- 
ments of  this  kind  the  feces  must  be  first  sterilized  by  saturated 
solutions  of  thymol  ; before  using  this  it  is  well  to  exclude  the 
action  of  peptonizing  bacteria  by  filtering  through  a Pasteur  filter. 

If  we  found  in  the  glycerin  extract  of  the  sterilized  feces  a sub- 
stance which  would  dissolve  boiled  egg-albumen  in  a solution  of 
0.2  per  cent.  HC1,  we  should  be  justified  in  concluding  that  it  was 
pepsin.  If  it  did  not  digest  in  HC1,  but  in  a one  per  cent,  solution 
of  sodium  carbonate,  it  would  probably  be  trypsin. 

For  the  demonstration  of  a diastatic  ferment  a dilute  solution  of 
starch  is  brought  into  the  incubator  with  about  five  c.c.  of  filtered, 
sterilized  feces.  After  a few  hours  the  HC1  and  soda  solutions  of 
the  boiled  albumin  are  tested  for  peptone  by  the  biuret  reaction, 
and  the  diastatic  test-tube  is  tested  with  a dilute  solution  of  iodin 
in  iodid  of  potassium.  If  the  starch  is  unchanged,  the  solution 
will  be  changed  to  blue ; if  not,  the  color  will  be  brown  or  yellow. 

In  this  way  we  have  confirmed  the  fact  that  pepsin  is  absent 
from  the  colon  contents,  but  trypsin  is  at  times  present,  since  the 
perfectly  sterile  extract  of  feces  will  digest  fibrin  and  albumin  in 
alkaline  solution. 

The  digestive  action  of  the  succus  entericus,  which,  according  to 
Griitzner,  has  a weak  fibrin-dissolving  property,  does  not  extend  to 
the  albumins,  and  therefore  it  will  not  confuse  the  result  stated 
above  as  pertaining  to  pepsin  and  trypsin. 


FATE  OF  DIGESTIVE  FERMENTS. 


69 


The  chief  digestive  action  of  succus  entericus  is  on  the  carbohy- 
drates. If  peptone  occurs  in  the  stools,  it  is,  in  the  author’s  opinion, 
a product  either  of  pepsin  or  trypsin  digestion,  not  exclusively  of 
bacterial  origin.  Undoubtedly,  there  are  proteolytic  bacteria — for 
instance,  the  bacillus  subtilis  of  Ehrenberg,  the  proteus  vulgaris  of 
Hauser,  the  bacillus  putrificus  coli  of  Bienstock,  and  the  bacillus 
liquefaciens  ilei  of  Macfadyen,  Nencki,  and  Sieber,  all  of  which 
exist  ordinarily  in  the  human  intestine;  and  their  first  products  of 
action  on  albumins  are  the  same  as  occur  in  normal  pancreatic 
digestion,  viz.:  albumoses,  peptones,  amido-acids,  and  ammonia; 
but  then  the  action  continues  uninterruptedly,  ending  in  the  forma- 
tion of  decomposition  products  stated  in  a previous  paragraph. 
The  bacterial  product  of  peptone  is  probably  of  no  use  to  the 
organism  in  which  it  occurs — it  is  a first  stage  to  proteid  putrefac- 
tion, and  these  proteolytic  parasites  need  peptone  for  their  own 
existence. 

The  remote  possibility  that  only  bacteria  could  produce  peptone 
in  the  colon  (feces)  might  be  excluded  by  the  fact  that  after  sterili- 
zation of  the  feces  by  a saturated  solution  of  thymol,  peptone  will, 
in  some  cases,  still  be  produced  when  the  above  tests  are  made.  It 
is  due  most  probably  to  trypsin,  which  is  present  in  the  stools 
when  they  have  traversed  the  intestines  rapidly. 

Starch-inverting  ferments  are  present  in  the  saliva,  pancreatic 
juice,  and  succus  entericus  ; hence,  if  such  a ferment  appears  in  the 
feces,  it  is  impossible  to  decide  upon  its  source. 

Amylopsin  and  steapsin  have  not  been  demonstrated  as  such  in 
normal  feces.  It  is  not  known  whether  pepsin  and  rennin  (chymo- 
sin)  occur  in  normal  feces.  We  have  found  a proteid-dissolving 
ferment  in  the  stool,  which  acted  in  a one  per  cent,  solution  of 
carbonate  of  sodium  only,  and  was  studied,  in  a case  of  complete 
atrophy  of  the  gastric  mucosa,  with  total  absence  of  HC1,  pepsin, 
and  chymosin,  and  also  of  the  proenzymes  of  these  ferments.  In 
the  wash-water,  bits  of  mucosa  were  found  that  proved  the  absolute 
destruction  of  the  glandular  apparatus  of  the  stomach. 

It  is  probable  that  this  ferment  was  trypsin.  There  was  a mod- 
erate gastrectasia,but  otherwise  no  anatomical  defect  was  observa- 
ble. The  stools  were  not  diarrheic.  Escherich’s  assertion  that  the 
colon  bacteria  do  not  live  upon  the  food  introduced, — as,  accord- 
ing to  his  opinion,  there  is  no  digestible  food  left  there  under  normal 
conditions, — but  that  they  live  upon  the  secretions  of  the  walls  of 
the  colon,  is  certainly  erroneous — if  this  statement  of  his  view  is 


70 


MOTOR  FUNCTIONS  OF  THE  STOMACH. 


correct  (quoted  from  Mannaberg,  in  Nothnagel’s  “ Erkrankungen 
des  Darms,”  p.  38). 

The  conception  of  some  writers  on  this  subject  that  food  mate- 
rials are  completely  used  up  in  the  digestive  tube,  is  not  proved  by 
actual  fact.  Even  meat,  when  eaten  in  a most  digestible  form,  is 
found  in  visible  traces  undigested  in  the  evacuations.  It  is  there- 
fore more  than  probable  that  the  colon  bacteria  live  at  the  expense 
of  the  ingested  proteid  food. 

Having  thus  far  reviewed  the  physiology,  anatomy,  and,  in  part, 
the  pathology  of  food  digestion  in  general,  let  us  now  return  to  the 
special  pathology  of  the  functions  of  the  stomach,  as  a preparation 
for  a better  comprehension  of  its  diseased  states. 

Qualitative  and  Quantitative  Methods  for  Testing  the  Motor 
Functions  of  the  Stomach. — The  motor  or  peristaltic  function 
is  the  most  important  one.  A man  may  be  able  to  live  without 
the  secretory  and  resorptive  functions  of  his  stomach,  as  the 
intestinal  digestion  and  secretion  would  suffice  for  amylolysis  and 
proteolysis,  and  he  depends  upon  the  small  intestine  altogether 
for  the  digestion  and  absorption  of  fats ; so  that  even  in  the  total 
absence  of  gastric  resorption  and  the  falling  away  of  secretions  of 
HC1,  pepsin,  and  rennin  ferments,  life  could  be  maintained. 

But  if  the  motor  function  is  interfered  with,  the  food  would 
remain  in  the  stomach  and  accumulate.  If  a normal  gastric  juice 
were  even  possible  when  the  peristalsis  is  paralyzed,  the  food  could 
be  only  partly  digested.  Carbohydrates  and  fats  would  not  be 
digested.  When  the  limit  of  distention  was  reached,  the  food 
would  be  ejected  as  in  pyloric  stenosis  and  gastrectasia. 

In  all  cases  of  inhibition  or  loss  of  motor  power,  the  secretory 
power  is  seriously  disturbed,  or  may  cease  absolutely;  so  also  the 
resorptive  power.  (See  chapters  on  Supersecretion  and  Motor 
Insufficiency.)  Many  cases  of  total  absence  of  gastric  secretions 
have  been  reported  in  patients  whose  body-weight  remained 
normal  and  their  general  health  unimpaired.  The  stomach  has 
been  removed  experimentally  in  dogs,  and  the  animals  continued 
to  thrive  without  it,  if  precautions  were  taken  to  provide  finely 
divided  food.* 

* Schlatter,  of  Zurich  (“  Med.  Record,”  1897,  Lll,  909),  and  Dr.  Brigham  (“  Journ. 
Amer.  Med.  Asso.,”  Feb.  12,  1898)  have  successfully  removed  the  entire  stomach  from 
human  patients  in  whom  the  digestive  process  continued  practically  normal,  at  least  up 
to  the  date  of  publication.  Much  is  yet  to  be  learnt  from  the  future  of  these  two  cases. 
Even  a year  of  artificial  life  under  the  constant  care  of  physicians  does  not  prove  that  the 
stomach  can  be  dispensed  with. 


TESTING  THE  GASTRIC  MOTOR  FUNCTIONS.  J I 

There  have  been,  up  to  very  recently,  six  different  methods  pro- 
posed for  determining  the  motor  functions  of  the  human  stomach  : 
the  methods  of  Leube,  Ewald  and  Sievers,  Klemperer,  Fleischer, 
Einhorn,  and  Hemmeter. 

Leube’s  method  of  estimating  the  duration  of  gastric  digestion — 
i.  e.t  to  determine  after  a definite  average  time  of  six  to  seven  hours 
after  a meal  of  50  gm.  bread,  200  gm.  beefsteak,  and  a glass  of  water, 
or  two  hours  after  an  Ewald  test-breakfast,  whether  solid  contents 
are  still  to  be  found  in  the  stomach — will  serve  the  practitioner 
with  a simple  and  ready  method,  which  follows  naturally  in  the  line 
of  drawing  test-meals  from  the  stomach  ; it  is,  however,  subject  to 
too  many  physiological  variations  to  permit  of  accurate  deductions. 

Ewald  has  proposed  the  use  of  salol,  which,  according  to  Nencki, 
is  not  decomposed  by  acids  in  the  stomach,  but  is  converted,  by 
the  alkaline  juices  of  the  duodenum,  into  salicylic  acid  and  phenol. 
He  and  Sievers  found  that  the  appearance  of  salicyluric  acid — the 
product  of  the  decomposition  of  the  salol  in  the  urine — would 
indicate  that  the  salol  had  actually  passed  out  of  the  stomach. 

Normally,  salicyluric  acid  will  appear  in  the  urine  from  forty  to 
seventy-five  minutes  after  taking  one  gm.  of  salol.  Delay  in  its 
appearance  will  indicate  a retardation  in  the  passage  of  food  into 
the  intestines. 

Salicyluric  acid  is  recognized  in  the  urine  by  the  violet  color 
produced  on  the  addition  of  neutral  ferric  chlorid  solution.  This 
method  necessitates  frequent  urination  of  the  patient — every  five 
minutes,  at  least;  otherwise  the  result  will  not  be  accurate. 

Brunner,  Riegel,  and  Eichhorst  found  that  the  time  in  which  the 
reaction  occurred  in  the  healthy  individual  varied  from  forty 
minutes  to  two  hours.  This  was  to  be  anticipated,  as  the  period 
during  which  a test-meal  may  remain  in  the  stomach  may  vary 
normally  between  two  and  three  hours. 

A.  Lockhart  Gillespie  found  that  in  the  dog  salol  was  not  decom- 
posed above  the  mid-ileum,  and  suggested  that  salol  can  pass  un- 
changed through  the  stomach-wall  and  become  altered  in  the  blood* 
its  derivatives  appearing  in  the  urine. 

The  duodenum  was  severed  close  to  the  stomach,  and  the  pyloric 
end  of  the  stomach  pulled  through  the  abdominal  wall.  Although 
it  was  thus  impossible  for  the  drug  to  reach  the  bowel,  the  dog’s 
urine  contained  salicyluric  acid,  notwithstanding  the  complete 
failure  of  the  test  for  that  body  in  the  contents  of  the  stomach 
(“  Edinburgh  Med.  Journ.,”  Nov.,  1898). 


72 


METHODS  FOR  TESTING  THE  GASTRIC  PERISTALSIS. 


CHAPTER  VIII. 

METHODS  FOR  TESTING  THE  GASTRIC  PERISTALSIS. — 
(Continued.) 

As  Evvald’s  salol  test  is  not  applicable  in  private  practice,  because 
of  the  frequent  micturition  that  is  necessary.  It  is  impossible  to 
examine  females  by  this  method  for  the  same  reason ; and,  also, 
because  the  excretion  of  salicyluric  acid  depends  upon  the  chang- 
ing energy  of  the  heart’s  action,  intra-arterial  pressure,  the  amount 
of  water  in  the  blood,  and  the  changeable  function  of  the  kidneys 
themselves. 

Huber  improved  this  method  somewhat  by  ascertaining  that 
salicyluric  acid  disappears  from  the  urine  in  twenty-four  hours,  after 
the  administration  of  salol  to  healthy  persons  ; but  in  patients  with 
impaired  gastric  peristalsis,  the  reaction  continues  to  be  distinct 
much  longer — sometimes  for  forty-eight  hours.  According  to 
Fleischer  and  Hecker,  the  duration  of  excretion  of  potassium  iodid 
in  the  urine  of  healthy  individuals  varies  from  twenty-nine  to  fifty 
five  hours  ; of  sodium  salicylate,  from  twenty-one  to  twenty-nine 
hours ; and  in  cardiac  and  nephritic  patients  this  may  vary  from 
eighty  to  ninety-six  hours.  It  is  evident  that  methods  of  so  vari- 
able a character  are  not  satisfactory  for  exact  research;  nor  even, 
on  account  of  the  great  loss  of  time,  of  much  value  for  compara- 
tive tests. 

Klemperer’s  method  consists  in  the  introduction  of  ioo  gm.  of 
neutral  olive  oil  into  the  perfectly  clean  stomach,  after  lavage, 
through  a stomach-tube.  Oil  or  fatty  acids,  which  are  formed  in 
traces,  are  not  absorbed  from  the  stomach.  After  two  hours,  all 
oil  yet  remaining  is  washed  out  by  repeated  lavage,  dissolved  in 
ether,  and  weighed  after  removal  of  the  .ether  by  distillation.  In 
the  normal  subject  Klemperer  could  find  but  20  to  30  gm.  of  oil; 
the  remaining  70  to  80  gm.  had  passed  into  the  intestine.  If  larger 
amounts  are  found, — for  instance,  50  to  60  gm.,  or  more, — they  are, 
according  to  Klemperer,  an  evidence  of  motor  insufficiency.  This 
method  requires  much  time  and  skilled  chemical  analysis,  and  is 
also  open  to  the  same  objection  as  that  of  Leube. 

Fleischer  (“  Spez.  Path.  u.  Therap.  d.  Magen-  u.  Darmkrankh.,” 
p.  791)  has  proposed  a method  to  determine  the  gastric  peristalsis 


PLATE  III. 


Author’s  Method  of  Recording  Gastric  Peristalsis. 

Patient  with  intragastric  bag  within  stomach  and  pneumograph  in  place,  both  connected 
with  the  kymograph. 


LIBRARY 

OF  THE 

UNIVERSITY  of  ILLINOIS, 


PLATE  IV. 


Author’s  Method  for  Determining  Location  and  Capacity  of  the  Stomach. 

The  apparatus,  not  including  kymograph.  G.  Intragastric  bag  distended.  F.  The 
esophageal  tube  attached  to  it.  H.  Intragastric  bag  collapsed  in  the  shape  in  which  it 
is  introduced.  A.  Graduated  pressure  bottle  elevated,  filled  with  water.  B.  Stop- 
cock. D.  Lower  graduated  bottle,  empty  at  first.  The  bag  is  distended  after  it  is 
swallowed  by  connecting  it  at  E with  D ; the  stop-cock.  B,  is  turned  on,  and  the  water 
then  runs  from  A to  D,  displacing  the  air  in  D and  forcing  it  into  the  bag.  Both 
bottles  being  graduated,  the  amount  of  air  in  G is  always  known,  and  can  be 
utilized  as  an  indication  of  the  gastric  capacity. 


LIBRARY 

LiltNOlS.' 


IODOFORM  TEST  FOR  GASTRIC  MOTILITY.  73 

by  giving  o.i  gm.  iodoform  in  a gelatin  capsule  during  meals; 
this  compound  does  not  decompose  in  acid  media,  but  does  break 
down  in  the  juices  of  the  duodenum,  which  are  less  acid  than  those 
of  the  stomach,  and  one  of  its  resultants  is  potassium  iodid, 
which  can  be  tested  in  saliva  by  starch  paper,  which,  when 
dipped  into  the  saliva,  colors  blue  on  being  touched  with  a 
drop  of  fuming  nitric  acid.  Naturally,  the  potassium  iodid  can 
also  be  detected  in  the  urine;  but  the  fact  which  gives  this 
method  the  preference  over  Fwald’s  salol  test  is  that  the  KI  can 
be  detected  in  the  saliva. 

This  method  gives  varying  results,  as  we  have  discovered.  In 
twenty-three  apparently  normal  cases  in  which  we  have  tried  it,  the 
reaction  coloring  the  starch  paper  first  occurred  just  one  hour 
after  the  meal  in  twelve  cases ; in  six  cases  it  occurred  first  in  one 
hour  and  twenty  to  twenty-two  minutes  ; in  two  cases,  in  one  hour 
and  forty-one  minutes;  and  in  one  case,  in  two  hours.  In  two 
cases  it  took  two  hours  and  a half  to  demonstrate  KI  in  the 
mouth,  after  giving  o.i  gm.  iodoform. 

The  time  of  the  appearance  of  the  first  red  and  the  subsequent 
blue  coloring  of  the  starch  paper  was  carefully  noted.  Fleischer 
states  that  after  a test-breakfast  the  reaction  in  the  saliva  should 
occur  in  from  fifty-five  to  one  hundred  and  five  minutes,  which 
is  still  a considerable  margin  for  variations — too  great  for  practical 
purposes. 

Nevertheless,  the  method  is  interesting,  and,  with  exactly  known 
meals,  might  be  available  for  hospital  work. 

In  Leube’s,  Ewald’s  and  Sievers’,  Klemperer’s,  and  Fleischer’s 
methods,  it  will  be  observed  that  the  gastric  motility  was  deter- 
mined by  something  that  was  administered  (salol,  iodoform,  and 
food)  or  poured  into  the  stomach  (oil),  and  by  the  absorption  of  the 
product  of  breaking  down  in  the  supposedly  alkaline  duodenum, 
and  its  subsequent  appearance  in  the  secretions  and  excretions 
(potassium  iodid  in  the  saliva  and  salicyluric  acid  in  the  urine) — an 
expression  in  terms  of  time  being  arrived  at,  to  denote  the  intensity 
of  the  gastric  peristalsis. 

In  two  methods  the  expression  is  derived  from  the  quantity  of 
oil  or  food  retained  in  the  stomach  after  two  hours,  but  here  also 
the  result  depended  upon  the  passage  of  something  into  the  duo- 
denum. In  all  of  these  methods,  therefore,  the  fundamental  idea 
is  the  rate  of  expulsion  of  gastric  contents  into  the  duodenum,  as 
if  that  were  the  only  object  of  the  motor  functions  of  the  stomach. 

6 


74 


METHODS  FOR  TESTING  THE  GASTRIC  PERISTALSIS. 


It  is  probable  that  this,  which  is  only  a part  of  the  purpose  of 
the  gastric  peristalsis,  was  so  much  dwelt  upon  because  it  offered 
the  most  expedient  means  for  experimenting,  and  a greater  possi- 
bility of  solution  of  the  problem.  However,  a second  and  most 
important  purpose  of  the  gastric  peristalsis,  and  one  concerning 
which  none  of  the  methods  referred  to  thus  far  can  instruct  us,  is 
the  moving  about  of  the  ingesta  within  the  stomach — (i)  so  that  they 
may  be  made  into  a more  homogeneous  mass;  (2)  that  they  may 
be  brought  into  thorough  contact  with  the  gastric  juice;  and  (3)  to 
stimulate  the  secretion  of  this  juice  by  the  mechanical  stimulation 
of  the  walls  of  the  organ. 

The  secretion  of  the  gastric  glands  is  not  only  stimulated  by  the 
mechanical  irritation  of  the  stomach-walls  during  peristalsis,  but  by 
the  contraction  of  a liberal  supply  of  muscular  fibers,  which  arise 
from  the  muscularis  mucosae,  and  are  spun  around  the  bases  of 
the  gland  tubules  (see  frontispiece  lithograph  of  normal  gastric 
mucosa) ; the  glands  are  no  doubt  themselves  contracted  and 
their  contents  expelled. 

In  some  of  the  batrachians  this  contraction  of  the  gastric  gland 
tubules  by  electric  stimulation  is  visible  under  the  microscope. 

Dr.  Max  Einhorn  has  described,  in  the  “ New  York  Medical 
Journal,”  September  15,  1894,  an  instrument  which  records  the 
gastric  movements  by  dots  on  a narrow  piece  of  paper. 

This  apparatus  consists  of  a ball  about  ^ of  an  inch  (14  mm.) 
in  diameter,  which  is  made  up  of  two  hollow  metallic  hemispheres 
screwed  together.  Within  this  is  contained  a second  smaller  ball, 
which  is  attached  to  the  outer  sphere  by  a non-conductor  so 
that  it  is  insulated  from  it. 

The  central  smaller  ball  bristles  with  small  metallic  spikes  which 
radiate  in  all  directions  from  the  center  to  the  inside  of  the  two 
hemispheres,  but  not  touching  them. 

A tiny  platinum  sphere  completes  the  interior  of  this  apparatus; 
it  lies  within  the  larger  round  capsule  and  moves  about,  knocking 
at  the  spikes.  When  it  does  so,  it  completes  an  electric  circuit 
between  the  outer  hemispheres  and  the  spikes  of  the  central  ball — 
for  two  insulated  wires,  one  connected  with  the  hollow  ball,  the 
other  with  the  spiked  ball,  run  up  in  a very  fine,  thin,  rubber  tube 
and  are  connected  with  the  two  poles  of  an  electric  battery.  On 
connecting  the  ball  with  another  part  of  the  apparatus,  the  “ ticker  ” 
(very  much  like  the  instrument  used  at  the  stock  exchanges  for 
reporting  the  variations  in  stock  by  telegraph),  each  motion  of  it 


METHODS  FOR  TESTING  THE  GASTRIC  PERISTALSIS.  /5 

will  be  recorded  by  lines  or  dots  on  the  paper.  The  ball  is 
swallowed  and  brought  into  the  stomach  by  the  aid  of  a draft 
of  water.  It  must  be  borne  in  mind  that  the  paper  records  the 
motions  of  the  ball  only ; this  does  not  mean  that  it  records  every 
motion  of  the  gastric  peristalsis. 

In  animals  upon  which  we  experimented  at  the  biological  labo- 
ratory of  the  Johns  Hopkins  University,  a rubber  stomach-shaped 
bag  was  fitted  exactly  to  the  interior  of  the  animal’s  stomach 
and  connected  with  a manometer  on  the  Ludwig  kymographion. 
Records  were  taken  with  the  animal’s  abdomen  intact  and  com- 
pared with  those  taken  with  the  abdomen  opened,  so  that  the  gastric 
peristalsis  could  be  viewed  by  the  experimenter. 

The  physiological  peristalsis  is  essentially  the  same  whether  the 
animal’s  stomach  is  normally  contained  within  the  abdomen  or 
exposed  to  view,  provided  in  the  latter  case  it  is  kept  warm. 

In  our  experiments  the  animals  were  placed  in  a large  metal 
case  with  a glass  top  ; underneath  the  animal  holder  about  two 
inches  of  water  was  contained  in  the  bottom  of  the  case,  which  was 
kept  at  the  desired  temperature  by  a number  of  Bunsen  burners 
beneath  the  case.  Thermometers  were  suspended  from  different 
parts  of  the  case  to  register  the  temperature,  for  it  is  most  essential 
that  after  an  animal’s  abdomen  has  been  opened  it  should  be  kept 
at  a constant  temperature  by  moist  steam  ; this  also  insures  the 
viscera  against  becoming  dry. 

In  a similar  manner  Ludwig  and  H.  Newell  Martin  studied  the 
physiology  of  the  mammalian  heart;  Schatz  conducted  his  funda- 
mental investigations  on  the  contractions  of  the  uterus  ; Engelmann 
carried  on  his  pioneer  work  on  the  contraction  of  the  involuntary 
muscle-fibers  of  the  ureter.  Phluger  and  Heidenhain  have  done 
similar  accurate  work  on  excised  organs,  and  the  results  have  been 
repeatedly  confirmed  by  other  competent  investigators. 

These  epoch-making  experimentations  are  mentioned  to  em- 
phasize the  fact  that  experiments  conducted  on  organs  isolated 
either  entirely  (Martin,  Ludwig,  Engelmann)  or  partially  (Schatz, 
Phluger)  are  capable  of  giving  perfectly  physiological  contractions 
or  peristalses  which  differ  nowise  from  the  perfectly  normal  ones. 

It  is  frequently  urged  that  these  experiments,  on  account  of  the 
operations  and  the  anesthesia  necessary,  do  not  present  perfectly 
physiological  conditions,  and  that  therefore  the  deductions  made 
therefrom  are  not  logical,  nor  represent  the  true  state  of  normal 
functioning. 


7 6 


METHODS  FOR  TESTING  THE  GASTRIC  PERISTALSIS. 


It  is  undeniable  that  we  never  get  at  the  absolutely  exact  normal 
functioning  of  an  organ — the  stomach,  for  instance — during  an 
experiment,  as  ether  and  chloroform  have  an  inhibiting  effect  on 
gastric  peristalsis.  But  we  are  enabled  to  produce  unconscious- 
ness of  the  animal  after  a brief  ether  narcosis  by  brain  compression, 
after  which  the  ether  is  no  longer  necessary,  and  then  the  gastric 
peristalsis  continues  perfectly  normal.  The  stomach  of  the  rabbit 
will  show  normal  peristalsis  after  complete  excision  and  suspension 
on  a hook  or  clamp  in  a warm,  moist  chamber. 

What  brought  us  to  the  idea  of  using  an  intragastric  thin  rubber 
bag  of  the  shape  of  the  stomach  to  record  the  peristalsis,  after  many 
attempts  with  a small  spherical  bag  that  did  not  exactly  fill  out  the 
entire  lumen  of  the  stomach,  was  the  repeated  observation  that  the 
small,  round  bag,  such  as  Professor  Moritz,  of  Munich,  used,  did 
not  record  every  peristaltic  movement  that  was  visible  to  the  eye 
when  the  abdomen  was  opened. 

We  frequently  noticed  peristaltic  constrictions  of  the  antrum 
pyloricum  when  the  rubber  bag,  of  about  12  cm.  in  diameter,  was 
at  the  cardia  or  fundus,  and  recorded  no  movement  but  that  due  to 
the  pressure  caused  by  the  descent  of  the  diaphragm.  We  con- 
cluded, after  three  months’  experimentation,  that  a small  intra- 
gastric apparatus  could  not  possibly  record  every  peristaltic 
movement. 

Sometimes  one  could  witness  very  strong  tonic  contractions  of 
seemingly  every  muscle-fiber  of  the  stomach, — it  gave  that  impres- 
sion,— by  which  the  whole  organ  contracted  from  all  sides  by 
shortening  of  every  circular,  oblique,  and  longitudinal  fiber,  and  at 
the  same  time  the  bag  gave  no  record  of  movement,  although 
when  it  was  lying  in  the  fundus  it  was  clearly  being  lifted  up, — it 
would  not  record  until  it  was  compressed  by  food  or  the  opposite 
gastric  wall. 

For  these  reasons  a bag  was  devised  which  had  the  exact  shape 
of  the  stomach,  but  could  readily  be  swallowed,  and  when  dis- 
tended within  the  organ,  exactly  adapted  itself  to  its  interior,  filling 
every  nook  and  corner  in  it.  If  a little  food  was  needed  in  the 
organ,  we  simply  did  not  blow  the  bag  up  so  far  as  to  fill  it  out 
completely. 

Our  apparatuses  has  been  demonstrated  many  times  on  a large 
variety  of  cases  in  the  clinical  amphitheater  of  the  University  of 
Maryland,  and  in  the  biological  laboratory  of  the  Johns  Hopkins 
University,  is  adjusted  with  great  ease.  By  a pneumograph  the 


library 

UNIVERSITY  of  ILLINOIS. 


y6  METHODS  FOR  TESTING  THE  GASTRIC  PERISTALSIS. 

It  is  undeniable  that  we  never  get  at  the  absolutely  exact  normal 
functioning  of  an  organ — the  stomach,  for  instance — during  an 
experiment,  as  ether  and  chloroform  have  an  inhibiting  effect  on 
gastric  peristalsis.  But  we  are  enabled  to  produce  unconscious- 
ness of  the  animal  after  a brief  ether  narcosis  by  brain  compression, 
after  which  the  ether  is  no  longer  necessary,  and  then  the  gastric 
peristalsis  continues  perfectly  normal.  The  stomach  of  the  rabbit 
will  show  normal  peristalsis  after  complete  excision  and  suspension 
on  a hook  or  clamp  in  a warm,  moist  chamber. 

What  brought  us  to  the  idea  of  using  an  intragastric  thin  rubber 
bag  of  the  shape  of  the  stomach  to  record  the  peristalsis,  after  many 
attempts  with  a small  spherical  bag  that  did  not  exactly  fill  out  the 
entire  lumen  of  the  stomach,  was  the  repeated  observation  that  the 
small,  round  bag,  such  as  Professor  Moritz,  of  Munich,  used,  did 
not  record  every  peristaltic  movement  that  was  visible  to  the  eye 
when  the  abdomen  was  opened. 

We  frequently  noticed  peristaltic  constrictions  of  the  antrum 
pyloricum  when  the  rubber  bag,  of  about  12  cm.  in  diameter,  was 
at  the  cardia  or  fundus,  and  recorded  no  movement  but  that  due  to 
the  pressure  caused  by  the  descent  of  the  diaphragm.  We  con- 
cluded, after  three  months’  experimentation,  that  a small  intra- 
gastric apparatus  could  not  possibly  record  every  peristaltic 
movement. 

Sometimes  one  could  witness  very  strong  tonic  contractions  of 
seemingly  every  muscle-fiber  of  the  stomach, — it  gave  that  impres- 
sion,— by  which  the  whole  organ  contracted  from  all  sides  by 
shortening  of  every  circular,  oblique,  and  longitudinal  fiber,  and  at 
the  same  time  the  bag  gave  no  record  of  movement,  although 
when  it  was  lying  in  the  fundus  it  was  clearly  being  lifted  up, — it 
would  not  record  until  it  was  compressed  by  food  or  the  opposite 
gastric  wall. 

For  these  reasons  a bag  was  devised  which  had  the  exact  shape 
of  the  stomach,  but  could  readily  be  swallowed,  and  when  dis- 
tended within  the  organ,  exactly  adapted  itself  to  its  interior,  filling 
every  nook  and  corner  in  it.  If  a little  food  was  needed  in  the 
organ,  we  simply  did  not  blow  the  bag  up  so  far  as  to  fill  it  out 
completely. 

Our  apparatuses  has  been  demonstrated  many  times  on  a large 
variety  of  cases  in  the  clinical  amphitheater  of  the  University  of 
Maryland,  and  in  the  biological  laboratory  of  the  Johns  Hopkins 
University,  is  adjusted  with  great  ease.  By  a pneumograph  the 


I 


author’s  method  for  recording  gastric  peristalsis.  77 

respiration  is  recorded  separately,  and  thus  one  is  enabled  to 
differentiate  the  active  from  the  passive  movements. 

A separate  seconds-pen  gives  on  the  same  paper  a record  in 
time,  so  that  the  experimenter  can  tell  at  a glance  the  duration, 
beginning,  and  end  of  the  peristalsis.  While  it  is  a most  satisfac- 
tory apparatus  for  recording  the  motor  function,  it  offers  a reliable 
means  of  ascertaining  the  size  and  exact  capacity,  and  finally  the 
intragastric  pressure.  No  apparatus  hitherto  devised  combines 
these  facilities  in  so  simple  a bit  of  mechanism  ; for,  taking 
away  the  kymograph,  which  should  be  in  every  medical  school, 
its  important  parts  are  simply  the  intragastric  bag  and  a mano- 
meter. 

In  practice,  a manometer  connected  with  the  intragastric  bag  will 
answer;  with  watch  in  hand  the  experimenter  is  able  to  count  the 
peristaltic  movements  as  they  are  conveyed  to  the  column  of  water. 
Einhorn,  in  his  new  book,  “ Diseases  of  the  Stomach,”  page  96, 
has  gathered  the  impression  that  the  apparatus  is  of  difficult  adjust- 
ment, because  in  our  first  report  ( loc . cit.)  we  stated  that  only  such 
patients  are  taken  as  have  become  accustomed  to  the  stomach- 
tube,  as  the  nausea  and  vomiting  first  attending  the  initial  intro- 
duction of  the  tube  make  an  exact  record  impossible  (we  lay  great 
stress  here  on  the  word  exact).  No  intragastric  instrument,  not 
even  Einhorn’s  electrode,  can  be  introduced  the  first  time  without 
some  nausea.  While  this  may  not  lead  to  emesis,  it  nevertheless 
has  a great  influence  on  the  number  of  gastric  movements,  as  most 
cases  we  have  tried  generally  show  more  contractions  in  the  first 
experiment  than  in  any  other.  If  the  record  is  to  be  exact,  and 
free  from  objections  that  may  be  urged  on  account  of  the  influence 
of  nervousness,  nausea,  suggestion,  etc.,  a certain  adaptation  and 
experience  of  the  patient  is  indispensable,  no  matter  what  instru- 
ment is  used.  Probably  none  of  these  apparatuses  will  be  regularly 
used  in  practice ; they  are  implements  for  the  trained  specialists, 
who  know  how  to  apply  them  and  how  to  interpret  their  results. 
Nevertheless,  our  intragastric  bags  are  used  regularly  at  the  Uni- 
versity of  Maryland  Hospital,  and  exact  results  obtained  thereby, 
even  at  the  first  attempt. 

Our  objections  to  the  Einhorn  gastrograph  are  : (1)  That  no 
differentiation  between  the  active  and  the  passive  movements 
produced  by  the  diaphragm  is  possible  thereby;  (2)  that  there 
is  no  coincident  record  of  time  in  seconds  on  the  paper;  (3) 
that  the  tonicity  or  intensity  of  a contraction  can  not  be  ad- 


yS  METHODS  FOR  TESTING  THE  GASTRIC  PERISTALSIS. 

equately  determined ; (4)  that  the  slow  but  very  extensive  gen- 
eral tonic  contractions — a narrowing  down,  as  it  were,  of  the 
entire  stomach  to  one  point  in  the  center — will  probably  be 
recorded  by  a single  dot,  such  as  would  be  made  by  an  inspiration 
also.  At  the  same  time,  when  we  reflect  that  a bag  12  cm.  in 
diameter  may  miss  some  of  the  contractions  and  fail  to  record  them, 
it  is  difficult  to  imagine  that  the  gastrograph  should  record  them 
all,  being  not  even  an  inch  in  diameter. 

Nevertheless,  Einhorn’s  apparatus  marks  an  epoch  in  the  history 
of  the  study  of  stomach  motions  and  their  physiology.  It  is  the 
first  attempt,  and  largely  a successful  one,  to  obtain  their  record 
by  mechanical  means. 

Passive  motions  caused  by  the  pulsations  of  the  aorta  and  the 
impulse  of  the  heart  ventricles  against  that  part  of  the  saccus 
caecus  cardiae  which  touches  the  arch  of  the  diaphragm,  and  also 
the  respiratory  passive  motions  due  mostly  to  the  muscles  of  res- 
piration, are,  to  a small  extent,  participants  in  the  causes  of  gastric 
movements;  but  they  can  not  of  themselves  produce  evacuations 
of  the  contents,  as  we  had  occasion  to  observe  in  the  clinic  on  a 
hysterical  girl,  who  had  no  active  stomach  movements,  no  genuine 
peristalsis  at  all,  all  of  her  gastric  movements  being  due  to  respir- 
ation and  circulation. 

This  girl  showed  a normal  state  of  the  secretions  after  an  Ewald 
test-meal,  but  at  the  same  time  there  was  stagnation  and  retention 
of  food.  It  is,  therefore,  most  essential  to  be  able  to  distinguish 
between  active  and  passive  movements,  for  a person  may  have  a 
great  many  movements  of  the  stomach  and  yet  have  no  genuine 
peristalsis  at  all. 

It  is  necessary  to  distinguish  between  methods  for  physiological 
study  of  gastric  peristalsis  and  methods  for  diagnostic  or  clinical- 
work.  Our  method  is  available  mainly  for  the  physiological  and 
clinical  laboratories,  though  it  will  give  valuable  information  even 
without  the  kymograph. 


THEORIES  CONCERNING  THE  MOVEMENTS  OF  THE  INGESTA.  79 


CHAPTER  IX. 

HEMMETER’S  METHOD  FOR  TESTING  THE  GASTRIC 
PERISTALSIS. 

Theories  Concerning  the  Movements  of  the  Ingesta. 

One  of  the  intragastric  stomach-shaped  rubber  bags  which  are 
used  in  our  clinic  consists  of  three  separate  compartments:  the 
first  filling  out  the  pylorus,  the  second  distending  the  middle  por- 
tion of  the  stomach,  the  third  occupying  a small  part  of  the  fundus 
and  the  saccus  caecus  cardiae.  (See  “ N.  Y.  Med.  Jour.,”  June 
22,  1895,  p.  772,  and  the  accompanying  illustration.)  Each  one 
of  these  compartments  records  on  the  kymograph  by  a separate 
tambour. 

In  the  report  referred  to  we  made  the  assertion,  from  the  results 
obtained  with  this  bag,  that  in  the  human  being  most,  if  not  all,  of 
the  peristaltic  waves  are  executed  by  and  start  at  the  pyloric  end. 
This  statement  was  made  before  Moritz’s  investigations  were  pub- 
lished in  the  “ Zeitschrift  fur  Biologie,”  proving  that  the  cardiac  end 
and  the  fundus  of  the  stomach  could  not  contract,  even  when 
stimulated  by  powerful  faradic  currents  on  both  the  mucous  and 
peritoneal  surfaces. 

One  week  before  our  results  were  published  in  the  “ New  York 
Medical  Journal,”  Dr.  S.  J.  Meltzer,  of  New  York,  published  his 
results  with  direct  and  indirect  faradization  of  the  digestive  canal, 
which  demonstrated  quite  conclusively  that  the  mucous  membrane 
of  the  digestive. canal  offers  a considerable  resistance  to  the  penetra- 
tion of  the  faradic  current  to  the  muscular  coat,  the  greatest  resist- 
ance being  found  in  the  mucous  membrane  of  the  stomach. 
Percutaneous  and  direct  faradization  of  the  stomach,  or  intestines 
can  not  produce  any  contraction  in  these  parts. 

Meltzer  stated  explicitly  the  kind  of  instruments  used, — the 
sliding  inductorium  (Schlittenapparat)  of  DuBois  Reymond,  a 
Grove’s  cell  prepared  anew  for  each  experiment, — and  also  the 
distance,  in  every  case,  of  the  primary  from  the  secondary  coil. 
His  device  of  including  the  sciatic  nerve  of  an  animal  (nerve- 
muscle  preparation  of  hind  leg  of  frog,  most  likely)  in  the  circuit 
is  practical,  and  has  for  a long  time  been  used  in  our  laboratory. 

There  is,  however,  a very  important  matter  which  physiologists 


8o 


METHODS  FOR  TESTING  THE  GASTRIC  PERISTALSIS. 


must  insist  on  knowing,  and  which  Meltzer  does  not  state,  per- 
haps because  it  was  not  very  readily  ascertained ; and  that  is,  the 
number  of  stimulations  to  the  second  used  by  him.  Involuntary 
muscle-fibers  are  much  slower  to  contract  than  voluntary  muscles, 
and  in  electrical  stimulation  experiments  they  contract  much  more 


Fig.  7.— Intragastric  Tissue  Rubber  BXg,  with  three  distinct  parts  and  three  separate  outlets 
for  recording  the  origin  and  direction  of  gastric  peristalsis.  Outside  of  the  mouth  the  triple 
tube  separates  into  its  three  component  tubes,  each  being  connected  with  a separate  tambour 
and  glass  ink  pen,  writing  the  gastric  contractions  and  relaxations  on  the  kymograph.  Part 
No.  1 records  the  contraction  of  the  pylorus;  part  No.  2,  the  middle  of  the  stomach;  and  part 
No.  3,  of  the  cardiac  end.  (See  double  plate  for  tracings  of  this  apparatus.) 


readily  when  the  number  of  stimulations  does  not  exceed  240  per 
minute.  The  best  contractions  are  obtained  at  a much  lower  rate 
of  stimulation. 

The  vibrator  on  the  DuBois  Reymond  inductorium  was  found, 
after  months  of  experimentation,  to  send  too  many  stimulations 
into  the  gastric  muscle  per  second.  Later  on,  when  we  used  the 


THE  MUCOSA  A NON-CON DUCTOR. 


8 1 


Kronecker  interrupter,  in  connection  with  a Jacquet  chronograph, 
and  no  more  than  ioo  stimulations  per  minute,  it  was  found  that 
the  preantral  sphincter  could  be  made  to  contract  with  the  distance 
of  primary  from  the  secondary  coil  = o,  and  both  electrodes  on 
the  mucosa. 

To  get  this  result,  it  is  best  to  starve  the  animal  for  twelve 
hours,  as  for  some  reason  yet  unknown,  the  contractions  are  more 
unlikely  to  occur  the  sooner  the  experiment  is  made  after  the  in- 
gestion of  food.  Still,  it  must  be  emphasized  that  the  mucosa  of 
the  stomach  is  practically  a non-conductor.  We  have  had  occa- 
sion to  try  this  in  the  physiological  laboratory,  with  a bit  of 
healthy  human  stomach-mucosa  which  one  of  our  students  tore 
off  from  the  wall  of  his  stomach  during  experimental  lavage  ; the 
piece  was  fifteen  mm.  long,  five  to  six  mm.  broad,  and  two  to  four 
mm.  thick.  The  gentleman  in  question,  after  trying  to  wash  his 
stomach  out,  and  not  succeeding  to  his  satisfaction,  connected  the 
end  of  the  tube  with  a suction  apparatus  (aspirator). 

This  was  followed  by  copious  hematemesis,  for  which  we  were 
hastily  summoned.  In  the  stomach-tube,  partly  projecting  from 
the  lower  opening,  was  a bit  of  fleshy  substance,  which,  on  micro- 
scopic examination,  proved  to  be  gastric  mucosa.  After  the 
hemorrhage  ceased,  the  young  man  was  treated  for  one  week  as  if 
he  had  gastric  ulcer.  He  did  not  experience  any  pain  during  the 
accident,  nor  thereafter ; the  only  thing  that  frightened  him  was 
the  blood.  He  made  a good  recovery.  This  bit  of  mucosa  was 
placed  in  a continuous  circuit  generated  by  a battery  of  three 
freshly  prepared  Grove’s  cells,  with  a milliamperemeter,  soon  after  it 
was  found;  the  meter  indicated  but  three  milliamperes.  As  it  was 
impossible  to  get  this  fresh  piece  of  mucosa  into  the  circuit  perfectly 
dry,  it  is  probable  that  the  indication  of  three  milliamperes  was 
brought  about  through  the  conducting  agency  of  the  moisture  on 
the  outside  of  the  tissue. 

In  the  biological  laboratory  of  the  Johns  Hopkins  University 
we  have  frequently  had  persons’  stomachs  connected  with  the 
kymograph,  and  an  intragastric  rubber  bag  blown  up  to  fill  out 
their  stomachs  exactly.  Through  the  intragastric  bag  ran  two 
insulated  wires,  one  ending  in  a small  brass  knob  near  the  pylorus, 
the  other  coming  out  against  the  mucosa  near  the  cardia  in  a 
similar  knob. 

Every  active  and  passive  motion  was  recorded  by  a manometer 
pen  (“  N.  Y.  Med.  Jour.,”  June  22,  1895,  p.  77 1).  But  the  strongest 


82 


METHODS  FOR  TESTING  THE  GASTRIC  PERISTALSIS. 


faradic  currents  (distance  of  primary  from  secondary  coil  — o) 
could  produce  no  contractions  of  the  stomach. 

Dr.  George  P.  Dreyer  and  myself  held  one  of  the  poles  in  the 
right  hand — the  plus,  for  instance — while  the  negative  was  in  the 
stomach  ; with  the  left  hand  we  touched  the  back  of  the  person’s 
neck,  thus  completing  the  circuit.  The  current  was  so  strong  that 
it  became  intolerable  to  us.  Although  this  current  made  its 
circuit  through  the  patient’s  stomach,  it  caused  no  contraction, 
as  was  evidenced  by  the  manometer  in  connection  with  the  intra- 
gastric  bag. 

Frequently  we  could  observe  contractions  of  any  skeletal  muscle 
upon  which  the  outer  electrode  was  placed, — for  instance,  the  gas- 
trocnemius,— and  still  the  stomach  did  not  contract.  This  proves 
that  in  some  conditions  the  gastric  mucosa  may  transmit  a current, 
yet  the  muscular  layer  give  no  evidence  of  contractions.  We  do 
not  wish  to  imply  that  it  is  absolutely  impossible  to  contract  the 
human  stomach  by  electrical  stimulation  ; but  the  current  required 
to  effect  this  must  be  so  strong  that  the  experiment  becomes 
hazardous. 

Einhorn  (“Diseases  of  the  Stomach,’’ pages  78-83)  and  Paul 
Cohnheim  (“  Archiv  f.  Verdauungskrankheiten,’’  Bd.  1,  S.  274) 
have  described  tiny  bits  of  mucosa  which  are  found  in  the  wash- 
water  and  vomit  of  many  gastric  sufferers.  We  can  confirm 
this  observation,  and  add  that  we  have  found  these  pieces  of 
gastric  mucosa  on  washing  out  the  stomachs  of  perfectly  healthy 
persons. 

It  has  occurred  to  us  that  in  rare  instances  in  which  a good 
contraction  of  the  stomach  was  obtained,  it  was  due  to  the  fact 
that  the  current  found  its  way  to  the  muscular  layer,  through  spots 
from  which  the  glandular  layer  had  been  cast  off.  It  must  not  be 
omitted  that  all  stomachs  experimented  upon  by  our  method  in 
this  series  were  washed  out  prior  to  the  experiment  to  insure 
absence  of  current-interrupting  food-particles  in  the  organ. 

Moritz  experimented  with  an  apparatus  very  similar  to  ours, 
except  that  his  rubber  intragastric  bag  was  round,  not  stomach- 
shaped. It  did  not,  therefore,  exactly  and  completely  fill  out 
the  organ,  nor  did  he  use  the  graduated  pressure  bottles,  by 
which  it  is  possible  to  determine  exactly  how  much  air  is 
blown  into  the  bag.  Instead  of  a pneumograph,  he  used  a per- 
forated cork  in  one  nostril  of  the  patient,  which  was  connected 
with  a second  manometer,  writing  on  the  Ludwig  kymograph. 


PHYSIOLOGY  OF  GASTRIC  MOVEMENTS.  83 

The  advantage  of  the  pneumograph  over  this  method  must  be  ap- 
parent. 

The  author’s  first  results  appeared  in  print  three  months  before 
those  of  Moritz  in  the  “ Zeitschrift  fur  Biologie,”  Bd.  xxxii,  which 
are  perhaps  the  most  important  contributions  to  the  physiology  of 
the  motor  function  since  the  investigations  of  Hofmeister  and 
Schiitz  (“  Archiv  f.  exper.  Pathol,  und  Pharm.,”  1886,  Bd.  xx).  In 
order  that  the  mechanism  of  the  gastric  peristalsis  may  be  better 
understood,  it  is  well  to  bear  in  mind  the  arrangement  of  the  mus- 
cular layers, — (1)  longitudinal,  (2)  oblique,  and  (3)  circular, — and 
what  was  said  under  the  head  of  anatomy  of  the  gastric  layers  and 
the  formation  of  the  sphincter  of  the  pylorus.  The  part  of  the 
stomach  near  the  pyloric  end  is  spoken  of  more  specifically  as  the 
antrum  pylori. 

The  line  of  separation  between  the  antrum  pylori  and  the  body 
or  fundus  of  the  stomach  is  made  by  a special  thickening  of  the 
circular  fibers,  forming  what  is  spoken  of  as  the  transverse  band  by 
older  writers — for  instance,  Beaumont,  in  his  “ Physiology  of 
Digestion,”  second  edition,  1847,  Pa£e  I04-  (A  pioneer  piece  of 
work,  very  fundamental  and  thorough  in  its  observations,  this 
book  remains  a monument  to  American  physiological  and  clinical 
observation.)  Recent  observers  describe  this  transverse  band  as 
the  sphincter  antri  pylorici,  and  locate  it  at  a distance  of  seven  to 
ten  cm.  from  the  pylorus. 

In  the  antrum  pylori  there  is  a very  strong  musculature,  and 
its  glands  contain  only  (or  rather  mostly)  chief,  central,  or  ferment 
cells.  The  exact  character  of  the  gastric  movements  during 
digestion  were  first  carefully  studied  on  the  human  being  by 
Beaumont ; his  facts  and  errors  have  influenced  physiologists 
more  or  less  up  to  the  present  time.  One  can  not  fail  to  suspect 
that  the  stomach  of  Alexis  St.  Martin  and  its  manner  of  peristalsis 
were  too  far  from  the  normal  to  permit  absolutely  correct  con- 
clusions. The  extensive  adhesions  which  Beaumont  describes 
certainly  acted  at  times  as  irritants,  at  others  as  impediments,  to 
normal  peristalsis. 

Professor  W.  H.  Howell’s  views  on  the  gastric  movements,  as 
expressed  in  the  “ American  Text-book  of  Physiology,”  page  317, 
will  serve  as  an  expression  of  a modern  physiologist.  He  says 
( loc . cit.)  the  movements  occur  in  two  phases : “ First,  the  feeble 
peristaltic  movement  running  over  the  fundus,  chiefly  on  the  side 
of  the  great  curvature,  and  resulting  in  pushing  the  fundic  contents 


84  METHODS  FOR  TESTING  THE  GASTRIC  PERISTALSIS. 

into  the  antrum  ; secondly,  the  sharp  contraction  of  the  sphincter 
antri  pylorici,  followed  by  a similar  contraction  of  the  entire  mus- 
culature of  the  antrum,  both  circular  and  longitudinal,  the  effect 
of  which  is  to  squeeze  some  of  the  contents  into  the  duodenum. 

“ It  is  possible  that  either  of  these  phases,  especially  the  first, 
might  occur  at  times  without  the  other,  and  in  the  first  phase  it  is 
possible  that  the  longitudinal  fibers  of  the  stomach  also  contract, 
shortening  the  organ  in  its  long  diameter,  and  aiding  the  propulsive 
movement,  but  actual  observation  of  this  factor  has  not  been  suc- 
cessfully made.  It  can  well  be  understood  that  a series  of  these 
movements  occurring  at  short  intervals  would  result  in  putting  the 
entire  semiliquid  contents  of  the  stomach  into  constant  circulation. 

“ The  precise  direction  of  the  current  set  up  is  not  agreed  upon, 
while  it  is  probable  that  the  graphic  description  given  by  Beaumont 
is  substantially  accurate.  A portion  of  this  description  may  be 
quoted  as  follows  : ‘ The  ordinary  course  and  direction  of  the  revo- 
lutions of  food  are,  first,  after  passing  the  esophageal  ring,  from 
right  to  left,  along  the  small  arch  ; thence,  through  the  large 
curvature,  from  left  to  right.  The  bolus,  as  it  enters  the  cardia, 
turns  to  the  left,  passes  the  aperture,  descends  into  the  splenic 
extremity,  and  follows  the  great  curvature  into  the  pyloric  end ; it 
then  returns  in  the  course  of  the  small  curvature.’ 

“ The  average  time  taken  for  one  of  these  complete  revolutions, 
according  to  observations  made  by  Beaumont,  seems  to  vary  from 
one  to  three  minutes. 

“ It  is  possible,  of  course,  that  this  typical  circuit  taken  by  food 
may  often  be  varied,  more  or  less,  by  different  conditions,  but  the 
muscular  movements  observed  from  the  outside  would  seem  to  be 
adapted  to  keeping  up  a general  revolution  of  the  kind  described. 
The  general  result  upon  the  food  may  be  easily  imagined.  It  be- 
comes thoroughly  mixed  with  the  gastric  juice  and  any  liquid 
which  may  have  been  swallowed,  and  is  gradually  disintegrated, 
dissolved,  and  more  or  less  completely  digested,  so  far  as  the  pro- 
teid  and  albuminoid  constituents  are  concerned. 

“ The  mixing  actions  are  aided,  moreover,  by  the  movements  of 
the  diaphragm  in  respiration,  since  at  each  descent  it  presses  upon 
the  stomach.  The  powerful  muscular  contractions  of  the  antrum 
serve  also  to  triturate  the  softened  solid  particles,  and  finally  the 
whole  mass  is  reduced  to  a liquid  or  semiliquid  condition,  in  which 
it  is  known  as  chyme,  and  in  this  condition  the  rhythmic  contrac- 
tion of  the  muscles  of  the  antrum  eject  it  into  the  duodenum. 


CRITICISM  OF  THEORIES  OF  BEAUMONT  AND  BRINTON.  85 

“The  rhythmic  spurting  of  the  contents  of  the  stomach  into  the 
duodenum  has  been  noticed  by  a number  of  observers,  through 
duodenal  fistulae  in  dogs,  established  just  beyond  the  pylorus.  It 
has  been  shown,  also,  that  when  the  food  is  entirely  liquid, — water, 
for  example, — the  stomach  is  emptied  in  a surprisingly  short  time 
— within  twenty  or  thirty  minutes;  if,  however,  the  water  is  taken 
with  solid  food,  then,  naturally,  the  time  it  will  remain  in  the 
stomach  may  be  much  lengthened.” 

Brinton  (“  Diseases  of  the  Stomach  ”)  advanced  the  view,  which 
differs  from  Beaumont’s,  in  assuming  a central  current  of  the  food, 
moving  from  the  pylorus  to  the  cardia  through  the  central  long 
axis  of  the  stomach.  There  are,  according  to  this  author,  two  cur- 
rents, one  along  each  curvature  running  from  the  cardia  to  the 
pylorus,  meeting  and  turning  inward  toward  the  center  of  the 
stomach  in  front  of  the  pylorus,  and  then  running  back  toward  the 
esophagus  as  a single  central  current,  there  dividing  to  make  again 
two  currents  as  before,  one  along  each  curvature. 

According  to  Poensgen  (“  Die  motor.  Verricht.  des  menschl. 
Magens,”  Strassburg,  S.  82),  Reymond,  Donders,  and  Lesshaft  ap- 
proved of  this  theory;  while  Penzoldt  and  P"oster  accept  the  great 
food-circle  of  Beaumont. 

Although  we  have  made  over  fifty  experiments  on  dogs,  cats,  and 
rabbits  to  observe  a food-circulation  within  the  stomach  corre- 
sponding to  these  views,  and  although  we  have  had  an  opportunity 
of  seeing  into  the  human  stomach,  through  fistulae,  during  diges- 
tion, we  have  not  been  able  to  confirm,  by  actual  observation,  either 
Beaumont’s  or  Brinton’s  views.  While  we  have  no  new  explana- 
tions to  offer,  it  has  occurred  to  us  that  the  piston-like  backward 
and  forward  movements  of  the  food  caused  by  the  antral  contrac- 
tions, and  especially  of  the  sphincter  of  the  antrum,  is  a sufficient 
force  to  effect  the  mixture  of  the  chyme  with  HC1  and  the  fer- 
ments such  as  are  found  in  it  when  it  leaves  through  the  pylorus. 
The  movements  do  not  differ  essentially  from  those  observed  in  the 
cat  by  Cannon  (“Amer.  Journ.  Physiol.,”  vol.  1). 

The  views  of  Beaumont  and  Brinton  date  from  the  epoch  when 
it  was  considered  all-important  that  food  must  be  properly  digested 
and  macerated  in  the  stomach  ; it  was  not  conceivable  then  that  by 
far  the  main  bulk  of  digestion  is  carried  on  in  the  intestines.  Hence 
the  complicated  theories  of  Beaumont  and  Brinton,  of  circular 
movements  of  food,  owe  their  origin  to  the  thought  that  such  a 
movement  was  necessary  to  mix  the  ingesta  with  the  gastric  juice. 
In  dogs  this  mixture  is  not  proved  to  occur  in  every  instance.  In 


METHODS  FOR  TESTING  THE  GASTRIC  PERISTALSIS. 


herbivora  (horse,  cow)  the  center  of  the  food-mass  in  the  stomach 
may  be  alkaline  or  neutral  in  animals  killed  one  hour  and  a quarter 
after  feeding. 

The  almost  vertical  position  of  the  stomach  was  unknown  to 
Beaumont  and  Brinton.  Like  many  clinicians  of  the  day,  they 
believed  the  organ  was  normally  in  a horizontal  position,  trans- 
versely across  the  upper  part  of  the  abdomen.  The  amount  of 
force  required  to  lift  the  food-mass  in  a vertical  line  upward  is 
considerable  ; it  is  necessary  to  imagine  a still  greater  force  to 
accomplish  the  vertical  ascent  on  the  side  of  the  lesser  curvature, 
in  order  to  conceive  of  a simultaneous  descent  on  the  side  of  the 
great  curvature,  which  descending  current  must  inevitably  interfere 
more  or  less  with  the  ascending  one. 

In  a number  of  experiments  in  which  the  stomachs  of  animals 
on  opening  the  abdomen  were  found  in  active  motion,  we  inserted 
long  needles  through  the  gastric  walls  to  determine  the  direction 
they  would  assume  under  the  pressure  of  the  ingesta.  According 
to  Beaumont,  the  ingesta  moving  from  the  saccus  csecus  along 
the  greater  curvature  to  the  pylorus  should  compel  the  points  of 
needles  to  be  directed  toward  the  pylorus  when  run  through  the 
greater  curvature,  and  along  the  lesser  curvature  they  should 
point  toward  the  cardia. 

If  Brinton’s  theory  were  true,  the  points  of  the  needles  at  both 
curvatures  should,  at  least  during  a large  period  of  gastric  diges- 
tion, be  directed  toward  the  pyloric  end.  If  needles  are  inserted  to 
a distance  of  y2  of  an  inch  along  both  curvatures  during  active 
gastric  peristalsis,  a great  diversity  of  movements  of  the  outside 
portions  of  the  needles  is  observable.  They  very  rarely  point  the 
same  way  along  either  curvature,  and  one  portion  of  them  may 
point  toward  the  cardia,  while  another  points  to  the  pylorus.  Only 
when  the  needles  are  inserted  very  deep,  so  that  they  dip  into  the 
central  or  axial  stream,  can  one  occasionally  observe  what  appears 
as  concerted  action.. 

During  active  peristalsis,  when  the  preantral  sphincter  at  times 
contracts  so  powerfully  as  almost  to  obliterate  the  lumen,  those 
needles  inserted  into  the  fundic  portion  of  both  the  greater  and 
lesser  curvatures  are  strongly  turned  toward  the  cardia,  but  simul- 
taneously those  few  needles  in  the  antral  and  pyloric  portions  are 
turned  toward  the  duodenum.  The  same  evidence  of  a central  or 
axial  current,  which  indicates  the  pumping  work  of  the  muscular 
antrum  in  pushing  back  solid  particles  into  the  fundus,  and  squeez- 
ing liquid  and  semiliquid  portions  into  the  duodenum,  can  be 


STUDIES  OF  PERISTALSIS  BY  X-RAYS. 


87 


obtained  by  the  intragastric  electric  lamp  when  introduced  during 
the  height  of  gastric  digestion.  These  lamps  can  be  seen  through 
the  abdominal  wall  in  dogs  whose  abdomens  have  been  shaved, 
when  introduced  in  a dark  room,  though  naturally  not  quite  so 
distinct  as  when  the  abdomen  is  opened. 

The  author  has  studied  gastric  peristalsis  in  the  human  subject 
by  means  of  the  X-rays.  (The  original  method  was  described  in  the 
“Boston  Medical  and  Surgical  Journal,”  June  18,  1896,  and  con- 
sisted of  introduction  of  a distensible  rubber  bag  into  the  stomach. 
The  X-rays  were  cut  off  by  a coating  of  argentic  oxid  on  the  inner 
side  of  the  bag.) 

A new  application  of  the  method  of  Boas  and  Levy-Dorn  for 
locating  the  site  of  obstructions  in  the  digestive  canal  by  means  of 
capsules  filled  with  bismuth  subnitrate — which  cut  off  the  X-rays, 
and  are  thus  visible — was  made  by  W.  B.  Cannon  for  the  study  of 
the  gastric  peristalsis  in  the  cat  (“  Amer.  Jour.  Physiol.,”  vol.  1,  p. 
359,  May,  1898).  His  results  are  valuable  as  confirming  other 
recent  experiments,  indicating  that  the  main  peristaltic  work  is 
carried  on  by  the  pyloric  end  of  the  stomach.  This  was  experi- 
mentally demonstrated  by  the  author  with  the  apparatus  pictured 
on  page  80  (“  New  York  Med.  Jour.,”  June  22,  1895).  The  fundus 
is  not  capable  of  exciting  effective  contractions.  As  will  be  shown 
further  on,  it  empties  the  ingesta  very  gradually  into  the  pyloric 
antrum  ; it  is  more  of  a reservoir  than  a food  titrator.  The  mixing, 
titration,  and  expulsion  is  carried  on  by  the  muscular  antrum  pylori. 
In  the  cat  the  stomach  is  emptied  by  the  formation  between  the 
fundus  and  the  antrum  of  a tube  along  which  constrictions  pass. 
The  contents  of  the  fundus  are  pressed  into  the  tube,  which, 
together  with  the  antrum,  is  slowly  cleared  of  food  by  waves  of 
constriction  (Cannon,  loc.  cit.).  The  author  has  made  observations 
on  human  subjects  with  thin  abdominal  walls  by  the  method  of 
Boas  and  Levy-Dorn.  Before  the  Rontgen  ray  apparatus  the  cap- 
sule of  bismuth  subnitrate  could  be  seen  oscillating  backward  and 
forward,  sometimes  slowly,  sometimes  with  surprising  rapidity, 
until  it  was  pressed  through  the  pyloric  sphincter,  which  generally 
appeared  to  occur  with  a rush.  But  never  was  any  circuit  of  the 
capsule  observed,  such  as  is  described  by  Beaumont,  Brinton,  or 
adopted  by  W.  H.  Howell.  With  the  method  used  by  Cannon — 
i.  e.y  mixing  subnitrate  of  bismuth  with  the  food — it  is  impossible  to 
judge  of  any  movement  of  individual  particles;  only  the  general 
body  and  contour  of  the  stomach  as  a whole  become  observable. 


88 


METHODS  FOR  TESTING  THE  GASTRIC  PERISTALSIS. 


We  agree  with  him  that  the  food  in  the  fundus  is  not  moved 
to  any  considerable  extent  by  peristalsis,  but  his  further  con- 
clusion that  it  is  consequently  not  mixed  with  gastric  juice,  may 
be  true  of  the  cat,  but  does  not  apply  to  the  human  being.  Food 
drawn  out  of  the  fundus  by  the  Einhorn  stomach-bucket,  which 
can  be  seen  before  the  X-ray  apparatus,  always  contains  gastric 
juice  if  any  is  secreted  at  all.  In  man  the  antrum  does  not  form 
into  a tube  as  in  the  cat,  though  an  approach  to  this  formation  is 
made;  during  powerful  contractions  the  impression  is  conveyed  as 
though  a second  sphincter,  about  ten  cm.  above  the  pylorus,  con- 
tracted and  shut  off  the  antrum  pylori  from  the  body  of  the 
stomach. 

The  author  has  observed  this  axial  food-current  at  the  clinic  in  a 
female  patient  with  very  thin  abdominal  parietes,  when  the  Einhorn 
intragastric  lamp  was  introduced  one  hour  after  a meal.  In  animals 
with  abdomen  opened  we  have  been  able  to  see  this  lamp  carried 
along  the  entire  greater  curvature,  from  the  pylorus  toward  the 
cardia,  during  active  digestion,  but  the  occurrence  is  so  rare  as  to 
appear  accidental. 

That  the  retrogressive  current,  which  is  set  up  by  contractions 
of  the  antrum  forcing  the  too  solid  food-particles  back  toward  the 
fundus,  must  inevitably  set  up  some  new  movements  among  the 
remaining  food-mass  in  the  fundic  end  is  natural,  but  we  have  no 
evidence  that  it  ever  reaches  that  systematic  circulation  described 
first  by  Beaumont  and  Brinton. 

It  should  not  be  overlooked  that  if  the  observations  of  Beaumont 
of  a complete  food-circuit  were  really  true  and  constituted  the  only 
movements  in  addition  to  the  duodenal  extrusion  which  the  food- 
mass  underwent,  there  must  always  be  a mass  of  food  in  the 
center  of  the  stomach  which  never  touches  the  gastric  wall ; if  all 
the  food  moves  about  along  the  periphery,  there  must  be  a central, 
quiet  portion. 

Brinton  was  aware  of  this  defect  in  Beaumont’s  statements,  and 
improved  upon  them  by  his  still  more  complicated  theory  of  piston 
movements  and  central  current  to  explain  the  axial  food-motions. 

If  the  conditions  described  by  these  authors  exist,  they  are  not 
well  explained  by  the  arrangement  of  the  muscularis  of  the  fundus, 
which,  as  far  as  the  work  of  Meltzer  ( loc . cit.),  Moritz  ( loc . cit.), 
Goldschmidt  (loc.  cit.)  and  the  author  show,  is  very  feeble  indeed  in 
its  contractions,  and  hardly  sufficient  to  propel  food  in  any  direc- 
tion ; yet,  according  to  the  above  theory,  powerful  contractions  are 


CONCLUSIONS  CONCERNING  PHYSIOLOGY  OF  PERISTALSIS.  89 

ascribed  to  it;  but  as  the  preantral  sphincter  is  only  seven  to  ten 
cm.  from  the  pylorus,  it  certainly  can  not  be  made  accountable  for 
the  movements  all  around  the  cardia  and  the  saccus  caecus. 

The  musculature  of  the  fundic  end  has  never  been  observed  in 
peristaltic  motion  by  us,  excepting  the  peristalsis  occasionally 
arising  from  the  antrum  and  traveling  upward  over  it.  During 
active  peristalsis  it  is  in  a condition  of  tonic  contraction  with  the 
intragastric  bag  in  the  fundus ; we  have  estimated  this  to  be  equal 
to  six  to  eight  cm.  of  water  (water  manometer). 

Moritz,  in  his  work  on  “ The  Motor  Function  of  the  Stomach,” 
studiously  avoids  referringto  any  systematic  food-circulation  within 
the  organ.  It  seems  rational  that  sufficient  churning  and  mixing 
is  effected  by  the  powerful  contractions  of  the  antrum  during  the 
general  tonus  of  the  fundus  to  explain  the  saturation  and  softening 
of  the  ingesta  by  gastric  juice. 

The  contrasting  relations  of  the  fundus  and  antrum  regarding 
active  peristalsis  are  evident  in  the  degree  of  pressure,  as  observed 
on  a water  manometer  in  connection  with  our  triple  intragastric 
bag.  In  the  fundus  the  pressure  is,  on  an  average,  equal  to  three 
to  six  cm.  of  water.  The  increase  of  intragastric  pressure  due  to 
cardiac  action  is  equal  to  one  to  two  cm.  (In  this  is  included  the 
pressure  due  to  every  new  heart  impulse  and  aortic  impulse.)  The 
inspiratory  increase  of  pressure  is  equal  to  six  to  twelve  cm. 
These  are  very  nearly  the  figures  Moritz  obtained,  and  we  add  them 
here  as  merely  in  support,  and  confirmatory,  of  his  views. 

Conclusions. — It  is  necessary  to  distinguish  the  movements  ot 
the  (1)  fundus,  (2)  preantral  portion,  (3)  antrum,  and  (4)  pyloric 
sphincter.  (1)  The  motor  apparatus  of  the  stomach  is  represented 
by  its  muscular  fibers.  Where  these  are  most  developed,  the 
peristalsis  is  strongest ; where  they  are  least  developed,  it  is  weakest. 
(2)  The  fundus  has  a thin  muscular  development,  hence  its  peri- 
stalsis is  insignificant,  and  consists  in  squeezing  its  contents  into  the 
tubular  preantrum  or  prepyloric  portion.  (3)  Waves  of  constriction 
along  the  preantrum  press  the  food  forward  and  backward  through 
this  portion  until  a mightier  wave-impulse  sweeps  it  into  the 
muscular  ampulla  just  in  front  of  the  pylorus,  the  antrum  pylori. 
(4)  The  final  expression  into  the  duodenum  is  executed  by  the 
antrum,  which  may  contract  as  a whole  or  form  into  two  spherical 
muscular  ventricles  by  a constriction  (rarely).  (5)  A food  circula- 
tion, in  the  sense  of  Beaumont  and  Brinton,  does  not  occur. 

The  physiology  of  the  motor  function  has  been  dwelt  upon 
7 


9o 


ABSORPTION  FROM  THE  STOMACH. 


more  extensively  than  seems  necessary  in  a condensed  statement  of 
gastric  pathology,  not  only  because  it  is  the  most  important  office 
of  the  stomach,  but  because  we  have  become  convinced  that,  in  a 
large  majority  of  disorders  of  secretion  and  absorption,  an  abnorm- 
ality in  the  motor  function  lies  at  the  foundation. 

The  exaggerated  or  diminished  peristalsis  can  on  careful  exam- 
ination be  detected  sometimes  before  the  secretory  and  absorptive 
anomalies  are  apparent.  The  secretory  disturbances  observed 
after  section  of  both  vagi  are  due,  according  to  Contejean,  to  the 
motor  paralysis  caused  at  the  same  time  (“Archiv.  de  Physiologic,” 
vol.  iv,  p.  640).  A similar  view  is  held  by  H.  Borutteau  (“  Phliiger’s 
Archiv,”  Bd.  lxv,  p.  26). 

The  relation  between  motility  and  secretion  and  absorption  is  not 
at  all  well  understood.  The  peristaltic  movements  effecting  a churn- 
ing motion  are  those  mostly  concerned  in  stimulating  secretion  ; 
when  these  movements  are  lost,  secretion  is  generally  disturbed. 

The  last  vestige  of  peristalsis  is  that  by  which  the  stomach 
is  emptied,  and  it  may  be  present  with  total  absence  of  secretion. 
In  stomachs  with  motility  much  impaired  and  secretion  arrested, 
the  absorptive  function  is  greatly  reduced  (atrophic  gastritis,  car- 
cinoma). In  temporary  arrests  of  these  functions,  the  secretive 
and  absorptive  functions  generally  return  with  improved  motility. 

In  our  drawing  (frontispiece),  the  manner  in  which  the  deep  ends 
of  the  fundus  glands  are  encircled  by  fibers  from  the  muscularis 
mucosae  is  very  evident.  From  this  it  is  conceivable  that  the  func- 
tion of  the  gland-cells  is  in  a manner  dependent  upon  the  contrac- 
tility of  the  fibers  of  the  muscularis  mucosae,  which  can  not  fail  to 
influence  the  blood-supply  to  these  cells  (see  Mall,  on  “ Circulation 
in  the  Dog’s  Stomach,”  chap.  1). 


CHAPTER  X. 

ABSORPTION  FROM  THE  STOMACH. 

Penzoldf  s and  Faber  s,  HerscheV  s,  Julius  Miller' s,  and  Hemmeter  s 
Tests  for  Gastric  Resorption. 

Remarkable  variations  exist  in  the  absorptive  power  of  the  gas- 
tric mucosa,  not  only  in  different  animals,  but  in  the  same  animals 
at  different  times  and  under  varying  conditions.  Absorption  is 


ABSORPTION  OF  STRYCHNIN. 


91 


largely  influenced  by  gastric  innervation  and  the  quality,  quan- 
tity, and  pressure  of  blood-supply.  Edkins  in  1892  (“  Journ. 
of  Physiol.,”  p.  460)  published  experiments  in  which  he  introduced 
a measured  quantity  of  salt  solution  into  the  stomach  of  cats  after 
ligation  of  the  pylorus  and  the  cardia ; after  an  hour  he  recovered 
exactly  the  same  quantity  again.  We  have  already  referred  to  the 
work  of  von  Mehring  (“Therap.  Monatshefte,”  1893),  which,  like 
that  of  Edkins,  shows  that  water  is  not  absorbed  from  the  stomach. 
Peptone,  grape-,  milk-  and  cane-sugars,  maltose,  dextrin,  and  alco- 
hol are  absorbed,  and  von  Mehring  demonstrated  that  a more  or  less 
active  secretion  of  water  from  the  walls  into  the  stomach  occurred 
simultaneously  with  the  absorption,  so  that  in  his  dogs  with  duo- 
denal fistulae  he  found  a larger  quantity  of  water  came  out  through 
the  fistula  than  the  dogs  had  taken  by  the  mouth.  Bouley  and 
Colin  (Colin,  “ Traite  de  physiologie  comparee,”  vol.  11,  p.  91)  intro- 
duced strychnin  into  the  stomach  of  animals  after  ligation  of  the 
pylorus — or  after  it  was  paralyzed  (as  they  claim)  by  vagotomy. 
It  is  stated  by  them  that  the  effect  of  strychnin  was  rapidly  evident 
in  the  cat,  dog,  and  pig,  that  itwas  retarded  in  the  cow,  and  that  there 
was  no  effect — at  least,  no  serious  effect — in  the  horse.  Tappeiner 
(“  Ueber  Resorption  im  Magen,”  “ Zeitschr.  f.  Biol.,”  1880)  intro- 
duced strychnin  into  the  stomach  of  cats;  0.03  gm.  of  this  alkaloid 
in  an  aqueous  solution  was  sufficient  to  kill  a cat  weighing  two 
kilos  in  eight  minutes.  Cats  whose  pylorus  was  tied  succumbed  to 
doses  of  0.05  gm.  and  more  only  after  an  hour  and  thirty  minutes  or 
even  later.  When  the  strychnin  solution  contained  alcohol,  it  was 
absorbed  almost  as  rapidly  as  when  the  pylorus  was  not  ligated. 
Similarly,  chloral  hydrate  was  not  absorbed  in  aqueous  solution,  but 
readily  in  alcoholic  solution,  from  the  stomachs  of  dogs  whose 
pylorus  was  ligated. 

In  the  experiments  of  Meltzer  on  the  absorption  of  strychnin  and 
hydrocyanic  acid  from  the  stomach  of  rabbits  (“  Journ.  Exper. 
Med.,”  vol.  1,  p.  529),  it  was  found  that  six  to  ten  milligrams  of  strych- 
nin introduced  into  the  full  stomach  with  the  pylorus  open  would 
rapidly  bring  on  tetanus,  and  it  is  intimated  that  absorption  takes 
place  in  that  case  from  the  intestines,  not  from  the  stomach.  When 
the  pylorus  is  closed,  even  such  large  doses  as  200  milligrams  of 
strychnin,  remaining  for  many  hours  within  the  empty  stomach, 
with  good  circulation  and  with  intact  innervation  of  the  vagi,  do 
not  produce  any  effect  at  all.  The  conclusion  is  justifiable  that  the 
gastric  mucosa  does  not  absorb  strychnin  to  any  considerable  ex- 


92 


ABSORPTION  FROM  THE  STOMACH. 


tent.  From  Meltzer’s  experiments,  which  apply  only  to  rabbits, 
it  is  not  evident  that  the  circulation  of  the  stomach  was  good,  for 
when  the  pylorus  or  the  cardia  is  ligated,  a normal  gastric  circula- 
tion becomes  impossible.  Injection  of  strychnin,  stained  with 
methylene-blue,  into  the  submucosa  (loc.  cit.),  which  was  in  two 
minutes  followed  by  tetanus,  although  the  cardia  was  tied  and  a 
tube  tied  into  the  pylorus,  does  not  prove  that  the  circulation  was 
normal.  The  same  objections  as  can  be  brought  against  the 
experiments  of  Talma  (loc.  cit.)  are  applicable  to  Meltzer’s;  the 
method  constitutes  too  violent  an  interference  with  gastric  circula- 
tion and  peristalsis.  The  author  has,  however,  been  able  to  con- 
firm Meltzer’s  conclusions,  for  in  rabbitts  in  whom  the  pylorus 
was  occluded  by  a rubber  balloon  introduced  through  the  mouth 
and  stomach  and  blown  up  in  the  duodenum  just  beyond  the 
pylorus,  it  was  discovered  that  strychnin  is  not  absorbed  from  the 
stomach.  Stenosing  the  outlet  beyond  the  pylorus  does  not  in  any 
way  injure  the  stomach  nor  disturb  circulation  or  innervation.  The 
rabbit  is  not  free  from  objection  as  an  experimental  animal,  as  its 
gastric  mucosa  is  rarely  in  an  entirely  normal  condition.  Meltzer 
found  that  distinct  differences  exist  in  the  absorptive  power  of 
different  parts  of  the  digestive  tract ; for  instance,  the  mucous 
membrane  of  the  esophagus  absorbs  strychnin  very  poorly.  The 
part  of  the  alimentary  canal  absorbing  best  is  the  pharynx  ; the 
rectum  absorbs  strychnin  next  best,  its  resorptive  power  excelling 
that  of  the  small  intestine.  Prussic  acid  is,  however,  absorbed  very 
well  from  the  stomach  even  when  the  pylorus  is  ligated ; it  seems 
to  produce  a hemorrhagic  surface  on  the  mucous  membrane  which 
facilitates  absorption. 

The  method  most  commonly  employed  to  test  gastric  resorption 
is  that  of  Penzoldt  and  Faber.  Three  to  five  grains  of  iodid  ot 
potassium  are  inclosed  in  a gelatin  capsule,  which  is  adminis- 
tered with  ioo  c.c.  = ounces  of  water.  Iodid  of  sodium  or 
potassium,  when  taken  internally,  will  appear,  and  can  be  tested 
for  in  the  saliva  and  in  the  urine,  where  it  is  excreted  in  from  six 
and  one-half  to  fifteen  minutes. 

The  test  is  generally  made  by  wetting  starch  paper  with  the  saliva 
of  the  patient  every  two  minutes  after  the  KI  is  taken,  and  touching 
the  wet  spot  with  fuming  nitric  acid.  The  first  appearance  of  a 
blue  color  indicates  that  the  iodid  has  reached  the  point  of  excre- 
tion, and  consequently  must  have  been  absorbed.  If  this  reaction 
first  occurs  after  fifteen  minutes,  then  the  rate  of  absorption 


herschel’s  test  for  absorption. 


93 


is  reduced.  This,  according  to  Zweifel  (“  Resorpt.  Verhaltnisse  d. 
menschl.  Magens,”  “ Deutsch.  Arch.  f.  klin.  Med.,”  Leipsic,  Bd. 
xxxix,  p.  349,  1886),  occurs  in  gastritis,  dilatation,  and  carcinoma; 
in  gastric  ulcer  the  resorption  is  said  to  be  normal,  or  nearly  so. 

Most  authorities  (J.  Wolff,  Zweifel,  Sticker,  Quetsch)  differ  very 
much  on  this  question,  but  agree  on  the  reduced  absorption  in 
carcinoma.  If  the  iodid  is  given  during  a meal,  the  reaction  occurs 
much  later. 

Herschel  (“Indigestion,”  London,  1895,  p.  1 1 5)  estimates  the 
absorptive  power  by  giving  two  decigrams  of  powdered  rhubarb, 
which  gives  a red  color  in  the  urine  with  liquor  potassae  normally 
in  fifteen  minutes.  Our  experience  with  this  method  is  that 
frequently  the  urine  is  so  highly  colored  in  digestive  diseases 
that  the  red  color  must  be  very  decided  to  be  recognized — in 
addition  to  which  it  suffers  from  the  same  objection  as  Penzoldt’s 
and  Faber’s  method.  In  the  first  place,  Brandi’s  experiments  have 
shown  that  sodium  iodid  is  absorbed  to  a very  slight  degree  or  not 
at  all  in  dilute  solutions. 

Not  until  its  solutions  reach  a concentration  of  three  per  cent, 
or  more  does  its  absorption  become  important.  Accordingly,  all 
soluble  inorganic  salts  are  practically  not  absorbed  in  the  stomach, 
since  it  can  not  be  supposed  that  they  are  normally  swallowed  in 
solutions  so  concentrated  as  three  per  cent.  Brandi  also  found  that 
condiments,  such  as  mustard  and  pepper,  and  also  alcohol,  very 
much  facilitated  the  absorption  of  sodium  iodid.  Perhaps,  these 
substances  act  by  stimulating  the  epithelial  cells,  or  by  causing  a 
marked  hyperemia  of  the  mucosa. 

The  absorption  time  does  not  vary  much  in  the  same  individual, 
except  when  the  stomach  is  full;  in  this  case  it  is  not  only  pro- 
longed, but  is  very  variable  in  the  same  individual.  This  prolon- 
gation, according  to  Sidney  Martin  (“  Diseases  of  the  Stomach,” 
London,  1895),  is  probably  due  to  a considerable  dilution  of  the 
iodid  by  the  stomach  contents,  and  also  to  the  fact  that  the  salivary 
glands  are  not  so  active  after  a meal  as  in  the  fasting  condition. 
One  must  not  overlook  the  fact  in  these  experiments  that  it  is  not 
only  the  absorptive  activity  of  the  stomach  that  is  being  investi- 
gated, but  also  the  excretory  activity  of  the  salivary  glands. 

In  Zweifel’s  experiments  it  is  probable,  from  what  we  know  of 
the  absorption  of  water  in  the  stomach,  through  the  observations 
of  Tappeiner  (“  Ueber  Resorption  im  Magen,”  “ Zeitschr.  f.  Biol.,” 
Miinchen,  Bd.  xvi,  p.  497,  1881)  and  von  Mehring  {loc.  cit.)y  that 


94 


ABSORPTION  FROM  THE  STOMACH. 


most  of  the  liquid  containing  the  iodid  passes  rapidly  into  the  duo- 
denum. Therefore,  we  may  be  testing  not  only  gastric  absorption 
and  excretory  activity  of  the  salivary  glands,  but  also  intestinal 
absorption. 

Zweifel  concludes  (loc.  cit.)  that  in  all  diseases  of  the  stomach 
there  is  a prolongation  of  absorption  time,  which  is  greatest  in  dila- 
tation and  carcinoma  and  least  in  chronic  gastric  catarrh,  and  very 
slight  in  ulcer  in  the  later  stages;  in  the  early  stages  of  ulcer,  how- 
ever, he  claims,  the  rate  of  absorption  is  also  prolonged. 

It  is  very  evident  that  no  differentiation  between  catarrh  and 
ulcer  is  possible  according  to  this  method,  and  thereby  one  of  the 
main  purposes  of  such  investigations — that  of  aiding  in  the  estab- 
lishment of  a diagnosis — is  thwarted. 

In  view  of  these  defects,  which  apply  equally  well  to  Herschel’s, 
Penzoldt’s,  and  Faber’s  methods  of  testing  absorption,  and  are 
caused  mainly  by  the  fact  that  water  is  not  absorbed  from  the 
stomach,  and  that  the  varying  secretory  activity  of  the  salivary 
glands  and  kidneys  is  a factor  influencing  absorption  time,  we 
have  devised  a method  which  is  available  for  experiments  on 
gastric  absorption  in  the  physiological  laboratory,  and  which  we 
have  successfully  tried  on  six  male  and  eight  female  patients  and 
ten  healthy  students.  The  methods  of  testing  the  urine  and 
saliva  were  discarded  entirely. 

Our  method  consists  in  washing  out  the  stomach  thoroughly; 
then,  by  means  of  our  method  of  duodenal  intubation,  the  entrance 
into  the  duodenum  is  plugged,  or  closed  up,  by  introducing  a 
small  rubber  balloon  into  it  and  blowing  it  up  just  in  front  of  or 
beyond  the  pylorus.  (A  method  having  the  same  object  in  view 
has  been  described  subsequent  to  the  author’s  publication,  by  Dr. 
F.  Kuhn,  in  the  “ Munchener  medizin.  Wochenschr.,”  Nos.  27,  28, 
and  29,  1896,  but  it  is  founded  upon  a different  principle  from 
ours — the  spiral  sound.) 

After  thus  mechanically  closing  the  pylorus,  a weighed 
amount  of  any  of  the  substances  which  von  Mehring  has  shown  are 
readily  absorbed,  or  of  any  harmless  inorganic  salt, — sodium 
chlorid  or  sodium  phosphate, — dissolved  in  100  c.c.  of  distilled 
water,  so  as  to  make  a three  per  cent,  solution,  is  poured  into  the 
organ  through  a tube.  This  is  indispensable  to  exclude  loss  of  the 
salt  solution  through  clinging  to  the  tongue,  mouth,  and  esophagus 
or  absorption  from  these  tissues. 

After  a lapse  of  ten  minutes  the  fluid  is  again  drawn  out  of  the 


author’s  method  for  testing  absorption.  95 

stomach  by  aspiration,  or  even,  if  necessary,  by  adding  known 
quantities  of  distilled  water,  until  the  last  washing  gives  no  indica- 
tion of  containing  any  trace  of  the  salt  by  a proper  chemical  test. 
This  entire  water  is  now  evaporated  to  dryness  and  the  residue 
weighed.  The  difference  between  the  amount  of  NaCl  poured  into 
the  stomach — which  in  a three  per  cent,  solution  is  three  gm.  in 
case  ioo  c.c.  are  used — and  the  amount  regained  indicates  the 
degree  of  gastric  absorption. 

To  simplify  matters,  the  practical  suggestion  of  Julius  Miller 
(Boas’  “ Archiv  fur  Verdauungskrankheiten,”  Bd.  i,p.  237,  “Zur 
Kennt.  d.  Sek.  u.  Resorpt.  im  menschl.  Magen  ”)  has  been  utilized 
and  can  be  recommended.  It  consists  in  noting  the  specific  gravity 
of  salt  solutions  before  pouring  them  through  the  tube,  and  after 
any  desired  time,  the  solutions  are  washed  out  or  aspirated,  and 
the  specific  gravity  again  determined. 

The  difference  between  these  specific  gravities  taken  before  the 
salt  solution  enters  the  stomach  and  after  it  is  regained  affords  a 
satisfactory  index  of  the  rate  of  absorption  from  the  stomach  if 
escape  of  the  solution  into  the  duodenum  is  prevented.  It  is  not 
necessary  to  evaporate  the  whole  solution  to  dryness  in  case  sodium 
chlorid  or  any  other  harmless  neutral  salt  is  used.  But  after 
measuring  the  total  quantity  of  liquid  regained, — say,  for  instance, 
it  amounts  to  one  liter  (1000  c.c.), — the  amount  of  NaCl  in  ten  c.c. 
can  be  determined  by  evaporation  in  platinum,  and  the  weight  of 
the  total  remaining  NaCl  calculated  by  multiplying  the  result  by 
100,  or  whatever  the  figure  may  happen  to  be. 

This  method  of  determining  the  rate  of  gastric  absorption  gives 
approximately  accurate  results,  even  without  duodenal  intubation 
and  mechanical  closing  of  the  pylorus,  provided  that  by  several 
preliminary  experiments  the  motility  of  the  patient’s  stomach  has 
been  relatively  determined. 

By  observing  what  portion  of  500  c.c.  of  water  he  will  pass  into 
the  duodenum  in,  say,  ten  to  twenty  minutes, — this  also  requiring 
the  drawing  out  again  of  the  remnant  of  the  500  c.c.  of  water  that 
was  taken  in  for  experiment, — von  Mehring  {loc.  cit .)  found  that  of 
500  c.c.  of  water  given  to  a large  dog,  through  the  mouth,  the 
entire  amount,  or  at  least  495  c.c.,  had  been  passed  out  of  the 
stomach  through  a duodenal  fistula  within  twenty-five  minutes. 

In  the  human  being  the  passage  of  water  out  of  the  stomach  is 
not  nearly  so  rapid.  Julius  Miller  {loc.  cit.)  found  that  the  human 
stomach  was  not  rid  of  even  200  c.c.  NaCl. solution  of  the  specific 


96 


ABSORPTION  FROM  THE  STOMACH. 


gravity  1028  in  thirty  minutes.  After  this  time  he  regained 
in  one  case  75  c.c. ; sometimes  he  regained  more  liquid  than 
he  poured  in. 

In  thirty  tabulated  measurements  which  he  gives  with  sodium  . 
chlorid  solution  (p.  240,  loc.  cit.),  he  regained  more  than  he  poured  in, 
five  times;  the  same  amount,  once;  and  a less  quantity,  twenty-five 
times.  But  his  figures  goto  prove  that  even  with  an  open  passage 
into  the  duodenum,  comparatively  small  amounts  of  salt  solutions 
are  passed  out  in  fifteen  minutes. 

Hence,  if  in  any  individual  the  average  amount  passing  into  the 
duodenum  in  fifteen  minutes  is  known  by  previous  experiments, 
the  closing  of  the  pylorus  is  not  necessary  to  reach  an  approximate 
result  concerning  the  rate  of  absorption.  Miller  confirms  von 
Mehring’s  conclusions  that,  contemporaneous  with  absorption,  a 
secretion  of  water  occurs  into  the  stomach. 

This  secretion  increases  with  the  concentration  of  the  solutions. 

In  the  five  instances  mentioned  where  more  was  regained  than  was 
poured  in,  the  specific  gravities,  which  are  a good  indication  of 
concentration,  were  1066,  1061,  1052,  1088,  and  1035.  (Regarding 
the  taste  of  three  per  cent,  solution  of  NaCl,  it  might  be  explained 
that  this  is  the  percentage  of  salt  in  the  water  of  the  Atlantic 
Ocean,  which  has  been  recommended  for  internal  use — A.  Levertin, 

“ Hygieina,”  xlvij,  xlviii.  “ Svenska  lakaresallsk  Forh.”  S.  138, 
1885.) 

In  the  studies  with  occlusion  of  the  pylorus  we  experimented 
also  with  known  solutions  of  sodium  sulphate,  peptone,  maltose, 
cane-sugar,  milk-sugar,  and  alcohol.  As  water  is  poured  out  on 
the  surface  of  the  mucosa,  in  return  for  salts  absorbed,  the  specific 
gravity  will  not  always  instruct  us  as  to  the  contents  of  NaCl, 
which  had  best  be  arrived  at  by  weighing. 

From  experiments  on  animals  it  is  known  that  a concentrated 
solution  may  cause  the  stomach  to  secrete  water,  thereby  diluting 
it,  but  that  at  the  same  time  it  is  possible  that  there  may  be  no 
resorption,  so  that  weighing  the  residue  from  evaporating  the 
liquid  regained  may  be  unavoidable  for  a correct  result. 

Maltose  was  found  a very  practical  substance  for  absorption  ex- 
periments, though  dextrose  will  also  answer  this  purpose,  as  their 
quantity  can  be  readily  determined  in  solution  by  titration  with 
Fehling’s  solution,  and  also  by  the  fermentation  test,  for  which  the 
Einhorn  saccharimeter  is  most  serviceable.  Maltose  will  not 
reduce  as  much  Fehling’s  solution  as  dextrose,  the  exact  relation 


TESTING  ABSORPTION  BY  MALTOSE.  97 

between  the  two  being,  according  to  Brown  and  Heron,  for  mal- 
tose, 60.8  ; for  dextrose,  ioo. 

According  to  Soxhlet,  one  c.c.  Fehling’s  solution  corresponds  to 
7.78  milligrams  maltose  in  one  per  cent,  solution  (provided  the 
Fehling’s  test  was  not  diluted).  Though  maltose  is  converted 
into  dextrose  in  the  stomach,  the  amount  converted  in  ten  to  fifteen 
minutes  is,  according  to  our  observations,  small  enough  to  be  dis- 
regarded. If  desired,  a test  by  Barfoed’s  reagent  may  be  made  to 
detect  if  any  dextrose  is  present  in  the  liquid  regained. 

The  amount  of  sodium  chlorid  in  the  solution  regained  can  also 
be  determined  by  titration  (Salkowsky  u.  Leube,  “ Die  Lehre 
vom  Harn”;  also,  Neubauer  u.  Vogel,  “ Analysen  d.  Urins  ”).  The 
method  is  given  in  the  laboratory  manual  of  Dr.  Edward  L.  Whit- 
ney (“  An  Introduction  into  the  Laboratory  Methods  of  Clinical 
Pathology,”  p.  18,  Baltimore,  1896).  Our  method  for  absorption 
testing  is,  in  brief,  the  following: 

To  determine  the  amount  of  500  c.c.  of  a three  per  cent.  NaCl 
solution  passed  into  the  duodenum  in  ten  minutes: 

1.  Allow  500  c.c.  three  per  cent.  NaCl  solution  to  run  into  a 
clean  stomach  through  a tube  and  remain  ten  minutes. 

2.  Draw  out  as  much  as  possible,  washing  out  the  last  with 
known  quantities  of  distilled  water. 

3.  Determine  the  amount  of  NaCl  as  stated  above,  and  add  the 
average  deficit  of  escape  into  the  duodenum. 

The  difference  between  the  original  amount  NaCl  and  the  amount 
regained  is  a fairly  accurate  index  of  gastric  absorptive  power;  or, 
by  our  method  of  duodenal  intubation,  occlude  the  pylorus  by 
blowing  up  a balloon  in  front  of  or  beyond  it ; pour  into  the  stomach 
through  a tube  a known  quantity — say,  100  c.c. — of  a one  per  cent, 
solution  of  maltose;  in  ten  to  twenty  minutes  aspirate  or  wash  out 
the  amount  of  maltose  left  as  above.  The  deficit  will  indicate  the 
amount  absorbed. 


98 


LOCATION,  SIZE,  AND  CAPACITY  OF  THE  STOMACH. 


CHAPTER  XI. 

METHODS  FOR  DETERMINING  THE  LOCATION,  SIZE, 
AND  CAPACITY  OF  THE  STOMACH. 

Percussion  and  Palpation. — Gastrodiaphany  of  Einhorn. 

Percussion  of  the  stomach  gives  varying  results,  according  to 
its  contents  and  to  the  degree  of  its  distention.  The  fundus  is 
closely  applied  to  the  concavity  of  the  diaphragm,  and  five-sixths  of 
its  volume  is  to  the  left  of  its  median  line;  only  one-sixth  to  the 
right  (observe  the  accompanying  illustrations  from  Eichhorst’s 
“Klin.  Untersuchungs-Methoden  ”).  The  highest  point  is  the 
fundus,  which  reaches  the  level  of  the  ninth  thoracic  vertebra.  The 
lesser  curvature  runs  along  the  left  of  the  spinal  column,  and  crosses 
to  the  right  at  the  level  of  the  first  lumbar  vertebra.  The  lesser 
curvature  is  entirely  covered  by  the  liver,  and  can  be  percussed  or 
palpated  only  when  it  is  located  lower  than  normal.  The  pylorus 
is  covered  by  the  right  lobe  of  the  liver,  about  three  to  four  cm. 
from  the  median  line  ; it  is  seven  cm.  lower  than  the  cardia.  The 
pars  pylorica  (antrum  pylori)  extends  further  to  the  right  than  the 
pylorus  itself.  The  greater  curvature  in  its  upper  part  is  largely 
covered  by  the  lung ; its  lower  and  anterior  part  is  in  appo- 
sition with  the  left  hypochondrium  and  epigastrium.  When  the 
stomach  is  full,  the  greater  curvature  is  two  to  four  cm.  above 
the  umbilicus.  To  the  right  of  the  median  line  it  ascends  along 
the  median  edge  of  the  gall-bladder,  and  is  continued  into  the 
pyloric  part. 

Distention  very  much  facilitates  percussion  and  palpation  of  the 
stomach. 

The  conviction  has  been  forced  upon  us  that  the  degree  to  which 
the  stomach  can  be  distended  is  a very  limited  one.  This  state- 
ment is  made  after  many  hundred  distentions  with  the  intragastric 
stomach-shaped  bag  in  connection  with  a manometer.  Most 
stomachs  that  are  in  a normal  state  will  refuse  to  be  distended 
more  than  100  c.c.  beyond  their  natural  capacity.  Only  in  patho- 
logical thinning  of  the  gastric  walls  and  in  atrophy  of  the  muscu- 
laris  is  an  overdistention  conceivable ; even  then  some  of  the  gases 
will  escape  by  the  cardia  before  painful  distention  will  ensue. 

For  these  reasons  distention  with  air  or  carbon  dioxid  is  an 


DISTENTION  OF  STOMACH  BY  AIK  OK  C02. 


99 


expedient  and  safe  way  of  determining  the  form  and  location  of 
the  stomach,  and  its  relation  to  any  tumors  that  may  be  present. 
There  is  no  better  way  of  differentiating  gastric  dilatation  from  gas- 
troptosis  (falling)  than  by  this  process  of  distention. 

This  method  is  carried  out  by  introducing  a stomach-tube,  to 
the  upper  end  of  which  is  attached  a double-bulb  pump  arrange- 
ment such  as  is  used  in  some  spray  apparatus  (Runeberg,  “ Deutsch. 


Fig.  8.— Location  of  the  Stomach — Dorsal  View, 
i.  Left  kidney.  2.  Right  kidney.  3.  Spleen.  4.  Lungs.  5.  Descending  colon.  6.  Ascending 
colon.  7.  Complementary  space  occupied  by  expanding  lungs  in  inspiration.  8.  Hepatic 
flexure.  9.  Splenic  flexure  of  colon.  The  stomach  occupies  the  space  colored  in  red. 


Archiv  f.  klin.  Med.,”  Bd.  xxxiv).  Bouveret  (“  Traite  des  Maladies* 
de  TEstomac,”  Paris,  1893)  recommends  that  the  air  be  forced  into 
the  stomach  by  blowing  with  the  mouth  through  the  tube.  Riegel 
and  Boas  are  very  fond  of  gastric  distention  by  carbon  dioxid  gas. 
A teaspoonful  of  bicarbonate  of  sodium,  and  about  the  same  amount, 
or  perhaps  a little  less,  of  tartaric  acid,  are  dissolved,  each  in  a 
separate  glass  containing  200  c.c.  of  water. 


IOO 


LOCATION,  SIZE,  AND  CAPACITY  OF  THE  STOMACH. 


First,  the  solution  of  tartaric  acid  is  administered,  and  immedi- 
ately afterward  the  sodium  bicarbonate.  The  patient  must  be 
in  the  dorsal  position,  with  knees  flexed.  Within  the  stomach  a 
brisk  evolution  of  C02  occurs,  at  once  distending  the  organ  so 
that  it  stands  out  prominently,  and  is  evident  as  a sharply  defined, 
arched  elevation.  The  greater  curvature  becomes  very  apparent; 
not  so  the  lesser  one.  The  patient  should  be  told  not  to  belch. 

The  stomach  under  distention  can  be  readily  palpated  or  per- 


Fig.  9. — Location  of  the  Stomach— Anterior  View. 

1.  The  stomach.  2.  Liver.  3.  Heart.  4.  Lungs.  5.  Complemental  pleural  spaces.  6.  Trans- 
verse colon. 


cussed.  If  tumors  were  made  out  before,  it  is  important  to  deter- 
mine their  seat  after  the  distention.  It  is  possible  thereby  in 
many  cases  to  demonstrate  the  connection  or  non-connection  of 
the  tumor  with  the  stomach  after  distention. 

Accordingly,  tumors  which,  when  the  stomach  was  empty,  were 
palpated  in  the  line  of  the  umbilicus  and  to  the  right,  for  which 
reason  it  might  be  doubted  whether  they  belonged  to  the  stomach, 
after  distention  may  move  upward  to  the  right,  and  toward  the 


DISTENTION  WITH  AIR  OR  C02. 


IOI 


anterior  arch  of  the  short  ribs.  One  may  see  and  feel  the  direct 
transition  of  the  tumor  mass  into  the  substance  of  the  stomach, 
or  trace  its  extent  toward  the  pylorus,  or  ascertain  that  it  is 
entirely  independent  of  the  stomach. 

Even  the  disappearance  or  the  becoming  less  distinct  of  a tumor 
is  very  important,  if  it  occurs  after  distention.  This  is  observed  in 
tumors  of  the  posterior  wall.  If  it  is  easily  movable,  very  close 


i.  Pronounced  liver  dullness.  2.  Lesser  liver  ness.  3.  Smaller  heart  dullness.  4.  Larger 
heart  dullness.  5.  Limits  of  stomach  percussion.  6.  Traube’s  semilunar  space.  7.  Left 
edge  of  short  ribs. 


and  tight  adhesions  may  be  excluded  ; if  it  is  absolutely  immov- 
able, it  is  abnormally  attached  or  fixed.  It  is  evident  that  disten- 
tion of  the  stomach  with  air  or  gas  not  only  enables  one  to  get 
a better  percussion  area,  but  it  serves  another  purpose:  that  of 
facilitating  the  palpation  of  tumors. 

Percussion  and  auscultation  over  the  stomach  frequently 
give  valuable  information  concerning  its  boundaries  without  the 


1 


Fig.  10.— Normal  Percussion  Limit  the  Adult  Stomach. — ( Eichhorst .) 


02 


LOCATION,  SIZE,  AND  CAPACITY  OF  THE  STOMACH. 


use  of  instruments.  So  does  the  elucidation  of  “ clapotement,” 
or  splashing  sounds.  But  when  the  stomach  is  not  distended 
or  no  instrument  is  used,  differentiation  of  colon  from  stomach 
becomes  difficult,  especially  if  the  abdominal  walls  have  any 
moderate  thickness.  Often  mere  inspection  will  disclose  the  loca- 
tion of  the  stomach  when  distended  by  its  own  gases.  In  his 
book  on  “ Diseases  of  the  Stomach,”  Riegel  gives,  in  addi- 
tion to  the  above,  ten  other  methods  for  determining  location, 
size,  and  capacity,  most  of  which,  being  more  or  less  falla- 
cious, we  must  refer  those  specially  interested  in  this  matter 
to  Riegel’s  book,  pages  41-56.  In  our  opinion,  all  of  these  latter 
methods  will,  before  many  years,  have  only  a historical  value. 
There  is  one  method  for  accomplishing  the  above  objects,  however, 
which  we  can  recommend  from  a very  large  experience,  and  which 
is  used  extensively  at  our  clinic,  and  of  the  accuracy  of  which 
we  have  had  many  opportunities  to  be  convinced. 

With  our  stomach-shaped  intragastric  rubber  bag  (see  plate  iv) 
and  the  pressure  bottles  A and  B,  the  location  and  capacity  can 
be  determined  with  great  ease.  The  rubber  bag  used  for  this  pur- 
pose has  no  sheath  or  guide  for  the  duodenal  tube.  The  stomach 
is  distended  by  blowing  up  the  bag  within  it;  the  amount  of  air 
necessary  thereto  is  measured  afterward  by  allowing  it  to  escape 
into  a spirometer.  A less  accurate,  though  quite  practical  method, 
is  to  catch  the  escaping  air  in  a glass  cylinder  filled  with  water  and 
inverted  over  a basin. 

It  might  be  claimed  that  our  method  is  a combination  of  von 
Kelling’s,  Schreiber’s,  and  Jaworski’s  methods,  and  it  does  indeed 
partake  of  part  of  the  devices  of  all  these.  (See  Riegel,  pp.  51,  52, 
and  54.)  Schreiber  used  a small,  round, — not  a stomach-shaped, 
— distensible  balloon,  but  no  pressure  bottles  nor  spirometer. 
Jaworski  used  two  pressure  bottles,  but  no  balloon  or  intragastric 
bag,  and  no  spirometer,  while  von  Kelling  used  simply  the  spir- 
ometer to  measure  the  air,  which  he  forced  into  the  stomach  with  a 
double  bulb,  as  is  used  on  sprays. 

Our  method  of  arriving  at  the  capacity  of  the  stomach  is  really, 
then,  not  entirely  original,  as  it  combines  the  best  of  the  three  older 
methods,  but  it  is  most  convenient  and  reliable.  The  bag,  as  has 
been  shown,  can  at  the  same  time  be  used  for  determining  the 
nature  of  the  motor  function.  It  can  be  asserted,  from  ’observa- 
tions on  a large  number  of  patients,  that  there  is  no  other  single 
method  which  is  so  useful,  combining  instruction  concerning  size, 


Fig.  ii. — Stomach  Distended  by  Air  or  CO*.  Showing  Stomach  in  State  of 
Gastroptosis. — ( From  the  Author's  Clinic .) 


104  LOCATION,  SIZE,  AND  CAPACITY  OF  THE  STOMACH. 

location,  and  capacity  of  the  stomach  with  that  concerning  its 
motor  function. 

The  method  is  as  easy  in  its  application  as  any  which  Riegel 
describes.  The  capacity  can,  for  practical  purposes,  be  read  off  on 
bottle  B,  from  the  amount  of  air  that  has  been  displaced  into 
the  intragastric  bag.  The  cost  of  the  bag  is  one  dollar,  and  a 
good  idea  of  the  motor  function  can  be  had  from  a water  man- 
ometer in  connection  with  it  after  distention  ; with  one  hand  on  the 
epigastric  region,  the  respiratory  movements  can  be  felt,  and  thus 
distinguished  from  the  active  movements  as  expressed  by  the  rise 
and  fall  of  the  water  column  in  the  manometer.  It  may  thus  be 
used  without  the  kymograph.*  Langerhans  (“Archiv  fur  Verdau- 
ungskrankheiten,”  Bd.  in,  S.  312)  prefers  the  use  of  the  intragas- 
tric rubber  bag  for  the  recognition  of  gastroptosis. 


GASTRODIAPHANY. 

Gastrodiaphany  of  Einhorn. — In  1889  Dr.  Max  Einhorn  suc- 
ceeded in  transilluminating  the  human  stomach  in  the  dark  by 
means  of  a small  Edison  lamp  attached  to  a soft-rubber  tube  ; from 
the  lamp  through  this  tube,  insulated  conducting  wires  ran  to  a 
storage  battery.  (See  illustration,  p.  105.)  At  some  distance  from 
the  rubber  tube  was  a current-interrupter.  By  this  apparatus  the 
inventor  claimed  to  be  able  to  ascertain  the  exact  position  and  size 
of  the  stomach,  and  to  recognize  tumors  and  thickenings  of  the 
front  wall  by  their  lack  of  translucency. 

In  1867  Milliot  had  succeeded  in  transilluminating  the  stomachs 
of  animals  by  platinum  wires  contained  in  glass  tubes  and  con- 
nected with  a Middeldorph’s  apparatus. 

Fleischer,  in  his  text-book  (“Path.  u.  Therap.  der  Magen-  u. 
Darmkrankh.”  p.  789),  claims  to  have  succeeded,  together  with 
Hiifler,  in  transilluminating  the  human  stomach  before  Einhorn. 


*In  the  shops  of  Baltimore  small  toy  balloons  are  sold  which  are  made  of  very  thin 
but  quite  tough  rubber,  which  my  assistants  have  frequently  used  for  intragastric  disten- 
tion. These  balloons  accompany  a game  called  “ pillow  dex,”and  are  sold  six  for  twenty- 
five  cents.  For  studying  the  motor  function  they  answer  as  well  as  the  more  expensive 
stomach-shaped  bags,  as  I have  assured  myself  that  on  distention  they  fill  every  inch  of 
space  in  a dog’s  stomach.  P'or  determining  the  capacity,  however,  the  stomach-shaped 
bag  is  more  accurate. 


ELECTR0D1APHANY  OF  THE  STOMACH. 


105 


If  this  is  really  so,  Fleischer  did  not  publish  his  investigations,  so 
far  as  we  know,  and  certainly  is  not  entitled  to  name  the  method 
after  himself. 

To  Einhorn  is  due  the  credit  of  developing  the  method  as  an 
aid  to  diagnosis.  The  patient,  in  a fasting  condition,  drinks  from 
two  glasses  to  a liter  of  water  ; the  apparatus  is  passed  into  the 
stomach  just  as  the  lavage  tube  is  passed,  and  connected  with 
the  storage  battery.  The  stomach  transmits  the  electric  light 
through  the  abdominal  walls,  becoming  visible  as  a red  zone  at 
the  place  which  corresponds  to  its  location.  The  observation  is 
executed  in  a dark  room. 

In  case  the  anterior  gastric  wall  is  occupied  by  a tumor,  the  light 
will  not  be  transmitted  at  that  spot,  but  all  around  it  the  rays  will 
penetrate,  thus  evincing  a dark,  shaded  area  in  a luminous  zone. 


Fig.  12.— The  Electrodiaphane. 


We  are  in  the  habit  of  marking  the  ribs,  particularly  the  um- 
bilicus, xiphoid  cartilage,  and  symphysis  pubes,  with  phosphorus, 
so  that  they  can  be  seen  in  the  dark  and  serve  as  landmarks  to  the 
exact  abdominal  area  in  which  the  light  permeates.  In  1891  Dr. 
Howard  A.  Kelly  prompted  us  to  attempt  transillumination  of 
the  colon  by  this  method,  and  the  author  demonstrated  it  to 
the  Clinical  Society  of  Maryland  in  that  year.  Later  Heryng  and 
Reichmann  (“Therap.  Monatshefte,”  1892)  published  the  first 
account  of  transillumination  of  the  colon.  The  water-circulating 
diaphane  devised  by  these  clinicians,  to  prevent  heating  of  the  lamp, 
possesses  no  advantages  whatsoever  over  Einhorn’s  instrument. 

We  have  been  able  to  illuminate,  in  successive  portions,  the 
entire  colon  in  this  manner,  and  demonstrated  prolapse  of  the 


106  LOCATION,  SIZE,  AND  CAPACITY  OF  THE  STOMACH. 

colon  thereby.  As  the  duodenum  is  but  ten  to  twelve  inches  long, 
a diaphane  of  proportionate  length  has  been  introduced  into  the 
ileum  in  our  clinic.  We  are  not  aware  that  this  extension  of 
electrodiaphany  to  the  small  intestine  has  been  practised  before 
we  published  an  original  device  for  intubating  the  duodenum  ; it 
would  be  impossible  without  such  a method. 

Notwithstanding  the  conservatism  of  Riegel  and  Fleiner  (“  Lehr- 
buch  d.  Krankh.  d.  Verdauungsorgane,”  p.  223)  and  the  objections 
of  Boas  and  Debove  and  Reinond,  we  consider  the  method  valua- 
ble. It  certainly  is  convenient  for  the  rapid  diagnosis  and  the 
differentiation  between  gastrectasia  and  gastroptosis. 

For  the  recognition  of  tumors,  a much  stronger  light  than  that 
used  by  Einhorn — namely,  eight  to  ten  volts — may  be  useful,  and 
one-half  of  the  lamp  coated  by  a reflecting  mirror  of  mercury, 
which  can,  of  course,  be  controlled  by  turning  the  tube  outside  of 
the  mouth.  At  a demonstration  which  we  were  requested  to  give 
before  the  Clinical  Society  of  Maryland  (1891),  the  apex  impulse  of 
the  heart  was  visible  in  the  dark  after  transillumination. 

According  to  Einhorn,  the  method  can  be  carried  out  both  in 
the  erect  and  the  reclining  position.  He  advises  to  permit  the 
patient  to  drink  only  one  to  two  glasses  of  water  (200  to  450  c.c.), 
which  amount  will  not  distend  the  stomach  beyond  its  natural 
capacity  and  position.  When  a stomach  is  distended  with  C02,  or 
filled  with  water,  it  is  unavoidably  enlarged  somewhat.  Heryng 
and  Reichmann  recommend  examining  the  patient  in  an  erect  posi- 
tion and  with  the  stomach  filled  with  from  one  to  two  liters  of 
water.  In  this  position  and  with  that  quantity  of  water,  the  organ 
can  not  fail  to  be  increased  beyond  its  natural  size  and  moved  out 
of  its  natural  situation.  Kuttner  and  Jacobson  (“  Berliner  klin. 
Wochenschr.,”  1893,  Nos.  39  and  40)  assert  that  the  transillumi- 
nated  area  projected  on  the  belly-wall  does  not  correspond  to  the 
stomach  alone,  but  also  to  light  that  is  diffused  through  loops  of 
intestine  adjacent  to  the  stomach,  and  filled  only  with  gas.  They 
found  that  the  image  is  covered  up  wherever  the  liver  is  superim- 
posed upon  the  stomach,  or  intestinal  loops  filled  with  feces,  or 
tumors  of  the  anterior  wall  intervene  between  the  source  of  the 
light  and  the  abdominal  parietes.  It  is  possible  to  determine  only 
the  inferior  and  left  lateral  limits  of  the  stomach  by  diaphany 
when  the  organ  is  in  its  normal  position,  for  the  lower  edge  of  the 
liver  prevents  the  transillumination  of  the  remaining  parts.  It  is 
therefore  not  possible  to  make  the  diagnosis  of  all  cases  of  dilata- 


DISTINGUISHING  DILATATION  FROM  PTOSIS.  10? 

tion  by  gastrodiaphany  alone,  for,  as  we  shall  show,  there  are  dila- 
tations in  which  the  stomach  does  not  sink  down  to  any  marked 
degree. 

But  in  gastroptosis,  where  the  stomach  has  sunk  down  as  a 
whole  and  is  adjacent  to  the  anterior  abdominal  wall,  gastro- 
diaphany will  give  characteristic  pictures,  and  enable  one  to  deter- 
mine both  the  upper  and  lower  limits.  When  the  stomach  has 
sunk  down,  it  loses  its  surface  contact  with  the  diaphragm,  and 
therefore  the  transilluminated  figure  will  show  no  respiratory 
movement. 

In  dilatation  the  stomach  lies  in  the  normal  position,  or  very 
nearly  so,  with  its  upper  portions,  which  can  not  be  transilluminated. 
In  this  condition  the  area  of  light  on  the  belly-wall  will  show  respira- 
tory movements  on  account  of  the  contact  of  the  stomach  with  the 
diaphragm.  Kuttner  and  Jacobson  hold  that  when  the  transillumi- 
nated zone  shows  distinct  respiratory  movement,  the  lesser  curva- 
ture is  in  its  normal  position,  and  if  the  zone  is  below  the  umbilicus, 
— i.  e low  position  of  the  greater  curvature, — these  signs  together 
indicate  a dilatation,  provided  transillumination  through  the  intes- 
tines can  be  excluded.  The  so-called  vertical  position  of  the 
stomach  may  effect  a low  situation  of  the  transillumination,  but 
not  a simultaneous  respiratory  movability  of  the  lower  light  zone, 
because  in  this  case  the  lesser  curvature  has  moved  away  from  the 
diaphragm.  It  is  conceivable  that  gastrodiaphany  may  aid  in  the 
recognition  of  tumors  of  the  anterior  wall  at  a time  when  these 
can  not  be  detected  by  other  methods  of  investigation.  In  such 
cases  the  transillumination  will  be  impossible  because  of  thickening 
of  the  gastric  walls.  According  to  these  observers  gastrodiaphany 
is  a valuable  method  for  distinguishing  between  dilatation  and  gas- 
troptosis. 

Meltzing  ( loc . cit.)  made  a large  number  of  experiments  on  healthy 
individuals  with  the  electrodiaphane,  after  which  he  came  to  the 
conclusion  that  the  empty  stomach  occupies  a larger  area  in  the 
epigastrium  than  could  be  hitherto  evidenced  by  percussion  or 
gaseous  distention.  This  is  due,  he  argues,  to  the  fact  that  per- 
cussion can  only  give  the  note  from  that  portion  of  the  stomach 
which  is  directly  adjacent  to  the  abdominal  wall.  The  large  curva- 
ture, however,  is  not  adjacent,  and  therefore  can  not  be  made  out 
by  percussion.  The  same  relative  condition  must  evidently  pre- 
vail when  the  stomach  is  filled  with  gas  or  water.  This  investiga- 
tor found  that  the  greatest  differences  existed  in  the  respiratory 


108  LOCATION,  SIZE,  AND  CAPACITY  OF  THE  STOMACH. 

movability  of  the  transilluminated  area  according  to  the  position 
of  the  patient.  He  holds  that  it  is  not  due  to  direct  contact  of  the 
stomach  with  the  diaphragm,  and  that  movability  which  is  evident 
in  the  reclining  position  may  disappear  almost  entirely  in  the  erect 
position.  He  declares  that  the  differential  diagnosis  between 
dilatation  and  gastroptosis  by  the  presence  or  absence  of  respira- 
tory movability  of  the  illuminated  area  is  not  reliable.  In  a later 
publication  Meltzing  (“  Archiv  f.  Verdauungskrankheiten,”  Bd.  11, 
. H.  4)  attempted  to  prove  the  position  of  the  electric  lamp  within  the 
stomach  by  the  use  of  a magnetic  sound,  and  claims  to  have  found 
that  the  results  of  both  methods  agree  within  the  breadth  of  one 
finger.  Kuttner,  Jacobson,  Renvers,  Langerhans,  Meinert,  and 
recently  Kelling  have  proved  without  doubt  that  the  method  is 
liable  to  give  erroneous  results.  In  the  first  place,  the  illuminated 
area  may  not  belong  to  the  stomach  exclusively,  and,  secondly,  we 
are  not  sure  whether  the  location  of  the  strongest  intensity  of  the 
light  really  corresponds  to  the  location  of  the  lamp.  These 
sources  of  error  may  arise  in  two  ways  : 1.  The  inferior  border  of 
the  stomach  may  appear  lower  than  the  lamp  really  is — a deception 
which  can  be  brought  about  when  the  greater  curvature  and  the 
lamp  lying  in  it  are  pushed  away  from  the  abdominal  wall  by  a 
distended  intestinal  loop,  and  the  irradiation  is  spread  around  this 
entire  loop  in  a downward  direction.  When  the  lamp  is  allowed 
to  wander  along  the  greater  curvature  in  a stomach  filled  with 
water,  one  may  occasionally  observe,  during  the  transillumination, 
that  a circular  or  elliptical  very  bright  spot  suddenly  appears  below 
the  border-line  of  the  gastric  limit  indicated  by  the  passing  lamp ; 
that  this  bright  area  does  not  belong  to  the  stomach  can  be  dem- 
onstrated by  the  high  tympanitic  tone  which  the  circular  bright  spot 
will  give  on  percussion.  I have  repeatedly  observed  this  phenome- 
non during  transillumination,  and  can  not  explain  it  in  any  other 
way  than  that  the  rays  of  light  from  the  lamp  are  deviated  ante- 
riorly through  a distended  intestinal  loop  superimposed  partially 
on  the  greater  curvature.  I have  also  made  several  experiments 
on  the  dead  subject  in  the  method  indicated  by  Kelling, — a number 
of  the  subjects  were  frozen  before  the  experiment  so  that  mova- 
bility of  the  abdominal  viscera  was  impossible, — and  been  convinced 
that  the  transilluminated  area  was  two  inches  lower  than  the  real 
position  of  the  lamp. 

2.  The  lower  border  of  the  stomach  may  appear  too  high.  This 
may  occur  when  the  lamp  lying  in  the  greater  curvature  is  cut  off 


CRITICISM  AND  LIMITATION  OF  THE  METHOD.  1 09 

from  the  abdominal  wall  by  opaque  objects  not  transmitting  light — 
such  as  intestinal  loops  filled  with  feces  or  neoplasm. 

In  order  to  obtain  reliable  results  from  gastrodiaphany,  it  is 
important  that  the  patient’s  bowels  should  be  cleared  out  by  enema, 
which  will  evacuate  the  colon,  and  about  twelve  hours  before  the 
enema  is  given  a saline  purge  or  a dose  of  castor  oil  will  remove 
fecal  accumulations  from  the  small  intestine.  The  bladder  must 
be  emptied  before  the  examination,  for  when  the  stomach  is  very 
low,  it  has  in  some  of  my  cases  been  superimposed  upon  the  bladder, 
and  the  latter  was  found  to  be  capable  of  being  transilluminated  by 
the  light  in  the  fallen  stomach.  This  precaution  is  especially 
necessary  when  it  is  desired  to  illuminate  the  small  intestine. 

We  have  experimented  with  incandescent  lamps  requiring  a 
current  of  from  eight  to  ten  volts.  This  intensity  of  light,  while 
it  is  of  advantage  when  it  is  desirable  to  determine  the  topograph- 
ical limits  of  palpable  tumors,  is  a disadvantage  when  we  wish  to 
simply  transillumine  the  gastric  wall  that  is  free  from  neoplasm. 
The  stronger  the  lamp  is,  the  more  deceptive  will  be  the  irradiation 
through  adjacent  loops  of  the  intestine  and  colon.  The  most 
important  literature  of  the  subject  is  presented  by  Oppler,  volume 
hi  of  the  “Archiv  fur  Verdauungskrankheiten,”  page  334.  The 
following  guiding  maxims  may  be  deducted  from  the  literature, 
which  I have  subjected  to  a critical  review  to  determine  the 
actual  value  of  the  method ; these  rules  I know  from  personal 
experience  are  important  to  the  practitioner  in  using  this  method  : 
(1)  The  stomach  of  the  patient  must  be  empty  and  all  remnants 
of  food  and  gas  must  be  evacuated  as  far  as  possible.  (2)  The 
intestine  must  also  be  evacuated  of  its  contents  and  of  gas  by 
a purge  and  by  enema.  (3)  The  bladder  must  be  evacuated. 
(4)  The  transillumination  must  be  conducted  in  a completely  dark 
room.  (5)  For  determining  the  size  and  location  of  the  stomach, 
a lamp  of  five  candle-power  should  be  used.  For  determining  the 
limits  of  palpable  tumors,  a lamp  of  eight  normal  candle-power  is 
advisable.  (6)  The  diaphany  should  be  conducted  in  the  erect  as 
well  as  in  the  reclining  position.  (7)  In  the  reclining  position  the 
lamp  gravitates  away  from  the  anterior  gastric  wall,  and  frequently 
no  light  effect  is  at  all  observable.  Even  in  the  erect  position,  when 
the  empty  stomach  is  transilluminated,  no  complete  light  image  of 
the  stomach  can  be  observed  on  the  abdominal  wall,  but  only  cer- 
tain undefined  areas  of  light  resembling  spots  or  discs.  (8)  The 
results  of  diaphany  correspond  more  and  more  closely  to  the  real 


I IO 


LOCATION,  SIZE,  AND  CAPACITY  OF  THE  STOMACH. 


condition,  the  thinner  and  freer  from  fat  the  abdominal  walls  are.-  In 
cases  where  the  walls  are  thin,  the  limits  agree  well  with  the  actual 
limits  of  the  stomach,  but,  as  a general  thing,  those  obtained  by 
diaphany  are  somewhat  lower  than  the  actual  limit  of  the  stomach. 
(9)  If  the  lamp  is  allowed  to  glide  along  the  greater  curvature  of  the 
empty  stomach  by  drawing  out  the  tube,  a series  of  light  spots  will 
be  observed,  which  will  indicate  approximately  the  position  of  the 
greater  curvature,  provided  a lamp  has  been  used  not  exceeding 
four  to  five  candle-powers,  and  only  the  bright  center  of  the  light 
discs  are  taken  into  consideration.  (10)  Excessive  development 
of  fat  in  the  subcutaneous  tissue  and  omentum  and  strongly 
developed  abdominal  walls  render  the  results  of  the  illumination 
fallacious.  This  also  occurs  when  a stronger  lamp  has  been  intro- 
duced, because  in  that  case  the  more  illuminated  center  of  the 
light  discs  can  not  be  recognized,  and  the  adjacent  organs  will 
also  refract  the  light.  (11)  Megalogastria,  which  has  been 
observed  in  individuals  with  thick  abdominal  walls,  seems  to  be 
due  to  this  deception.  But  even  deducting  any  possible  irradiation 
of  light  beyond  the  limits  of  the  organ,  it  is  certain  that  the 
greater  curvature  of  the  empty  stomach  is  at  a lower  level  than  has 
hitherto  been  assumed.  This  is  not  invariably  the  case,  however, 
and  from  our  own  critical  observations,  conducted  on  a sufficiently 
large  material,  we  consider  such  extreme  variations  as  Meltzing 
described  (loc.  cit.)  as  exceptional.  (12), When  the  stomach  is  filled 
with  from  500  to  1500  c.c.  of  water,  a continuous  picture  is  obtained 
in  form  of  a luminous  disc.  (13)  By  this  method  the  lower  edges 
of  the  right  and  left  lobes  of  the  liver  and  the  anterior  margin  of  the 
spleen  can  be  accurately  determined.  The  former  shuts  off  the  light 
at  the  right  superior  boundary,  and  the  spleen  at  the  left  superior 
boundary  of  the  luminous  area.  (14)  When  the  stomach  is  thus 
filled,  the  position  of  the  greater  curvature  is  somewhat  lower  than 
in  the  empty  stomach,  and  it  is  from  four  to  ten  centimeters 
lower  in  the  erect  than  in  the  reclining  position.  Meltzing 
and  Martius  assert  that  a line  connecting  the  anterior  superior 
spines  of  the  ilium  is  exceeded  in  the  majority  of  cases.  If  a lamp 
of  only  four  candle-powers  has  been  used,  we  should  consider  a 
stomach  illuminated  beyond  this  line  as  dilated  or  prolapsed  beyond 
a doubt.  Much  depends  in  these  cases  upon  the  strength  of  the 
light  and  the  amount  of  water  introduced  into  the  stomach.  (15) 
Concerning  the  respiratory  movements  of  the  illuminated  figure,  I 
should  say  that  in  my  experience  it  moves  downward  distinctly 


CRITICISM  AND  LIMITATION  OF  DIAPHANY.  Ill 

during  inspiration  when  the  body  is  in  the  reclining  position, 
but  in  the  upright  position  the  movements  are  very  slight,  and  in 
case  there  is  gastroptosis,  there  are  no  respiratory  movements 
whatever.  In  the  rare  cases  of  extreme  dislocation  of  the  stomach, 
we  could  observe  no  respiratory  movement  even  in  the  reclining 
position.  (16)  Filling  the  stomach  with  1500  c.c.  of  water  lowers 
the  greater  curvature  somewhat.  If  only  300  or  400  c.c.  are 
introduced,  the  lower  margin  of  the  stomach  may  even  rise  a little 
higher  than  the  line  it  occupied  when  empty.  Full  distention 
with  water  enlarges  the  transilluminated  area  toward  the  right  of 
the  median  line. 

The  method  of  electrodiaphany  has  been  extolled  by  a number 
of  investigators,  and  severely  criticized  by  others.  In  the  existing 
chaotic  condition  of  the  various  opinions,  and  as  the  facilities  for 
obtaining  the  electric  current  in  physicians’  offices  in  the  cities  are 
becoming  greater  with  every  day,  insuring  a more  frequent  and 
extensive  application  of  this  method,  the  author  considers  it  his 
duty  to  sift  the  opinions  presented,  and  subject  them  to  critical 
analysis,  along  the  guiding  lines  of  a large  experience.  No  matter 
how  classical  or  well  established  the  authority  that  presents  an 
opinion,  a writer  with  an  analytical  mind  will  see  the  utility  and 
results  of  any  method  through  the  spectacles  of  his  individual 
experience. 

From  that  standpoint  I feel  justified  in  emphasizing  the  fact  that 
electrodiaphany  will  give  rise  to  serious  deceptions  unless  sup- 
plemented by  other  well-established  methods,  and  that  the  diag- 
nosis should  never  be  based  upon  transillumination  alone.  Electro- 
diaphany can  be  satisfactorily  replaced  by  other  methods  of 
examination.  With  these  limitations,  we  believe  the  method  to 
be  a valuable  diagnostic  aid,  serviceable  for  the  determination  of 
the  normal  and  abnormal  topography  of  the  abdominal  organs. 

The  abnormal  shape  and  situation  of  the  stomach,  so-called  loop 
form  and  vertical  position,  may  be  easily  recognized  in  many  cases. 
In  very  rare  cases  diaphany  may  suggest  the  presence  of  a tumor 
that  is  not  demonstrable  by  any  other  method. 

It  may  be  possible  to  detect  tumors  on  the  lower  edge  of  the 
liver  thereby,  and  possibly  enlargement,  tumor,  and  dislocation  of 
the  spleen.  It  does  not  present  a useful  means  to  determine  dis- 
turbances of  the  peristaltic  functions  or  gastric  atony.  When  a 
small  quantity  of  water  is  introduced  into  a healthy  stomach,  the 
lower  curvature  should  rise  somewhat  higher.  If  this  does  not 


I 12 


LITERATURE  ON  GASTRODIAPHANY. 


take  place,  we  might  suspect  gastric  atony.  If  the  transilluminated 
figure  does  not  alter  its  size  on  introducing  a small  and  then  a large 
amount  of  water,  this  would  be  suggestive  of  motor  insufficiency. 
When  the  luminous  area  shows  up  very  low  upon  the  abdomen, 
great  caution  is  required  to  differentiate  between  (i)  physiological 
megalogastria,  (2)  dilatation,  (3)  gastroptosis.  The  respiratory 
movabilities  which  we  have  already  described  do  not  suffice  to 
make  a differential  diagnosis,  for  in  megalogastria  (normal  large 
stomach),  as  well  as  in  dilatation,  the  respiratory  movability  is 
often  very  slight  in  the  erect  position,  and  in  gastroptosis  there 
may  be  slight  respiratory  movement  in  the  reclining  position. 
Only  in  total  gastroptosis  do  we  find  the  respiratory  movement 
entirely  absent. 

These  evidences  suffice  to  show  that  electrodiaphany  is  useful 
only  in  association  with  other  methods  of  clinical  diagnosis. 


LITERATURE 

ON  GASTRODIAPHANY. 

1.  Boas,  “Ueber  die  Bestimmung  der  Lage  und  Grenzen  des  Magens  durch 
Sondenpalpation,”  “ Centralbl.  f.  innere  Medicin,”  1896,  No.  6. 

2.  Boas,  “ Diagnostik  und  Therapie  der  Magenkrankheiten,”  1895,  Theil  11, 
p.  148. 

3.  Boas,  “Ueber  den  heutigen  Stand  unserer  Kenntnisse  von  Pathol,  u. 
Therap.  der  Motilitatsstorungen  des  Magens,”  “Therap.  Monatsh.,”  1896, 
Heft  1,  11. 

4.  Briiggemann,  “Ueber  den  Tiefstand  des  Magens  bei  Chlorose.”  Inaug.- 
Diss.,  Bonn,  1895. 

5.  Einhorn,  “New-Yorker  medicin.  Monatsschrift,”  November,  1889. 

6.  Einhorn,  “Berliner  klinische  Wochenschrift,”  1892,  No.  51. 

7.  Epstein,  “ Die  Anwendung  der  Gastrodiaphanie  beim  Saugling,”  “ Jahr- 
buch  f.  Kinderheilkunde,”  N.  F.  xli,  Heft  hi,  iv. 

8.  Hirschler,  “Ueber  Gastrodiaphanie”;  referirt  nach  “Wien,  klinische 
Wochenschr.,”  1894,  No.  31. 

9.  Heryng  und  Reichmann,  “ Ueber  elektrische  Magen-  und  Darmdurch- 
leuchtung,”  “Therap.  Monatsh.,”  Marz,  1892. 

10.  Kelling,  “ Archiv  fur  Verdauungskrankheiten,”  Band  11,  1896. 

11.  Kelling,  “ Physikalische  Untersuchungen  iiber  die  Druckverhaltnisse  in 
der  Bauchhohle,  sowie  iiber  die  Verlagerung  und  die  Vitalcapacitat  des 
Magens,”  “ Volkmann’sche  Vortrage,”  N.  F.  cxliv. 

12.  Kelling,  “ Ueber  die  Fehlerquellen  der  Magendurchleuchtung,”  “ Archiv 
fur  Verdauungskrankheiten,”  Band  ill,  Heft  1. 

13.  Kuttner,  “ Einige  Bemerkungen  zur  elektrischen  Durchleuchtung  des 
Magens,”  “ Berliner  klinische  Wochenschr.,”  1895,  No.  37. 

14.  Kuttner,  “ Zur  Durchleuchtung  des  Magens,”  ebenda,  1896,  No.  38. 


LITERATURE  ON  GASTRODIAPHANY.  I I 3 

15.  Kuttner  und  Dyer,  “ Ueber  Gastroptose,”  “Berliner  klinische  Wochen- 
schr.,”  1897,  No.  20. 

16.  Kuttner  und  Jacobson,  “ Ueber  die  elektrische  Durchleuchtung  des 
Magens  und  deren  diagnostische  Verwertbarkeit,’’  “ Berliner  klinische  Woch- 
enschr.,”  1893,  No.  39. 

17.  Langerhans,  “ Magendurchleuchtung  und  Magenaufblahung,”  “Wiener 
medicinische  Blatter,”  1895,  No.  45. 

18.  Leo,  “Ueber  Gastroptose  und  Chlorose,”  “Deutsche  med.  Wochen- 
schr.,” 1896,  No.  12. 

19.  Martius,  “ Naturforscherversammlung,”  Wien,  1894;  referirt  nach 
“Wiener  med.  Presse,”  1894,  No.  40. 

20.  Martius,  “Ueber  die  wissenschaftliche  Verwertbarkeit  der  Magensdurch- 
leuchtung,”  “ Centralbl.  f.  innere  Medicin,”  1895,  No.  49. 

21.  Meinert,  “ Zur  Fragevon  der  diagnostischen  Verwertbarkeit  der  Magens- 
durchleuchtung,”  “ Centralbl.  f.  innere  Medicin,”  1895,  No.  44. 

22.  Meinert,  “ Ueber  normale  und  pathologische  Lage  des  menschlichen 
Magens  und  ihren  Nachweis,”  ebenda,  1896,  Nos.  12,  13. 

23.  Meinert,  “ Zur  Aetiologie  der  Chlorose,”  Bergmann,  Wiesbaden,  1895. 

24.  Meinert,  “ Ueber  einen  bei  gewohnlicher  Chlorose  des  Entwickelungs- 
alters  anscheinend  constanten  pathologisch-anatomischen  Befund,  und  liber 
die  klinische  Bedeutung  Desselben,”  “ Volkmann’sche  Sammlung,”  N.  F., 
1895,  1 1 5,  116. 

25.  Meltzing,  “ Magendurchleuchtungen,”  “ Zeitschrift  f.  klinische  Medi- 
cin,” Band  xxvii,  Heft  11,  ff. 

26.  Meltzing,  “ Die  Controle  der  Magendurchleuchtung  mittels  der  Magnet- 
sonde,”  “ Archiv  f.  Verdauungskrankheiten,”  Band  ii.  Heft  iv. 

27.  Meltzing,  “ Gastroptose  und  Chlorose,”  “ Wiener  medicin.  Presse,”  1895. 
Nos.  30-34. 

28.  Mikulicz,  “ Wiener  medicin.  Presse,”  1881,  No.  45  ff.,  und  “ Wiener  med. 
Wochenschr.,”  1883,  Nos.  23,  24. 

29.  Milliot,  “ Internationaler  medicin.  Congress  zu  Paris  ” ; citirt  nach 
“ Schmidt’s  Jahrbuchern,”  Band  cxxxvi,  S.  143. 

30.  Pariser,  “ Berliner  medicinische  Gesellschaft,”  6.  Juli,  1892. 

31.  Reichmann,  “Ueber  die  elektrische  Durchleuchtung  des  Magens  fur 
diagnostische  Zwecke,”  “ Gazeta  lekarska,”  1896,  No.  32. 

32.  Renvers,  “ Verein  fur  innere  Medicin,”  4,  iv,  1892. 

33.  Rosenheim,  “Berliner  klinische  Wochenschr.,”  1896,  No.  13. 

34.  Schwartz,  “Ueber  den  diagnostischen  Werth  der  elektrischen  Durch- 
leuchtung menschlicher  Korperhohlen,”  “ Beitrage  zur  klinische  Chirurgie,” 
Band  xxiv,  Heft  ill. 

35.  Van  der  Weijde,  “ De  Doorschijnung  van  de  Maag,”  “ Nederl.  Tijdschr. 
voor  Geneeskunde,”  1895,  Deel  11,  No.  12. 


14  STOMACH-TUBE  AND  TECHNICS  OF  ITS  INTRODUCTION. 


CHAPTER  XII. 

THE  STOMACH-TUBE  AND  TECHNICS  OF  ITS 
INTRODUCTION. 

Examination  of  Stomach  Contents.  — Test-meals  : Their  Effect  upon  the 
Amount  of  Acid  Secreted. — Literature. 

No  other  kind  but  a soft  elastic  stomach-tube  should  be  used,  and 
before  introducing  it  for  the  first  time  in  any  patient,  we  should 
always  carefully  instruct  him  or  her  regarding  the  object  and  utility 
of  the  procedure  and  its  harmlessness.  Whenever  we  can  do,  so  we 
give  very  timid  patients  an  opportunity  of  observing  with  what 
ease  more  experienced  patients  introduce  the  tube  on  themselves. 
This  has  a most  comforting  effect.  Weak  and  old  persons  should 
always  be  treated  on  the  bed,  several  thick  towels  being  placed  on 
the  patient’s  chest  and  beneath  the  chin ; if  the  case  is  to  be  ex- 
amined in  an  erect  position,  linen  gowns  are  drawn  over  the  breast 
and  lap,  or  an  additional  rubber  sheet  to  protect  the  clothing.  Dr. 
Fenton  B.  Turck,  of  Chicago,  has  devised  a useful  rubber  pocket, 
which  is  suspended  under  the  chin  during  lavage,  and  protects  the 
garments  of  the  patients  from  the  mouth  discharges.  If  the  throat 
and  fauces  are  very  tender  (often  found  in  excessive  smokers),  it  is 
advisable  to  precede  the  introduction  of  the  tube  by  spraying  the 
throat  with  a three  per  cent,  solution  of  cocain  hydrochlorate  or 


the  following  anodyne  spray  : 

R . Three  per  cent,  solution  of  cocain  hydrochlorate  in  • 

benzoinol, 2 fluidounces 

One  per  cent,  solution  of  menthol  in  liquid  vaselin 

oil,  . fz  of  a fluidounce. 

Use  in  atomizer  for  spraying  the  throat.  Mix. 


Every  patient  should  possess  his  or  her  own  tube,  especially 
in  private  practice.  In  hospital  practice  a special  tube  should  in- 
variably be  obtained  for  every  carcinomatous,  syphylitic,  and 
tuberculous  patient,  and  its  use  limited  to  that  particular  person. 
After  the  tube  has  been  used  it  should  be  carefully  washed,  first 
with  soap  and  warm  water,  rinsed  out  by  a current  of  warm  water 
and  disinfected  by  placing  it  in  a six  per  cent,  solution  of 
carbolic  acid  or  a saturated  solution  of  boric  acid  or  thymol, 
in  which  the  instrument  should  be  kept  coiled  until  it  is  used 


HOW  TO  INTRODUCE  A STOMACH-TUBE. 


15 


again.  Much  has  been  written  about  the  construction  of  the 
lower  end  of  the  tube.  The  author’s  experience  is  that  the  Ewald 
tube  as  pictured  on  page  124  answers  every  purpose.  The  lower 
end  of  the  tube  should  be  open,  as  there  can  be  no  doubt  that 
this  facilitates  the  entrance  of  chyme  into  the  tube  when  the  con- 
tents are  drawn,  and  also  the  entrance  and  exit  of  water  during 
lavage.  Two  larger  lateral  openings  at  opposite  sides  of  the 
tube  and  about  two  inches  apart,  are  advantageous  for  the  same 
object. 

The  Ewald  tube  possesses  also  six  to  eight  smaller  openings, 
which  may  not  favor  the  aspiration  of  thick  chyme,  yet  are  valua- 
ble for  lavage,  when  it  is  desirable  to  produce  a mechanical  effect 
on  the  mucosa  by  having  many  fine  streams  fall  upon  it.  They 
have  the  disadvantage  of  rendering  the  tube  more  difficult  to  clean. 
When  there  is  reason  to  suppose  a gastric  or  esophageal  ulcer, 
neoplasm,  or  stenosis,  I prefer  a tube  that  is  closed  at  the  lower 
end,  because  this  form  is  more  likely  to  pass  over  these  structural 
abnormalities  without  injuring  them.  If  the  patient  is  quiet  and 
composed,  it  is  safe  to  let  him  introduce  the  tube  himself  even  at  the 
first  opportunity,  the  main  points  to  impress  upon  him  being  three  : 
(1)  To  swallow  several  times  when  the  tube  has  reached  the  root 
of  the  tongue  ; (2)  to  breathe  deeply  and  regularly;  (3)  to  push  the 
tube  with  both  hands  as  soon  as  it  has  turned  downward  into  the 
esophagus.  Introducing  the  finger  into  the  mouth  to  depress  the 
tongue  is  rarely  necessary.  Involuntary  or  intentional  coughing 
must  be  suppressed  by  exercise  of  self-control,  as  it  will  inevitably 
prevent  the  point  of  the  tube  from  entering  the  esophagus  and 
turn  it  back  into  the  mouth.  The  more  passive  and  quiet  a patient, 
the  easier  can  the  procedure  be  carried  out. 

In  addition  to  the  execution  of  lavage  the  stomach-tube  is  useful 
for  the  following  diagnostic  purposes  : (1)  To  draw  the  contents  of 

the  stomach  for  chemical  and  microscopical  analysis  ; (2)  to  estab- 
lish the  permeability  of  the  esophagus;  (3)  to  determine  the  lower 
border  of  the  stomach  by  palpating  the  tube  through  the  abdom- 
inal walls.  This  method  was  originally  proposed  by  Leube,  but 
has  been  deserted  even  by  him  on  account  of  its  inaccuracy.  In 
many  cases  it  is  not  possible  to  palpate  a tube  through  the  abdom- 
inal walls,  and  even  where  palpable,  it  is  not  possible  to  differen- 
tiate a dilatation  from  a descent  or  ptosis. 

It  is  very  important  to  use  graduated  wide^mouthed,  transparent 
glass  bottles  of  about  one  quart  (one  liter)  capacity  for  lavage.  At 


I 1 6 STOMACH-TUBE  AND  TECHNICS  OF  ITS  INTRODUCTION. 


least  two  such  bottles  are  needed — one  to  pour  the  water  into  the 
funnel,  the  other  to  catch  the  outflow.  This  outflow  should 
always  be  measured,  and  efforts  to  regain  the  entire  quantity  that 
has  entered  the  stomach  must  be  made  before  an  additional  supply 
is  poured  in.  Neglect  of  this  precaution  may  produce  dangerous 
overdistention  of  the  organ. 

It  is  not  necessary  to  lubricate  the  stomach-tube  with  any  oil  or 
vaselin — there  is  generally  mucus  enough  in  the  esophagus  to 
facilitate  the  passage.  It  is  sufficient  to  moisten  it  with  water. 

In  the  “ New  York  Medical  Journal  ” for  December  28,  1895,  volume  lxii, 
No.  26,  page  822,  a new  double-current  stomach-tube  has  been  described  by 
the  author,  through  which  the  inflow  and  outflow  goes  on  uninterruptedly  at 


Fig.  13— Hemmeter’s  Double-current  Stomach  Lavage  Tube. 

A.  Hard  rubber  inflow.  B.  Soft  rubber  double  tube.  C.  Hard  rubber  part  of  outflow.  D.  Stop- 
cock controlling  inflow.  E.  Reservoir.  F.  Outflow  openings.  G.  Soft  outflow  tube.  /.  In- 
flow opening. 

the  same  time.  This  tube  is  recommended  only  as  a time-saver  for  the  spe- 
cialist in  practice;  the  simple  tube  will  fulfil  every  requirement ; it  is  the  safest 
instrument,  even  though  in  lavage  of  progressed  gastrectasia  it  may  require 
much  more  time. 

From  20  measurements  of  female  patients,  the  author  has  found  that 
the  average  distance  from  the  incisor,  teeth  to  the  deepest  portion  of  the 
stomach  is  55  cm.,  and  in  36  measurements  of  healthy  males  the  same  dis- 
tance was  found  to  be  60  cm.  In  cadavers  this  distance  is  in  both  sexes 
shortened  by  postmortem  rigor,  according  to  the  author’s  experience,  it  having 
been  found  to  be  52.5  cm.  on  the  average  for  females  in  12  different  subjects. 
In  12  male  cadavers,  the  average  distance  from  the  incisor  teeth  to  the  deepest 
part  of  the  stomach  was  54  cm. 

In  ten  cases  of  dilatation  of  the  stomach,  the  average  distance  from  the  in- 


TECHNICS  OF  INTRODUCING  STOMACH-TUBE. 


II 7 


cisor  teeth  to  the  deepest  portion  of  the  stomach,  as  measured  by  as  rigid  a 
sound  as  could  safely  be  introduced,  was  69  cm. 

The  author,  on  visiting  Professor  F.  Penzoldt,  in  Erlangen,  in  July,  1895,  was 
surprised  to  find  this  pioneer  of  digestive  pathology  still  advocating  the  use  of 
a guide  in  the  shape  of  a flexible  stick  or  whalebone,  which,  during  introduction, 
is  inserted  into  the  gastric  tube  to  facilitate  its  entering  the  esophagus  after  it 
curves  over  the  base  of  the  tongue. 

In  his  most  recent  contribution  to  the  subject,  Penzoldt  (Joe.  cit.,  27)  gives 
minute  details  as  regards  the  method  of  application  of  the  Leitungsstab  or  Man- 
drin  within  the  tube,  and  says  that  it  should  be  oiled  to  facilitate  its  removal 


when  the  tube  has  reached  the  middle  of  the  esophagus.  He  also  suggests 
catching  the  tip  of  the  lavage  tube  between  the  index  and  middle  fingers  of  the 
left  hand,  which  are  inserted  into  the  patient’s  mouth,  and  bending  the  tip 
down  over  the  base  of  the  tongue  until  it  enters  the  esophagus.  This  is  the 
method  advocated  by  his  teacher,  Professor  Leube  (Joe.  cit.t  2),  and  also  by 
Rosenheim  (36). 

In  the  writer’s  experience  the  intratubal  whalebone  guide  and  the  insertion 
of  the  fingers  into  the  patient’s  mouth  are  superfluous.  The  tube  can  always 
be  introduced  without  a guide,  and  without  touching  the  patient.  The  main 
object  is  that  the  point  of  the  tube,  when  it  has  reached  the  wall  of  the  pharynx, 


Fig.  14. — Illustrating  the  Principle  of 
Siphonage. 


Fig.  15. — Bulb  Used  for  the  Aspiration 
of  Test-meals  with  Patients  having 
Very  Relaxed  Abdominal  Walls. 


A.  Stomach  end.  B.  End  going  to  collect- 
ing flask. 


1 1 8 STOMACH-TUBE  AND  TECHNICS  OF  ITS  INTRODUCTION. 

shall  be  deflected  downward.  This  will  occur  without  exception,  and  in  a 
very  natural,  easy  manner,  if  the  patient  is  directed  to  swallow  at  this  moment. 
In  the  moment  of  this  act  of  deglutition  the  point  of  the  tube  is  bent  downward 
into  the  esophagus  ; the  physician  must  carefully  watch  this  moment,  and  at  the 
very  onset  of  the  act  of  swallowing  rapidly  push  the  tube  over  the  descending 
epiglottis.  If  the  patient  should  show  difficulty  in  breathing  after  the  tube  is 
introduced,  leave  it  quietly  in  place  and  encourage  the  patient  to  breathe 
deeply.  Boardman  Reed  (“  International  Medical  Magazine,”  Oct.,  1898,  p. 
693)  has  correctly  observed  that  the  nervous  spasm  of  the  glottis  occasionally 
encountered  during  the  introduction  is  relieved  by  “ bringing  into  action  the 
auxiliary  respiratory  muscles  and  making  rhythmical  forced  inspirations.” 

Beginners  in  using  the  tube  need  have  no  fear  that  it  will  enter  the  trachea. 
To  make  it  enter  the  trachea  is,  in  the  writer’s  experience,  a difficult  undertak- 
ing, and  requires  special  training  and  dexterity.  He  was  present  on  an  occa- 
sion when  a class  of  ten  students  were  taking  a private  course  in  diseases  of 
the  throat,  during  which  lesson  they  were  trying  to  mop  the  larynx.  What 
they  really  did  was  to  mop  out  the  superior  portion  of  the  esophagus,  showing 
plainly  that  it  is  not  as  easy  to  enter  the  larynx  as  the  esophagus.  Direct 
the  patient  to  keep  taking  deep  inspirations,  and  as  soon  as  the  tip  or  point  of 
the  tube  is  felt  touching  the  pharyngeal  wall,  tell  him  to  swallow,  and  almost 
immediately  the  tube  follows  into  the  esophagus  and  can  be  pushed  into  the 
stomach  without  further  resistance.  The  double  tube  is  still  in  its  experimental 
stage  and  can  not  be  recommended  as  practical.  Personally,  I use  the  single 
tube  almost  exclusively. 

It  is  not  necessary  for  the  patient  to  open  his  teeth  any  wider 
than  just  to  admit  the  tube  ; at  the  same  time,  caution  him  not  to 
bite  on  it,  but  to  breathe  naturally.  In  case  the  tube  is  to  be  intro- 
duced into  highly  nervous  and  hysterical  patients,  or  such  who 
have  not  sufficient  self-control,  it  is  best  to  have  their  hands  held 
by  a trained  nurse  or  assistant.  It  is  always  best  to  use  both  hands 
in  pushing  the  tube.  After  it  has  passed  the  glottis,  catch  hold  of 
the  tube  two  inches  from  the  mouth  and  rapidly  complete  the 
introduction.  Avoid  seizing  the  tube  further  away  from  the  mouth, 
as  then  it  will  kink  on  pushing  it.  No  patient  should  be  subjected 
to  gastric  lavage  without  a previous  examination  of  the  thorax. 
Penzoldt  tells  of  a case  in  which  the  stomach  should  have  been 
washed  out  in  the  morning,  but  on  account  of  lack  of  time  this  was 
postponed  until  the  evening.  On  the  same  afternoon  the  patient 
died  of  rupture  of  an  aortic  aneurysm  into  the  esophagus. 

Lavage  and  introduction  of  the  tube  are  contraindicated — 

I.  In  all  constitutional  and  local  conditions  which  could  be  aggra- 
vated or  life  endangered  by  the  irritation  and  exertion  of  lavage. 
Among  these  could  be  mentioned: 

1.  Pregnancy. 


CONTRAINDICATIONS  TO  LAVAGE. 


I 19 

2.  Heart  disease  in  a state  of  defective  compensation — heart 
neuroses,  angina  pectoris,  myocarditis,  and  fatty  heart  in  an  ad- 
vanced stage. 

3.  Aneurysm  of  the  large  arteries. 

4.  Recent  hemorrhages  of  all  kinds,  including  apoplexies,  pul- 
monary, renal,  vesical,  gastric,  rectal  hemorrhages,  and  hemorrhagic 
infarctions. 

5.  Advanced  pulmonary  tuberculosis. 

6.  Advanced  pulmonary  emphysema,  with  bronchitis. 

7.  Apoplexy  and  cerebral  hyperemia. 

8.  Advanced  cachexia. 

9.  Presence  of  continued  or  remittent  fever. 

II.  The  stomach  and  intestinal  diseases  which  are  contraindica- 
tions for  the  use  of  tube  are : 

1.  Ulcer,  with  recent  hematemesis  and  evidences  of  blood  in  the 
stools. 

2.  Palpable  carcinoma  of  the  pylorus,  with  vomiting  of  coffee- 
ground  material  and  the  classical  symptoms  of  cancer. 

3.  Stomach  or  intestinal  troubles,  with  acute  fever. 

4.  Gastric  mucosa  easily  started  to  bleeding. 

5.  Secondary  gastric  affections  whose  dependence  upon  a distinct 
and  more  important  primary  disease  is  evident. 

These  are  not  invariable  rules,  however ; cases  may  occur 
under  some  of  these  exceptions  that  at  times  peremptorily  require 
lavage  on  account  of  depressing  self-intoxication  from  the  stomach 
or  advanced  gastric  fermentation.  Thus,  according  to  Boas,  it  has 
been  employed  with  success  in  pregnancy,  and  the  author  has 
washed  out  the  stomach  in  cases  of  typhoid  fever  with  favorable 
result,  and  also  performed  lavage  in  a case  of  aortic  regurgitation, 
with  Bright’s  disease  and  gastrectasia,  where  much  relief  was 
experienced  from  the  procedure.  Professor  Moritz  has  frequently 
passed  the  stomach-tube  in  pregnant  women  to  ascertain  the  intra- 
gastric  pressure  (25). 

In  a normal  position  of  the  abdominal  viscera  the  location  of  the 
cardia  corresponds  to  the  spinous  process  of  the  ninth  thoracic 
vertebra.  By  counting  off  this  process  on  the  back  of  the  patient 
and  placing  the  upper  eye  of  the  tube  against  it,  one  can  measure 
the  length  of  tube  necessary  to  reach  the  stomach  by  applying  it 
from  this  point  along  the  back,  passing  alongside  of  the  ear  to  the 
front  incisor  teeth.  At  this  point,  which  reaches  the  incisors,  it  is 
of  assistance  to  make  a mark  on  the  rubber  with  ink  or  to  tie  a 


120  STOMACH-TUBE  AND  TECHNICS  OF  ITS  INTRODUCTION. 

string  around  it;  this  will  avoid  passing  the  tube  out  or  in  to  dis- 
cover whether  it  has  reached  the  stomach  after  being  introduced. 

In  dilatations  and  falling  of  the  organ,  the  length  of  tube  required 
can  only  be  learned  after  a previous  lavage.  When  the  tube  is 
used  to  draw  out  a test-meal,  direct  the  patient  to  contract  his 
abdominal  muscles  as  if  in  the  act  of  having  a stool.  Frequently 
the  accompanying  nausea  will  bring  this  about  involuntarily.  If 
no  contents  arise,  push  the  tube  gently  further  in  or  pull  it  slowly 
out,  trying  different  levels.  If  the  abdominal  walls  are  flabby, 
external  manual  compression  will  sometimes  produce  the  desired 
result.  If  all  these  manipulations  are  of  no  avail,  the  stomach  is 
either  empty  or  the  tube  is  plugged  up  with  food-particles  too  large 
to  pass. 

To  find  out  which  is  the  case,  allow  300  c.c.  of  pure  water  to  run 
in  and  then  lower  the  funnel  and  siphon  out ; if  nothing  but  com- 
paratively clear  water  returns,  the  test-meal  has  passed  into  the 
duodenum.  One  should  be  very  cautious  in  moving  the  tube  out 
and  in  when  no  stomach  contents  appear  in  the  funnel,  as  it  is 
possible  that  the  eyes  of  the  tube  may  have  sucked  in  the  gastric 
mucosa  itself,  and  by  moving  too  suddenly,  a piece  may  be  torn 
away.  If  there  is  the  least  resistance,  avoid  moving  ; rather  force 
a little  air  through  the  tube  with  a rubber  bulb  or  pour  in  a small 
amount  of  water,  which  will  push  away  the  adherent  mucosa  or 
the  food-particle,  and  the  next  attempt  will  bring  up  the  test-meal. 

If  the  stomach  is  already  empty,  the  test-meal  must  be  given 
again  at  another  time.  I do  not  recommend  any  apparatus  for 
aspiration,  not  even  the  rubber  bulb,  except  in  cases  of  advanced 
dilatation  or  relaxed  abdominal  walls,  when  the  rubber-bulb  aspir- 
ator becomes  necessary  ; with  patience  the  simple  expression  method 
will  suffice.  For  small  samples  of  test-meals  the  Einhorn  stomach 
bucket  (Einhorn,  “ Diseases  of  the  Stomach,”  p.  63)  is  an  available 
instrument.  Before  using  the  tube,  all  artificial  teeth  should  be 
removed,  and  tight  apparel,  especially  corsets,  should  be  loosened. 

In  very  rare  cases  of  intense  food  and  mucous  putrefaction,  and 
in  extensive  gastrectasis,  a recurrent  tube  may  be  used  with 
success.  To  give  an  idea  of  the  time  it  takes  to  cleanse  some 
stomachs,  we  quote  Dr.  Herman  Strauss,  assistant  to  Professor 
Riegel,  who  claims  to  have  washed  out  rice-particles  after  forty 
liters  of  water  had  been  allowed  to  flow  in  and  out.  After  person- 
ally washing  a dilated  stomach  for  one  hour,  we  found  bread  and 
stringy  mucus  in  the  last  washing.  F.  B.  Turck  asserts  that  food 


TEST- MEALS. 


I 2 I 

remnants,  even  after  the  stomach  has  been  washed  clear,  may 
adhere  to  the  walls  of  the  organ  ; for  the  removal  of  these  he 
recommends  his  gyromele  (“Chicago  Clin.  Review,”  1895).  From 
examination  of  many  hundred  stomachs  at  autopsies  we  should 
judge  that  food  adherence  to  the  walls  of  the  stomach  occurs  very 
rarely. 

Test-meals. — The  test-meal  most  frequently  employed  is  that 
of  Ewald  and  Boas,  consisting  of  a roll  or  a piece  of  wheat-bread 
and  500  c.c.  of  water  or  tea,  without  milk  or  sugar.  The  time  for 
examination  is  one  hour  after  the  meal. 

Leube  and  Riegel  advocate  a test-dinner  of  4CO  c.c.  soup,  a por- 
tion of  beefsteak  or  roast  beef,  potatoes,  and  a roll.  The  time  for 
examination  is  three  to  four  hours  after  this  meal. 

Jaworski  and  Gluczinski  employ  the  white  of  a hard-boiled  egg 
and  100  c.c.  water. 

Klemperer  recommended  y2  of  a liter  of  milk  and  70  gm.  of 
wheat-bread,  and  examined  two  hours  later. 

WILLMP 


Fig.  16. — The  Esophageal  Tubal  Probe. 


Germain  See  used  60  to  80  gm.  scraped  meat  and  150  gm.  white 
bread.  Examination  two  hours  later. 

The  Ewald  and  Boas  test-breakfast  seems  the  most  convenient, 
and  in  cases  of  enfeebled  digestion,  when  much  food  is  retained 
from  previous  meals,  the  least  confusing. 

Fleiner’s  test-meal  consists  of  soup,  roast  beef,  and  potato  puree; 
he  examines  three  to  four  hours  after  the  meal. 

Double  Test-meal  Used  by  the  Author. — At  our  clinic,  the  Hospital 
of  the  University  of  Maryland,  we  generally  use  a double  test-meal, 
consisting  of : 

8 A.  m. — One  small  piece  of  beef,  scraped  and  broiled  =80  gm. ; 1 soft-boiled 
egg ; 30  gm.  boiled  rice  ; 1 glass  of  milk  = 250  c.c.,  and  a piece  of  bread. 

Four  to  five  hours  later  an  Ewald  test-meal  is  given,  and  one  hour 
after  this  the  stomach  contents  are  drawn.  In  giving  a test-meal, 
always  insist  on  good  chewing,  and  urge  that  all  food  substances  be 
very  finely  cut  up,  so  that  they  can  not  plug  up  the  tube,  even  if  not 
digested. 

9 


122  STOMACH-TUBE  AND  TECHNICS  OF  ITS  INTRODUCTION. 

The  double  test-meal,  about  which  the  late  Dr.  Henry  Salzer,  of 
Baltimore,  was  quite  enthusiastic,  really  offers  some  advantages 
over  others.  In  the  first  place,  it  permits  of  as  easy  a study  of  the 
various  stages  of  the  digestion  and  of  the  motility  and  degree  of 
retention  as  Riegel’s  test-dinner;  but  the  main  advantage  of  the 
double  test-meal — a full  meal  at  8 or  9 a.  m.  and  an  Ewald  test- 
meal  at  12  m.  or  1 p.  m.,  examination  at  1 or  2 p.  m. — is  that,  after 
drawing  it,  we  may,  in  a large  number  of  instances,  recognize 
conditions  of  gastric  motility  and  secretion  before  we  analyze  the 
contents.  For  instance,  disappearance  of  the  entire  breakfast-meal 
points  to  a normal  digestion. 

Absence  of  all  proteids, — beef  and  egg, — and  presence  of  consid- 
erable carbohydrates, — rice  and  bread, — points  to  hyperchlorhy- 
dria  ; and,  again,  absence  of  all  carbohydrates  and  presence  of  some 
of  the  beef  and  egg  point  to  hypochlorhydria,  subacidity,  ana- 
cidity  or  achylia.  Presence  of  the  entire  meal,  with  perhaps  milk 
uncurdled,  means  impaired  motility,  with  atrophy  of  gastric  mucosa, 
absence  of  acid,  enzymes,  and  proenzymes.  If  the  entire  meal 
has  disappeared,  the  status  of  the  gastric  secretions  may  be  ascer- 
tained from  the  Ewald  test-meal,  which  is  still  present. 

The  objection  which  has  been  made,  that  the  double  meal  is 
uncleanly  to  handle  during  analysis,  has  also  been  urged  against 
Riegel’s.  Whether  the  morsels  of  an  Ewald  test-meal  are  nicer  and 
more  esthetic  to  handle  than  remnants  of  our  double  test-meal  is  a 
matter  concerning  which  it  does  not  pay  to  quarrel.  It  is  a very 
important  matter  to  state  what  test-meal  is  used  in  giving  out  the 
various  acidities  obtained,  because  some  test-meals  are  greater 
stimulants  to  the  gastric  secretion  than  others. 

The  Ewald  test-breakfast  really  makes  very  slight  demands  upon 
the  working  capacity  of  the  stomach. 

The  total  acidity  one  hour  after  an  Ewald  test-breakfast  is  nor- 
mally about  60*;  the  lowest  total  acidity  observed  by  us  one  hour 
after  a test-breakfast  of  this  kind  in  a healthy  individual  was  22. 
Fleiner,  who  uses  a test-meal  of  soup,  roast  beef,  and  potato  puree, 
asserts  that  two  to  three  and  a half  hours  after  this  test-meal 
the  total  acidity  is  normally  70  to  100  (Prof.  Wilhelm  Fleiner, 
“ Lehrbuch  d.  Krankheiten  d.  Verdauungsorgane,”  p.  186).  Dr. 
Julius  Friedenwald  has  confirmed  that  the  gastric  secretion  of  HC1 


*For  the  significance  of  these  figures  the  reader  is  referred  to  the  chapter  on  Titration 
of  Stomach  Contents. 


AMOUNTS  OF  ACIDS  SECRETED  AFTER  VARIOUS  MEALS.  I 23 


appears  sooner,  and  reaches  a higher  degree  after  the  double  test- 
meal  than  after  an  Ewald  meal. 

An  amount  of  HC1  equal  to  o.  I to  0.25  per  cent,  may  be  regarded 
as  normal;  above  this,  is  hyperacidity.  The  total  acidity  can  not 
correctly  be  regarded  as  an  unfailing  indication  of  the  amount  of 


Fig.  17.— Stomach-pump  used  only  for  Rapid  Evacuation  of  Poisons. 


HC1  present;  the  latter  should  always  be  determined  separately 
in  addition  to  the  total  acidity. 

Apparently  there  are  climatic,  barometrical,  and  geographical  fac- 
tors which  influence  the  total  acidity.  In  170  cases  at  Riegel’s 
clinic,  Strauss  found  the  total  acidity  after  a test-breakfast  equal  to 


124  STOMACH-TUBE  AND  TECHNICS  OF  ITS  INTRODUCTION. 

68  ; in  92  cases  at  Berlin  after  a test-breakfast  the  average  total 
acidity  was  estimated  at  47 ; the  average  amount  of  free  hydro- 
chloric acid  at  Riegel’s  clinic  was  found  to  be  37.  Normal  values 
one  hour  after  a test-breakfast  of  a roll  and  water  are,  for  average 
total  acidity,  40  to  60 ; for  free  HC1,  20  to  30,  for  our  clinic  at  the 
University  of  Maryland,  Baltimore,  and  in  private  practice.  These 
were  also  the  figures  obtained  formerly  at  the  Maryland  General 
Hospital. 

Four  hours  after  the  complex  meal  of  Salzer, — i.  e .,  50  to  60  grs. 
beef,  500  c.c.  milk,  70  grs.  rice,  and  one  egg, — the  total  acidity  on 
the  average  was  found  to  be  95  and  the  free  HC1  46,  at  the 
author’s  clinic.  It  should  be  emphasized  that  these  figures  repre- 
sent only  relative  values.  One  often  finds  every  symptom  of  hyper- 
acidity with  relief  following  the  use  of  alkalies,  when  the  total 
acidity  was  found  to  be  only  56  (one  hour  after  an  Ewald  break- 
fast), the  free  HC1  only  24.  On  the  other  hand,  cases  have  pre- 


sented themselves  showing,  under  the  same  conditions,  a total 
acidity  of  80  and  free  HC1  = 50,  still  no  symptoms  of  hyper- 
acidity. All  this  goes  to  show  that  some  stomachs  may  do  their 
work  normally  very  well  on  relatively  low  amounts  of  free  HC1, 
and,  of  course,  suffer  from  hyperacidity  from  comparatively  slight 
increase  of  free  HC1,  which  would  not  affect  a stomach  used  to 
higher  amounts  of  acid.  (See  Hemmeter,  “ Archiv  fur  Verdauungs- 
krankheiten,”  Bd.  iv,  S.  30.) 

Most  observers  that  can  speak  with  authority  on  the  subject 
agree  that  the  total  acidity  should  not  be  employed  to  express 
hyperacidity,  but  only  the  amount  of  free  HC1,  as  this  is  the 
only  acid  which,  when  increased,  gives  rise  to  the  complex  of 
symptoms  technically  recognized  as  hyperacidity. 

Before  closing  this  chapter  it  might  be  added  that,  where  it  is 
impossible  to  use  the  tube  on  account  of  prejudice  of  the  patient,  to 
obtain  a test-meal,  emesis  may  be  resorted  to.  The  stomach  con- 


LITERATURE. 


125 


tents  obtained  after  a test-meal,  as  a rule,  filter  slowly,  and  if  much 
mucus  is  present,  with  great  difficulty.  The  filtration  can  be  accel- 
erated by  rubbing  the  material  first  through  a small,  coarsely 
grained  sieve  (strainer),  then  through  a finely  grained  strainer,  and 
then  filtered  through  Swedish  filter-paper. 


LITERATURE 

ON  THE  HISTORY  AND  TECHNICS  OF  THE  STOMACH-TUBE. 

1.  Abercrombie,  “ Diseases  of  the  Stomach." 

2.  Arnott,  quoted  by  Alderson,  on  the  “ Dangers  Attending  the  Use  of  the 
Stomach-pump,”  "Lancet,"  January  4,  1879. 

3.  Avicenna,  “Liber  Canonis,"  etc.,  1544,  Ausg.  Venice,  Liber  1,  fen.  iv, 
Chap,  xx,  p.  83. 

4.  Benedict,  A.  L.,  "Conservatism  in  the  Use  of  the  Stomach-tube,”  "Am. 
Med.  and  Surg.  Bull.,”  1898,  xn. 

5.  Berger,  C.,  " Ueber  die  Technik  der  Einfiihrung  des  Magenschlauches,” 
" Reich’s  Med.  Anz.,”  Leipzig,  1898,  xxm. 

6.  Bush,  F.,  " London  Medical  and  Physic.  Journal,”  1822. 

7.  Canstatt,  "Text-book,”  Erlangen,  1846,  Vol.  in,  Cap.  vi. 

8.  Capivacceus,  Hieronymus,  " Medic.  Practic.,”  Liber  1,  Cap.  liii,  Venice, 
1590. 

9.  Dapper,  " Die  unbekannte  neue  Welt,”  etc.,  Amsterdam,  1753,  S.  566. 

10.  Ewald,  C.  A.,  " Klinik  d.  Verdauungskrankheiten,”  Berlin,  i890-’9i. 

11.  Ewald,  C.  A.,  "A  Ready  Method  of  Washing  Out  the  Stomach,”  " Irish 
Gazette,”  August  15,  1874. 

12.  Hemmeter,  John  C.,  "An  Apparatus'for  Washing  Out  the  Stomach  and 
Sigmoid  with  a Continuous  Current,”  etc.,  "New  York  Med.  Journal,”  March 
30,  1895. 

13.  “ Hieronym.  Fabric,  ab  Abquapendente,”  " Chirurg.  Schrift,”  ed.  Joh. 
Scultetus,  Niirnberg,  1716,  11  Theil,  Cap.  39,  S.  92. 

14.  Hieronymus  Mercurialis,  " Die  Morbis  venenosis  et  venenis,”  Venetiis, 
1583,  Liber  1,  Cap.  22. 

15.  Hunter,  John,  "Proposals  for  the  Recovery  of  People  Apparently 
Drowned,”  “ Sammlung  auserlesener  Abhandlungen,”  iv,  S.  144. 

16.  Jackson,  "Extracts,”  " Records  of  the  Boston  Society  for  Medical  Im- 
provement,” Vol.  vi,  p.  261. 

17.  Jlirgensen,  " Zur  lokal.  Therapie  der  Magenkrankheiten,”  " Deutsch. 
Archiv  f.  klinische  Medizin,”  Band  vn,  p.  239,  1870. 

18.  Knapp,  M.  J.,  "The  Clinical  Report  of  Four  Cases  of  Lavage  of  the 
Stomach  by  the  Aid  of  Knapp’s  Director,”  "Med.  Rec.,”  New  York,  1898, 
liii,  313. 

19.  Kussmaul,  " Behandl.  d.  Magenerweit.  durch  eine  neue  Methode,  mit  der 
Magenpumpe,”  " Deutsch.  Archiv  f.  klinische  Med.,”  vi,  455. 

20.  Leube,  " Die  Magensonde,”  Erlangen,  1879. 

21.  Leube,  "Deutsche  Archiv  f.  klinische  Med.,”  Band  xxxiii. 

22.  Martius  and  Liittke,  " Die  Magensaure,”  Stuttgart,  1892. 


126 


LITERATURE. 


23.  Moritz,  “ Zeitschrift  f.  Biologie,”  xxxn,  p.  314,  Leipzig,  1895. 

24.  Murdoch,  F.  H.,  “The  Use  and  Abuse  of  the  Stomach-tube,”  “ N.  Y. 
Med.  Jour.,”  16,  1,  1897. 

25.  Nicander,  “Alex.  Phar.,”  Edit.  Paris,  1857,  p.  155. 

26.  “ Oribasius,  Collecta  medicinalia  of,”  Vol.  viii,  Cap.  vi. 

27.  Pechlini,  Joh.  Nicol.,  “ Observation  Physico-medical,”  Liber  1,  observ. 
50,  S.  1 16,  Hamburg,  1691. 

28.  Penzoldt,  F.,  “Allgem.  Behandl.  d.  Magen-  u.  Darmkrankheiten,”  in 
“ Handbuch  der  speciell.  Therapie  innerer  Krankh.,”  Vol.  iv,  p.  289. 

29.  Penzoldt,  F.,  “ Die  Magenerweiterung,”  Erlangen,  1875. 

30.  Ploss,  “ Der  Magenkatheter  a Double  Courant,”  etc.,  “ Deutsche 
Klinik,”  1870,  No.  8. 

31.  Reed,  B.,  “ How  to  Introduce  a Tube  into  the  Stomach  with  the  Least 
Possible  Embarrassment  of  the  Patient,”  “ Internat.  Med.  Mag.,”  Phila., 
1898,  VII. 

32.  Rosenheim,  “ Krankheit.  d.  Speiserohre  u.  d.  Magens,”  Wien  und  Leip- 
zig, 1891. 

33.  Rumsaeus,  “ Organum  Salutis,  or  an  Instrument  to  Cleanse  the  Stomach,” 
l649' 

34.  Ryff,  W.  H.,  “Gross.  Chirurgie,”  Frankfurt-a.-M.,  1559,  Theil  1,  p.  37. 

35.  Scultetus,  Joh.,  “ Wundartzneyisches  Zeughaus,”  Frankfurt,  Ulm,  1679, 
S.  108. 

36.  Socrates,  J.  C.,  “ Griindliche  u.  vollstandige  Beschreib.  d.  Peniculi  Ven- 
triculi  Singularis,”  etc.,  Lips.  u.  Frankfurt,  1713;  “ Breslauer  Sammlung  von 
Natur  u.  Medizin,”  etc.;  “ Geschichten,”  1719,  Classe  v,  Art.  ill. 

37.  Sorbierus,  in  “ Sorberiana,”  Paris,  1694. 

38.  Van  Helmont,  “ Doctrina  inaudita  de  causa,”  etc.,  “ Lithiasis,”  1646, 
Cap.  vii,  34,  S.  140. 

39.  Veronensis,  Joh.  Arculani,  “ Practica,”  etc.,  Venice,  1557,  p.  82. 

40.  Welch,  William  H.,  Pepper’s  “American  System  of  Medicine,”  Vol.  11, 
p.  607. 


ANALYSIS  OF  STOMACH  CONTENTS. 


2 7 


CHAPTER  XIII. 

METHODS  FOR  QUALITATIVE  AND  QUANTITATIVE 
ANALYSIS  OF  STOMACH  CONTENTS. 

Presence  of  Bits  of  Gastric  Mucosa. — Examination  of  Stomach  Contents 
for  Mucus,  Saliva , Bile , Duodenal  Secretions , Blood , and  Pus. — Tests 
for  Blood  in  Sto?nach  Contents.  — Demonstration  of  the  Presence  of  Iron 

in  Stomach  Contents  or  Vomited  Matter. — Spectroscopical  Examination  of 

Stomach  Contents  for  Blood. — Examination  of  Portions  of  Mucosa  or 

Tissue  found  in  the  Wash-water  or  Vomited  Matter. — Literature. 

The  stomach  contents  should  be  examined  for — 

1.  The  character  and  amount  of  the  undigested  food. 

2.  The  presence  and  kind  of  bacteria  and  yeast  fungi. 

3.  The  bile,  mucus,  pus,  and  blood. 

4.  The  total  acidity. 

5.  The  amount  of  free  hydrochloric  acid. 

6.  The  presence  of  inorganic  acids,  as  lactic,  butyric,  or  acetic 
acids. 

7.  The  combined  hydrochloric  acid  and  acid  salts. 

8.  The  presence  of  products  of  digestion, — viz.,  syntonin,  pro- 
peptone, albumoses,  peptone. 

9.  The  presence  of  pepsin  and  rennin ; if  these  are  absent,  their 
proenzymes. 

10.  The  products  of  starch  digestion,  dextrin,  erythrodextrin, 
achroodextrin,  and  maltose. 

11.  Fragments  of  mucosa. 

12.  Fragments  of  neoplasms. 

Character  and  Amount  of  Undigested  Food. — The  exami- 
nation for  undigested  food-particles  may  demonstrate  the  presence 
of  substances  eaten  twenty-four  hours  before  the  expression  of 
contents,  and  thus,  at  once,  establish  an  atony,  dilatation,  or 
stenosis.  As  already  pointed  out,  excess  of  rice  and  bread  and 
absence  of  beef  and  egg  indicate  a higher  acidity,  while  absence 
of  bread  and  rice  and  presence  of  egg  and  beef  indicate  sub-  or 
anacidity.  This,  of  course,  can  be  most  conveniently  studied 
when  the  contents  are  drawn  out  about  five  hours  after  the  first  of 
the  double  meal,  as  employed  by  the  author. 


128 


ANALYSIS  OF  STOMACH  CONTENTS. 


Bacteria. — For  bacteriological  examination,  a few  slides  are 
stained  with  methylene-blue,  and  also  cultures  made,  the  latter 
especially  when  there  is  any  disease  of  the  air-passages  the 
microbes  of  which  may  get  into  the  stomach  with  swallowed  mucus 
or  run  down  unconsciously  during  sleep.  This  is  particularly 
important  in  pulmonary  or  laryngeal  tuberculosis.  Instead  of 
methylene-blue,  Lugol’s  solution  of  iodin  should  be  used  on 
other  slides  for  examining  bits  of  tissue,  mucosa,  and  cellular 
detritus. 

The  normal  stomach  contains  many  micro-organisms ; only 
the  presence  of  very  large  numbers  of  bacteria  has  a pathological 
significance,  if  by  culture  experiments  they  can  be  shown  to  be  still 
capable  of  multiplication. 

Microbes  only  propagate  luxuriantly  when  stagnation  of  gastric 
contents  occurs.  The  secretory  disturbances  are  then  a secondary 
effect,  a consequence  of  the  stagnation.  But  primary  reduction  of 
HC1  secretion  has  been  known  to  cause  a luxuriant  gastric  flora, 
since  it  is  the  HCl  which,  to  a great  extent,  inhibits  their  develop- 
ment and  also  destroys  a large  number  of  them.  If  there  be 
deficient  peristaltic  power,  the  diminution  of  HCl  causes  further 
disturbances  in  the  stomach  and  intestines  by  accumulation  of  bac- 
teria. But  no  degree  of  gastric  acidity,  no  matter  how  great,  can 
destroy  all  bacteria  introduced. 

Germ  growth  in  the  walls  of  the  stomach  and  in  adherent  food- 
masses  has  been  reported  by  F.  B.  Turck  (“  N.  Y.  Med.  Journ.,” 
Nov.  23,  1895).  This  has  been  observed  by  us  in  ulcer,  ulcus  car- 
cinomatosum,  and  carcinoma. 

Hyperacidity  is  as  detrimental  in  its  consequences  as  anacidity, 
because  it  inhibits  normal  intestinal  digestion,  which  is  the  best 
means  of  combating  fermentation  and  putrefaction.  Hydrochloric 
acid  undoubtedly  inhibits  or  checks  gastric  fermentation  to  a cer- 
tain extent,  but  all  ferment-producing  microbes  are  not  destroyed 
by  it  in  the  stomach.  Therefore,  one  frequently  finds  gastric 
fermentation  with  hyperacidity  of  HCl,  and,  reversely,  fermenta- 
tion may  be  absent  where  hydrochloric  acid  is  entirely  absent, 
provided  the  peristole  is  good. 

This  will  again  impress  the  importance  of  an  intact  gastric  peris- 
talsis, a certain  time  of  action  being  indispensable  for  organized 
ferments  to  set  up  their  characteristic  decomposition  even  at  the 
body  temperature;  with  a good  motility,  however,  the  gastric 
chyme  may  reach  the  intestine,  meeting  a vigorous  digestion 


BACTERIA  OF  THE  STOMACH.  1 2g 

before  the  bacteria  get  a chance  to  forge  ahead  of  the  normal  unor- 
ganized ferments. 

The  most  frequent  of  fungi  in  gastric  contents  is  ordinary  yeast, 
and  there  should  be  no  difficulty  in  recognizing  it.  Unless  occur- 
ring in  large  numbers  and  sprouting,  it  has  no  pathological  signifi- 
cance. Two  more  germs  found  in  the  contents  are  of  interest — the 
sarcinae  and  the  Oppler-Boas  bacillus,  the  latter  occurring  in  the 
gastric  contents  of  carcinoma.  Sarcinae  may  be  seen  under  the 
microscope  without  staining  ; they  are,  indeed,  preferably  to  be 
examined  that  way,  as  they  stain  so  deeply  with  anilin  dyes  as  to 
look  like  black  patches. 

Sidney  Martin  recommends  drying  and  fixing  a drop  of  stomach 
contents  on  the  slide  or  cover- 
glass,  and  placing  in  a very 
dilute  solution  of  gentian  vio- 
let for  three  minutes,  washing 
out  in  water,  drying,  and 
mounting  in  Canada  balsam. 

The  gentian  violet  must  be  so 
diluted  as  to  be  nearly  trans- 
parent. Y east  can  similarly  be 
stained  by  magenta  or  methyl- 
ene-blue solution  (two  per 
cent.).  If  the  latter  is  used,  the 
preparation  requires  washing 
out  in  water. 

Sarcinae  can  hardly  be  said 
to  have  any  pathological  sig- 
nificance, according  to  Oppler  (“  Miinchen.  med.  Wochenschr.,” 
1894,  No.  29).  They  are  found  in  ectasias,  occurring  on  a non- 
malignant  basis,  and  in  very  atonic  conditions;  also  in  acute  and- 
chronic  gastritis,  in  ulcer,  in  the  gastric  neuroses,  and  the  gastrop- 
toses ; in  the  last-named  conditions  the  presence  of  sarcinae  is 
rather  the  exception  than  the  rule. 

Riegel  agrees  with  Oppler  in  the  assertion  that  sarcinae  are  very 
rarely  found  in  gastric  carcinoma.  They  are  generally  observed 
in  biscuit  or  bale-shaped  groups  of  four,  eight,  and  sixteen  individ- 
ual sarcinae  bunched  together;  their  occurrence  as  single  individ- 
uals is  seen  rarely. 

The  Oppler-Boas  bacillus  (Oppler,  “ Zur  Kenntniss  d.  Magenin- 
halts  bei  Carcinoma  Ventriculi,’’  “ Deutsche  med.  Wochenschr.," 


130 


BACTERIA  OF  THE  STOMACH. 


1895,  No.  5)  is  an  unusually  long  and  non-motile  bacterium,  which 
was  observed  in  many  cases  of  gastric  carcinoma.  (See  Fig.  19.)  In 
twenty  cases  of  carcinoma  Kaufmann  found  these  bacilli  nineteen 
times,  and,  according  to  his  investigations,  they  have  the  power  of 
abundantly  forming  lactic  acid  from  various  kinds  of  sugar.  In 
the  only  case  of  the  twenty  just  mentioned  in  which  the  Oppler- 
Boas  bacillus  was  absent,  the  lactic  acid  was  absent  also. 

According  to  Schlesinger  and  Kaufmann  (“  Wiener  klinische 
Rundschau,”  1895,  No.  15),  the  presence  of  a large  number  of  these 
bacilli  in  the  stomach  contents  is  an  indication  of  carcinoma,  and 
their  absence  is  of  similar  significance  to  the  absence  of  lactic  acid. 
If  a stenosis  of  the  pylorus  is  present,  then  the  absence  of  these 
bacilli  is  an  argument  against  carcinoma.  Riegel  (loc.  cit.)  confirms 
the  occurrence  of  these  bacilli  in  enormous  numbers  in  carcinoma, 
and  adds  that,  although  there  are  numerous  fungi  that  have  the 
property  of  forming  lactic  acid  in  stomach  contents,  this  can  not 
alter  the  significance  of  the  Kaufmann  and  Schlesinger  observation. 
He  does  not  consider  this  organism  as  pathognomonic  of  gastric 
cancer,  but  as  very  important  for  the  diagnosis.  Since  the  publi- 
cation of  the  first  edition  of  this  work,  the  writer  and  his  clinical 
assistants  have  examined  fifty  cases  of  gastric  carcinoma  particu- 
larly for  the  Oppler-Boas  bacillus.  They  were  found  in  every  case 
but  one.  We  examined  also  eighteen  cases  of  gastric  ulcer  without 
discovering  this  organism  in  a single  case,  and  consider  this 
examination  an  indispensable  adjunct  to  every  gastric  analysis. 

Our  knowledge  concerning  the  bacteria  occurring  in  normal  and 
pathological  stomach  contents  is  very  incomplete  as  yet.  It  ap- 
pears, however,  that  in  all  pathological  processes  we  are  not  con- 
fronted with  qualitatively  new  bacteria,  but  with  excessive  multi- 
plication of  those  normally  present.  The  disturbances  produced 
by  abnormal  augmentation  of  bacteria  in  the  stomach  are  ex- 
plained by  Minkowski  (“  Ueber  d.  Gahrung  im  Magen,”  Mit- 
theilung  a.  d.  Med.  Klin.  Konigsberg,”  edited  by  B.  Naunyn, 
Leipsic,  1888,  p.  156)  in  the  following  manner: 

1.  Substances  may  be  formed  which  irritate  the  mucosa  and  pro- 
voke catarrhal  inflammation. 

2.  Gas  may  be  formed  in  considerable  quantities,  causing  dis- 
tress by  distention,  and  increase  the  mechanical  insufficiency 
already  present. 

3.  The  fermentation  may  give  rise  to  toxins. 

4.  Putrefaction  of  albuminous  bodies  may  produce  alkaline 


MUCUS — BILE BLOOD — PUS.  I 3 I 

bodies  that  will  neutralize  the  hydrochloric  acid  or  what  little  of  it 
may  yet  be  secreted. 

5.  Gastric  fermentations  may  have  a detrimental  influence  on  the 
intestinal  functions. 

Examination  of  Stomach  Contents  for  Mucus,  Saliva,  Bile, 
Duodenal  Secretions,  Blood,  and  Pus. — The  presence  of  mucus 
is  evident  to  the  naked  eye  by  its  stringy  and  tenacious  character. 
Mucus  from  the  pharynx  is  distinguished  from  gastric  mucus  by 
its  occurring  in  clumps  and  being  discolored  by  dust-particles. 
The  chemical  demonstration  is  carried  out  by  dissolving  the  mucus 
in  liquor  potassae,  in  which  it  is  slightly  soluble,  and  from  which  it 
can  be  reprecipitated  by  acetic  acid.  When  pharyngitis,  laryngitis, 
and  bronchitis  can  be  excluded,  large  quantities  of  mucus  in  stom- 
ach contents  are  indicative  of  gastritis.  The  normal  stomach  does 
not  secrete  much  mucus.  Statements  repeatedly  made  to  the  con- 
trary can  only  be  explained  by  faulty  clinical  observation.  Mucus 
is  dissolved  or  digested  by  gastric  juice,  but  requires  twice  as  long 
as  albumin  for  its  solution  (Schmidt,  “ Deutsch.  Arch.  f.  klin.  Med.,” 
Bd.  lvii,  S.  72).  Gastric  mucus  may  occur  in  two  forms  : (i)  As  a 
glassy,  swollen,  transparent  mass  ; (2)  in  forms  of  fibers  or  shreds. 
These  states  of  mucus  are  to  a large  extent  conditioned  by  the 
amount  of  HC1  secreted.  When  there  is  deficiency  or  absence  of 
HC1,  the  mucus  swells  up.  When  HC1  secretion  is  normal  or  in- 
creased, the  mucus  may  be  increased  also,  but  if  so,  it  occurs  in 
forms  of  fibers,  strings,  or  shreds.  The  quantity  of  mucus  is 
inversely  proportional  to  the  quantity  of  HC1  secreted  ; the  largest 
amounts  are  found  with  total  absence  of  HC1.  Microscopical  exami- 
nation of  the  mucus  yields  unsatisfactory  results ; when  it  contains 
pigmented  alveolar  epithelia,  it  is  derived  from  the  respiratory 
passages.  Pavement  epithelium  suggests  its  origin  from  the  mouth 
and  pharynx,  but  if  the  gastric  juice  be  capable  of  digesting,  one 
finds  only  nuclei,  and  if  it  be  devoid  of  digestive  power,  entire 
cells  are  found.  The  spiral  or  snail  cells,  first  described  by  Ja- 
worski,  are  products  of  the  action  of  HC1  on  mucus,  and  have  no 
diagnostic  significance. 

If  the  gastric  contents  consist  largely  of  saliva , this  can  be 
demonstrated  by  the  potassium  sulphocyanate,  KCNS,  which  is 
a normal  constituent  of  healthy  saliva.  Potassium  sulphocyanate 
gives  a dark,  purplish-red  color  upon  the  addition  of  a solution  of 
chlorid  of  iron. 

Bile}  if  present  to  any  considerable  extent,  is  noticeable  at  once 


132 


ANALYSIS  OF  STOMACH  CONTENTS. 


to  the  naked  eye  by  the  compound  greenish-yellow  tinge  it  im- 
parts to  stomach  contents.  Very  slight  amounts  of  bile  and 
duodenal  secretions  are  occasionally  observed  under  normal  con- 
ditions, particularly  if  the  stomach  be  washed  out  early  in  the 
morning  before  breakfast,  for  there  is  no  absolute  closure  of  the 
pylorus  when  the  stomach  is  empty. 

Boas  has,  however,  pointed  out  that  constant  presence  of  very 
evident  admixture  of  bile  and  duodenal  secretions  points  to  stenosis 
of  the  descending  portion  of  the  duodenum  (Boas,  “ Deutsche  med. 
Wochenschr.,”  1791,  No.  28.,  “ Ueber  die  Stenose  des  Duodenum.”). 
As  a rule,  it  will  be  necessary  to  assure  one’s  self  of  the  presence  of 
bile  by  the  Gmelin  test,  or  the  demonstration  of  bile  acids  or  cho- 
lesterin. 

Gmelin’s  test  is  carried  out  by  adding  twenty  drops  of  fuming 
nitric  acid  to  ten  c.c.  of  officinal  nitric  acid  in  a test-tube.  Ten  c.c. 
of  stomach  filtrate  are  drawn  into  a pipet,  and,  holding  the  test- 
tube  with  the  HN03  in  the  left  hand  in  a slanting,  horizontal 
position,  the  filtrate  is  allowed  to  flow  slowly  from  the  pipet  held 
in  the  right  hand  over  the  nitric  acid.  If  the  stomach  contents 
contain  bile,  there  will  be  formed  several  characteristic  rings  of 
color,  which,  going  from  above  downward,  are  (1)  green,  (2)  blue, 
(3)  violet,  and  (4)  red,  but  only  the  green  color  is  an  evidence  of  the 
presence  of  bile. 

Better  results  are  obtained  by  using  a conical  glass  on  a broad 
foot  instead  of  a test-tube.  In  the  clinical  laboratory  they  are  of 
sixty  to  seventy-nine  c.c.,  or  about  two  ounces,  in  capacity.  It  is  of 
some  advantage  to  be  able  to  place  them  alternately  on  and  in  front 
of  a white  and  black  background  during  the  reaction.  First,  twenty 
c.c.  of  gastric  juice,  if  necessary  previously  filtered,  are  placed  in 
the  glass,  then  ten  c.c.  of  nitric  acid  added  by  a pipet,  which  is 
carefully  carried  to  the  bottom  of  the  vessel  ; here  the  nitric  acid 
is  very  gradually  permitted  to  escape  by  diminishing  the  pressure 
of  the  finger  on  the  end  of  the  pipet.  In  this  manner  it  is  easier 
to  get  the  nitric  acid  under  the  gastric  juice.  The  display  of  the 
colors,  yellow,  green,  blue,  violet,  and  red,  occurs  from  above 
downward  ; the  green  color  is  the  only  one  that  is  characteristic  of 
bile  elements. 

The  demonstration  of  the  bile  acids  is  affected  by  first  precipitat- 
ing all  albuminous  bodies  by  boiling  or  by  alcohol;  a few  drops  of 
a solution  of  cane-sugar  are  added,  and  then,  drop  by  drop,  pure 
concentrated  sulphuric  acid.  If  the  solution  is  now  heated,  a beauti- 


BLOOD  IN  GASTRIC  CONTENTS.  1 33 

ful  purple-red  color  is  obtained,  between  6o°  and  70°  C.  (Petten- 
kofer). 

The  presence  of  duodenal  secretions  is  demonstrated  by  testing 
the  stomach  contents  for  the  specific  ferment  activity  of  trypsin, 
amylopsin,  and  steapsin.  (See  pp.  56  and  57.) 

Pus. — Pus  is  rarely  found  in  the  gastric  contents,  but  if  so, 
purulent  inflammations  in  the  mouth,  tonsils,  pharynx,  retronasal 
fossae,  larynx,  and  bronchi  must  be  excluded  before  assigning  its 
cause  to  the  stomach.  In  one  case  in  which  we  found  pus  in  the 
stomach  it  came  from  an  ozena  ; in  another  it  was  traced  to  a 
tuberculous  softening  in  the  left  lung.  The  significance  of  pus  will 
be  considered  in  connection  with  acute  simple  and  with  phlegmon- 
ous gastritis. 

Test  for  Blood  in  Stomach  Contents. — Although  blood  may 
be  present  in  the  material  drawn  by  a stomach-tube,  or  in  vomit,  it 
is  not  always  easy  to  decide  whether  it  was  derived  from  the  lungs 
or  from  the  stomach.  Vomiting  may  produce  a cough,  and,  vice 
versa,  coughing  may  lead  to  an  attack  of  vomiting  ; and  in  cases 
where  either  organ  is  liable  to  hemorrhage,  as  in  tuberculous 
patients  with  a congestive  state  of  the  gastric  mucosa,  it  is,  except  in 
rare  instances,  impossible  to  decide  the  origin  of  the  blood. 

In  cases  with  copious  arterial  gastric  hemorrhage,  the  blood  is 
bright  red  and  clotted.  A slower  but  still  quite  profuse  hemorrhage 
generally  shows  as  a black  clot  or  mass  of  black  clots.  In  very 
slow  but  continuous  hemorrhage  the  blood  collects,  and  may  be 
partially  digested  or  decomposed  in  the  stomach  before  it  is 
vomited  as  a black,  coffee-ground  material.  The  diagnosis  of 
blood  in  the  vomit  is  not  always  easily  made.  There  are  four 
methods  of  determining  the  presence  of  blood,  and  by  one  or  more 
of  them  it  may  generally  be  accomplished. 

The  first  is  by  the  microscopical  demonstration  of  the  red  blood- 
corpuscles.  In  cases  of  suspected  ulcer,  all  vomited  matter  should 
be  microscopically  examined,  even  when  blood  is  not  evident  to  the 
naked  eye. 

The  second  is  known  as  the  guaiacum  test.  Two  or  three  drops 
of  freshly  prepared  tincture  of  guaiacum  are  added  to  five  c.c.  of 
stomach  contents  in  a test-tube,  and  ozonized  ether  poured  on  the 
surface ; if  blood  is  present,  a blue  color  develops  where  the  two 
liquids  meet.  Equal  parts  of  tincture  of  guaiacum  and  turpentine 
that  have  been  exposed  to  the  air  may  be  used  instead  of  ether. 
This  test  for  blood  is  fallacious,  as  almost  any  carbohydrate,  bile, 


134 


ANALYSIS  OF  STOMACH  CONTENTS. 


or  saliva  will  produce  the  same  color  in  the  total  absence  of 
blood. 

The  guaiacum  test,  which  was  originally  proposed  by  Almen 
and  Van  Deen,  becomes  more  reliable  when  executed  by  an  im- 
proved method  suggested  by  H.  Weber.  A considerable  quantity 
of  the  filtrate  is  extracted  or  mixed  with  water;  glacial  acetic  acid, 
to  the  amount  of  one-third  of  the  entire  quantity  of  water  and  fil- 
trate mixture,  must  be  added. 

Of  this  acid  extract  about  ten  c.c.  are  poured  off  after  settling ; 
then  ten  drops  of  tincture  of  guaiacum  and  twenty  to  thirty  drops 
of  turpentine  are  added.  If  blood  is  present,  the  mixture  becomes 
violet-blue ; in  case  blood  is  absent,  the  color  will  be  red-brown. 
The  blue  coloring-matter  that  indicates  blood  can  be  extracted  by 
shaking  the  mixture  with  chloroform.  Coffee-ground  vomit  will 
not  permit  of  the  correct  finding  of  blood  with  either  of  the  two 
preceding  tests. 

This  kind  of  vomit  may  have  to  be  differentiated  from  genuine 
tea  or  coffee  vomit,  or  from  bile,  by  Gmelin’s  test.  In  this  form  of 
vomit  the  corpuscles  are  disintegrated  and  the  hemoglobin  trans- 
formed into  insoluble  hematin.  Still,  there  are  two  ways  left  to 
diagnose  the  blbod  present,  if  any : first,  the  formation  of  crystals 
of  hemin,  and,  secondly,  the  demonstration  of  the  presence  of  iron. 

1.  Preparation  of  hemin  crystals  : Three  to  four  drops  of  the  thick 
sediment  is  mixed  on  a glass  slide  with  a little  common  salt,  then 
one  to  two  drops  of  glacial  acetic  acid  are  added,  and  the  mixture 
carefully  heated  over  a small  flame  of  a spirit-lamp  or  a Bunsen 
burner  until  bubbles  begin  to  form.  If  blood  is  present,  on  exam- 
ining the  preparation  with  the  microscope  reddish-brown,  oblong 
crystals  of  hemin  hydrochlorate  will  be  recognized;  their  color, 
form,  and  occurrence  are  characteristic.  This  test  may  fail  in  cases 
where  blood  is  present. 

2.  Demonstration  of  the  presence  of  iron  : Naturally,  the  patient 
whose  stomach  contents  are  to  be  examined  must  not  have  been 
taking  iron  in  any  form,  nor  any  raw  meats. 

Demonstration  of  the  Presence  of  Iron  in  the  Stomach  Con- 
tents or  in  Vomited  Matter. — In  case  one  is  dealing  with  coffee- 
ground  material  this  test  may  become  necessary.  Some  of  the  black 
sediment  is  placed  in  a porcelain  dish,  and  a few  crystals  of  potassium 
chlorate  and  two  to  three  drops  of  strong  hydrochloric  acid  are 
added.  On  heating  over  a flame  and  adding  a few  drops  of  a five 
per  cent,  solution  of  potassium  ferrocyanid,  4KCN,  Fe(CN)2  + H20, 


FRAGMENTS  OF  MUCOSA,  ETC.,  IN  GASTRIC  CONTENTS.  1 35 

Prussian  blue  will  be  formed.  Boas  and  Sidney  Martin  consider 
this  a very  delicate  test.  The  Prussian  blue,  upon  the  occurrence 
of  which  this  test  depends,  is  a complex  cyanid  of  iron,  4Fe(CN)3. 
3Fe(CN)2. 

Spectroscopic  Examination  of  Stomach  Contents  for  Blood. 

— A spectroscopic  examination  is  possible  when  the  red  blood- 
corpuscles  have  become  dissolved,  and  the  filtrate  of  gastric  con- 
tents contains  oxyhemoglobin.  The  compound  of  oxygen  with 
hemoglobin  is  distinguished  by  two  absorption  bands  in  the  spec- 
trum, which  occur  between  the  Fraunhofer  lines  D and  E in  the 
yellow  and  green.  If  after  the  recognition  of  these  lines  a reducing 
agent  is  added  to  the  solution  of  oxyhemoglobin, — for  instance,  if 
it  is  shaken  with  ammonium  sulphid, — the  two  bands  observed  be- 
fore fuse  into  a single  broad  band,  occupying  the  space  between  the 
two  distinct  and  separate  bands,  or  move  beyond  D toward  the  red  of 
the  spectrum.  (Compare  Eichhorst,  loc.  cit.,  p.  523  ; also  Richard 
C.  Cabot,  “ Clinical  Examination  of  the  Blood,”  Wm.  Wood  & Co., 
Publishers,  New  York,  1897,  and  von  Jaksch,  loc.  cit.) 

Examination  of  Portions  of  Mucosa  or  Tissue  Found  in  the 
Wash-water  and  Vomited  Matter.  — In  the  wash-water  from 
almost  every  stomach,  also  in  the  samples  of  test-meals  gained  by 
the  Ewald  expression  method,  and  in  vomited  matter,  small  portions 
of  the  superficial  mucosa  of  the  stomach  can  frequently  be  found 
on  careful  searching.  Stimulated  by  reading  the  accompanying 
literature,  particularly  the  work  of  Hayem,  Boas,  Einhorn,  and 
Cohnheim,  we  have  during  the  last  three  years  made  a study  of 
such  tiny  bits  of  mucosa. 

To  detect  them  more  easily,  the  stomach  is  best  washed  in  the 
morning,  before  breakfast,  with  500  c.c.  of  warm  water,  which  is 
poured  into  a shallow  papier-mache  or  hard-rubber  dish,  the  bot- 
tom of  which  is  colored  white  and  black  like  a checker-board ; on 
this  background  the  tiny  bits  of  tissue  from  the  mucosa,  or  from 
any  neoplasm  that  may  be  in  the  stomach,  can  be  more  easily 
recognized.  These  particles  are  usually  of  a reddish  color;  they 
may  seem  at  times  colorless,  so  that  in  a glass  or  pitcher  they  may 
be  overlooked,  while  on  the  dark,  flat  dish  they  are  quite  apparent. 
These  fragments  come  from  very  superficial  erosions,  which  are  pos- 
sibly caused  by  very  slight  local  congestions  or  by  traumatism 
(Ewald,  loc.  cit.). 

It  is  conceivable  that  the  contractions  of  the  muscularis  of  the 
stomach  may,  if  sufficiently  powerful,  effect  an  arrest  of  the  flow  of 


36 


ANALYSIS  OF  STOMACH  CONTENTS. 


circulation  in  the  folds  and  cause  intense  congestion  of  the  veins 
and  capillaries,  which  may  give  rise  to  small  hemorrhages  into  the 
mucosa.  These  hemorrhagic  areas  are  very  poorly  nourished  by 
the  blood-current,  and  may  eventually  succumb  to  the  autodigestive 
action  of  the  gastric  juice;  other  gastric  contractions  then  loosen, 
and  cast  off  these  tiny  spots  of  necrosis  (Hartung,  loc.  cit .). 

According  to  Virchow  (loc.  cit),  circulatory  derangements  of  the 
larger  vessels  of  the  stomach, — the  acute  and  chronic  gastritis  espe- 
cially,— if  accompanied  with  vomiting  and  colicky  contractions,  are 
the  cause  of  ulcers  and  erosions.  Small  erosions  represent  only 
the  superficial  stratum  of  the  mucosa,  generally  only  the  vestibule 
or  alveolus  and  the  first  third  of  the  gland-ducts  ; the  entire  lower 
half  of  the  mucous  membrane  is  rarely  cast  off  (Gerhardt,  loc.  cit). 
The  gland-duct  remaining  shows  nothing  pathological.  At  the 
sides  and  edges  of  the  sequestrated  portion  the  glands  become 
longer,  and  the  first  ones  that  are  intact  usually  curve  themselves 
over  the  defect,  partly  covering  it.  Recovery  takes  place  by  the 
simple  after-growth  of  the  remaining  portions  of  the  glands. 

In  three  stomachs  which  were  taken  immediately  after  death 
(not  later  than  two  hours  after),  we  observed  what  was  undoubt- 
edly a superficial  epithelial  sequestrum  resting  loosely  upon  the 
mucous  membrane  in  many  places  of  what  we  had  every  reason  to 
believe  was  a perfectly  normal  stomach.  The  autodigestion  in  this 
case  had  been  prevented  by  pouring  ninety  per  cent,  alcohol  into 
the  organ  about  fifteen  minutes  after  death.  In  places,  portions  of 
mucosa  half  as  large  as  a lentil-seed  could  be  dislodged  by  a gentle 
stream  of  water  from  a wash-bottle.  The  erosions  included  the 
inner  third  of  the  gland-duct  proper  (“inneres  Schaltstiick  ” of 
Stohr),  and  it  seems  that  even  before  they  were  dislodged  the 
process  of  repair  had  already  begun  ; for  underneath  small  areas 
of  necrosed  superficial  epithelium  that  were  lifted  from  the  true 
glandular  stratum  by  a thin  layer  of  lymph  containing  few  red 
blood-corpuscles,  cell  proliferation  was  going  on  in  the  parietal 
or  oxyntic  cells,  and  in  the  cylindrical  cells  of  the  adjoining  intact 
epithelium  formation  of  mitosis  and  karyokinetic  figures  were 
evident  in  picrocarmin  and  eosin  stains  of  these  sequestrations  of 
mucosa.  The  presence  of  mitosis  in  an  apparently  healthy  stomach 
somewhat  weakens  the  assumption  (Lubarsch)  that  this  is  a valu- 
able sign  of  carcinoma. 

It  seems  possible  that  a process  of  exfoliation  is  constantly  going 
on  in  the  lining  membrane  of  the  gastro-intestinal  tract,  just  as  in 


ETIOLOGY  OF  EROSIONS. 


1 37 


the  epidermis.  It  is  not  conceivable  that  the  constant  and  con- 
tinuous impact  and  friction  of  the  ingesta  should  go  on  daily 
without  causing  necrosis  of  epithelium  in  places.  If  we  should 
hold  the  normal  acid  chyme  in  the  palm  of  our  hands  for  three  or 
four  hours  three  times  or  more  every  day,  we  would  very  soon 
notice  dermatitis  and  exfoliations  of  the  epidermis. 

In  the  digestive  tract  (for  it  occurs  all  along  the  small  intestine) 
this  exfoliation  goes  deeper  than  in  our  hands  because  of  imme- 
diate autodigestion  of  the  exfoliated  spot.  Although  we  have 
examined  fifty  human  stomachs  with  especial  regard  for  this 
phenomenon,  we  have  failed  to  detect  evidence  of  this  process  in 
minute  areas  in  but  four  cases,  and  in  these  the  examination  was 
limited  to  a very  small  portion  of  the  stomach. 

Even  in  stomachs  obtained  within  one  hour  after  death,  and 
preserved  by  pouring  alcohol  or  solutions  of  formalin  into  the 
organ,  these  erosions  can  be  seen  in  places.  We  generally  request 
a strip  which  begins  in  the  esophagus,  runs  through  the  cardia, 
saccus  caecus,  entire  greater  curvature,  and  pylorus,  and  has  a piece 
of  duodenum  attached  to  it.  This  is  hardened,  and  in  many 
places  pieces  are  excised  half  an  inch  apart  and  embedded  in  cel- 
loidin,  cut  into  serial  sections  with  the  revolving  microtome, 
stained  in  eosin  and  hematoxylin  and  mounted  in  balsam.  In 
some  cases  we  sectioned  strips  running  along  the  lesser  cur- 
vature. 

In  this  way  it  was  found  that  most  of  these  erosions  and  exfolia- 
tions occur  in  the  vicinity  of  the  sphincter  antri  pylorici,  about 
seven  to  ten  cm.  from  the  pylorus.  At  this  point  the  muscu- 
laris  has  its  most  powerful  development,  and  the  peristalsis,  and 
consequently  the  impact  of  the  food  with  the  mucosa,  is  most 
vigorous  ; hence  the  epithelium  here  has  most  to  suffer  from  fric- 
tion. Slight  erosions  can  be  detected  in  the  lower  part  of  the 
esophagus,  where  no  peristalsis  normally  occurs  but  that  accom- 
panying deglutition.  So  the  conclusion  seems  justifiable  that  very 
tiny  exfoliations  and  erosions  occur  in  all  stomachs,  and,  in  adult 
life,  perhaps  at  all  times.  This  precludes  the  presumption  that  the 
pieces  of  mucosa  are  lesions  produced  by  the  stomach-tube. 

Boas  (loc.  cit.)  thinks  that  coughing  or  defecation  may  cause  the 
dislodgment  of  such  loosened  epithelium.  When  this  process 
reaches  such  an  exaggerated  type  as  described  by  Einhorn  {loc.  cit., 
“ Erosions  of  the  Stomach”),  it  is  very  probable  that  the  mucosa  is 
made  less  resistant  by  some  well-developed  gastric  disease  (one  of 

IO 


I38  LITERATURE  ON  EXFOLIATIONS  AND  EROSIONS. 

the  forms  of  gastritis,  carcinoma,  etc.),  for  his  patients  suffered 
from  pains,  emaciation,  and  weakness. 

Among  the  forty-six  stomachs  examined  by  myself  were  nineteen 
in  which  no  symptoms  referable  to  the  stomach  were  given  during 
life.  The  pieces  varied  from  five  mm.  in  length,  and  nearly  as  wide. 
Einhorn  recommends  intragastric  spraying  of  a solution  of  1 : 1000 
of  argentic  nitrate  for  the  excessive  exfoliation,  combined  with 
intragastric  galvanization,  diet,  and  tonics,  with  a hygienic  out- 
door life. 


LITERATURE 

ON  EXFOLIATIONS  AND  EROSIONS  OF  GASTRIC  MUCOSA. 

1.  Boas,  “ Diagnostik  u.  Therap.  d.  Magenkrankh.,”  “ Allg.  Th.,”  3d  ed., 
p.  220. 

2.  Boas,  “ Ueber  Gastritis  Adda,”  “Wiener  med.  Wochenschr.,”  1-11,  1895. 

3.  Boas,  “ Beitrag  zur  Symptomatologie  des  chronischen  Magenkatarrhs  und 
der  Atrophie  der  Magenschleimhaut,”  “ Munch,  med.  Wochenschr.,”  41  u.  42. 

4.  Cohnheim,  Paul,  “ Die  bedeut.  klein.  Schleimhautstiickchen  f.  d.  Diag- 
nose d.  Magenkrankh.,”  “ Archiv  f.  Verdauungskrankh.,”  Band  1,  S.  274. 

5.  Cramer,  “ Ueber  d.  Ablosung  d.  Magenschleimhaut  durch  die  Sondirung,” 
“ Miinch.  med.  Wochenschr.,”  p.  52,  1891. 

6.  Damaschino,  “Note  sur  un  nouveau  procede  pour  l’etude  de  lesions  de 
l’estomac,”  “ Gaz.  med.,”  1880. 

7.  Ebstein,  “Ueber  die  Losung  eines  Stuckes  d.  Pylorusschleimhaut  mit  d. 
Magensonde,”  “Berliner  klinische  Wochenschr.,”  1895. 

8.  Ebstein,  “ Beitrage  zur  Lehre  vom  Bau  der  sogenannten  Magenschleim- 
driisen,”  “ Schultze’s  Archiv,”  Band  vi,  p.  530. 

9.  Einhorn,  “ Clinical  Observations  on  Erosions  of  the  Stomach  and  Their 
Treatment,”  “ N.  Y.  Medical  Record,”  June  23,  1894. 

10.  Einhorn,  “State  of  the  Gastric  Mucosa  in  Secretory  Disorders  of  the 
Stomach,”  “ N.  Y.  Medical  Record,”  June  27,  1896. 

11.  Einhorn,  “Zur  Achylia  Gastrica,”  “Archiv  f.  Verdauungskrankh.,” 
Band  1,  Heft  2. 

12.  Ewald,  “ Klinik  d.  Verdauungskrankheiten,”  3d  ed.,  p.  191. 

13.  Ewald,  “ Ein  Fall  chronischer  Sekretionsuntiichtigkeit  des  Magens  ” 
(Anadenia  ventriculi  ?),  “ Das  Benzonapthol,”  “ Berl.  klinische  Wochenschr.,” 
26  u.  27,  1892. 

14.  Ewald,  “ Ein  Fall  v.  Atrophie  d.  Magenschleimhaut  mit  Verlust  d. 
HC1  Sekretion,  Ulcus  carcinomatosum  duodenale,”  “ Berl.  klinische  Wochen- 
schr.,” 1886. 

15.  Fenwick,  “Ueber  den  Zusammenhang einiger krankhafter  Zustande  des 
Magens  mit  anderen  Organerkrankungen,”  “ Virch.  Archiv,”  Band  118,  xil. 

16.  Gerhardt,  D.,  “Virch.  Archiv,”  Band  cxxvn,  p.  85. 

1 7.  Hammerschlag,  “ Zur  Kenntniss  des  Magencarcinoms,”  “ Wiener 
klinische  Rundschau,”  23,  1895. 

18.  Hartung,  O.,  “ Deutsche  med.  Wochenschr.,”  No.  38,  p.  847,  1890. 


LITERATURE  ON  EROSIONS.  I 39 

19.  Hayem,  “Gastritis  Parenchymatosa,”  “ Allg.  Wien.  med.  Zeitung,” 
1894,  pp.  2-17. 

20.  Hayem,  “ Resume  de  l’Anatomie  Pathologique  de  la  Gastrite  Chronique,” 
“ Gaz.  Hebdom.,’’  pp.  33,  34,  1892. 

21.  Jaworski  u.  Korcynski,  “ Ueber  einige  bisher  wenig  beriicksichtigte 
klinische  und  anatomische  Erscheinungen  im  Verlaufe  des  sogenannten 
Magenkatarrhs,”  “ Archiv  f.  klinische  Med.,”  47,  p.  578. 

22.  Klemperer,  “ Ueber  die  Dyspepsie  der  Phthisiker,”  “ Berlin,  klinische 
Wochenschr.,”  11,  1889. 

23.  Korcynski  u.  Jaworski,  “ Klinische  Befunde  bei  Ulcus  u.  Carcinoma  Ven- 
triculi,”  etc.,  “ Deutsche  med.  Wochenschr.,”  pp.  47-49,  1 886. 

24.  Kupfifer,  “ Epithel  u.  Driisen  d.  menschlichen  Magens,”  Munchen,  1883. 

25.  Langerhans,  “ Virch.  Archiv,”  Band  cxxiv,  p.  373. 

26.  Meyer,  “ Zur  Kenntniss  der  sogenannten  Magenatrophie,”  “ Zeitschr.  f. 
klinische  Med.,”  Band  xvi,  p.  366. 

27.  Rosenheim,  “ Ueber  atrophische  Processe  an  der  Magenschleimhaut  in 
ihrer  Beziehung  zum  Carcinom  u.  als  selbstandige  Erkrankung,”  “ Berliner 
klinische  Wochenschr.,”  51,  1881. 

28.  Sachs,  “Zur  Kenntniss  der  Magenschleimhaut  in  krankhaften  Zustan- 
den,”  “Archiv  f.  exp.  Pharm.  u.  Pathol.,”  Band  xxiv,  1888. 

29.  Schmidt,  “ Ein  Fall  von  Magenschleimhautatrophie  nebst  Bemerkungen 
tiber  die  sogenannte  schleimige  Degeneration  der  Driisenzellen  des  Magens,” 
“ Deutsche  med.  Wochenschr.,”  19,  1895. 

30.  Schmidt,  “ Fortgesetzte  Untersuchungen  iiber  die  Secretion  des  Magen- 
schleims,”  “Deutsche  med.  Wochenschr.,’’  Vereinsbeilage,  xm,  1895. 

31.  Schmidt,  Adolf,  “ Untersuch.  iiber  menschl.  Magenepithel,  normal  u. 
pathol.,”  “Virchow’s  Archiv,”  Band  143.  xix. 

32.  Stintzing,  “ Zum  feineren  Bau  u.  zur  Physiologie  d.  Magenschleimhaut,” 
“ Miinchener  med.  Wochenschr.,”  46,  1889. 

33.  Stohr,  “Zur  Kenntniss  des  feineren  Baues  der  menschlichen  Magen- 
schleimhaut,” “ Schultz’s  Archiv,”  Band  xx,  p.  221. 

34.  Virchow,  R.,  “Virch.  Archiv,”  Band  v,  p.  363. 

35.  Hemmeter,  J.  C.,  “ Zur  Histologie  d.  Magendriisen  b.  d.  Hyperaciditat,” 
“Archiv  f.  Verdauungskrankh.,”  Heft  3,  1898. 


CHAPTER  XIV. 

THE  DIAGNOSTIC  SIGNIFICANCE  OF  FRAGMENTS  OF 
GASTRIC  MUCOSA. 

One  of  the  first  to  utilize  these  fragments  for  diagnostic  purposes 
was  Boas,  who  attributed  great  importance  to  this  way  of  finding 
out  the  real  state  of  the  mucosa.  He  held  that  in  certain  con- 
ditions of  suppressed  secretion  the  differential  diagnosis  between  a 
possible  neurosis  and  a genuine  gastritis  with  glandular  atrophy 
was  only  possible  by  examination  of  such  pieces  of  mucosa. 


140 


SIGNIFICANCE  OF  FRAGMENTS  OF  MUCOSA. 


Rosenheim  ( loc . cit.),  Boas  ( loc . cit.),  and  Julius  Friedenwald  (“  Med- 
ical News,”  June  22,  1895)  emphasize  the  value  of  qualitative  and 
quantitative  testing  of  rennin  zymogen  to  differentiate  between 
chronic  gastritis  with  glandular  atrophy  and  carcinoma  on  the  one 
hand,  and  nervous  dyspepsia  and  secondary  gastritis  on  the  other. 
However,  Ewald  {loc.  cit.)  and  also  Einhorn  {loc.  cit.)  have  asserted 


Fig.  20. — Fragment  of  Mucosa  showing  a Normal  Condition  of  Glands  : very  slight 
round-celled  infiltration.  The  piece  became  detached  above  the  level  at  which  the  oxyntic 
cells  are  found.  X 600. 


that  absolute  deficiency  of  rennin  zymogen  is  not  pathognomonic 
of  atrophy  ; therefore  it  wmuld  indeed  seem  as  if  a certain  diagnosis 
could  only  be  made  by  a small  piece  of  mucosa. 

Is  there  any  clue  which  can  be  derived  from  these  pieces  regard- 
ing the  state  of  the  mucosa  in  the  secretory  disorders?  This 
we  will  try  to  answer  in  the  following.  Hayem,  to  whom  we 


HISTOLOGY  OF  THE  FRAGMENTS.  1 4 1 

are  indebted  for  the  best  histological  investigations  of  the  gastric 
mucosa,  emphasizes  that  the  individual  elements  of  the  mucosa, 
gland-ducts,  superficial  epithelium,  and  interstitial  tissue  can  become 
diseased  in  a variety  of  ways  ; the  various  portions  of  the  stomach, 
fundus,  pylorus,  and  cardia  may  exhibit  different  affections;  and. 
finally,  the  mucosa  may  at  different  parts  show  different  phases  of 
disease.  He  distinguishes  a parenchymatous  and  an  interstitial 
gastritis.  First,  the  parenchymatous  : 

1.  Gastrite  parenchymateuse  hyperpeptique  chloro-organique. 
Under  this  he  has  two  sub-classes:  ( a ) “D’emblee” — dyspeptic 
distress  coming  on  at  once — in  the  first  stage  of  digestion.  ( b ) 
“ Tardive  ” — dyspeptic  distress  coming  on  in  later  stages — in  one 
and  one-half  to  two  hours.  Under  this  hyperpeptic  parenchymatous 
gastritis,  Hayem  means,  clinically,  a hyperpepsia  with  hyperacidity 
and,  anatomically,  degeneration  of  the  principal  central  or  chief 
cells,  with  proliferation  of  the  parietal,  border,  or  oxyntic  cells. 

2.  Gastrite  parenchymateuse  muqueuse  (gastritis  mucipara),  by 
which  he  means  a mucous  degeneration,  a process  taking  place 
principally  in  the  vestibules  to  the  gland-ducts  (which  are  lined 
with  columnar  epithelium)  and  corresponds  to  the  Sehleimkatarrli 
of  most  German  writers.  This  is  associated  with  hypopepsia  and 
subacidity. 

3.  Gastrite  parenchymateuse  atrophique,  which  signifies,  anatom- 
ically, the  total  atrophy  of  the  glands  without  interstitial  pro- 
cesses, and,  clinically,  anacidity  or  achylia.  The  interstitial  forms 
he  separates  into  two  classes  : 

(a)  Those  in  which  the  round-cell  infiltration; 

(1 b ) Those  in  which  the  sclerosis,  i.  e .,  connective-tissue  prolifera- 
tion, predominates. 

These  processes  are  described  as  occurring  purely  as  such, 
or  mixed  with  forms  of  parenchymatous  gastritis,  and  as  leading 
to  sub-  or  anacidity.  In  order  to  bring  our  results  in  critical  con- 
sideration with  those  of  Einhorn  (loc.  cit.),  we  have  adopted  his 
classification  of  the  anatomical  conditions  found  in  these  frag- 
ments. There  is,  however,  one  objection  that  can  be  urged  against 
it,  and  that  is  the  apparent  fact  that  he  has  based  his  system 
upon  conditions  of  the  gland-tubes  and  interglandular  tissue 
exclusively,  and  mentions  the  state  of  the  cells  only  once  in  six 
types  described.  We  shall  therefore  supplement  his  categories 
by  adding  the  state  and  condition  of  the  vestibular  or  alveolar 
columnar  cells  (Vorraumzellen),  and  the  condition  and  numerical 


142 


SIGNIFICANCE  OF  FRAGMENTS  OF  MUCOSA. 


relations  of  the  chief  central  or  ferment  cells  (Hauptzellen),  and 
the  parietal,  border,  or  oxyntic  cells  (Belegzellen)  : 

I.  Normal. — The  gland-ducts  and  interglandular  tissue  exist  in 
normal  proportions.  The  columnar  epithelium  of  the  surface  and 
of  vestibule  is  normal,  with  scattered  cells  showing  at  their  free 
ends  slight  mucoid  metamorphosis.  Average  number  of  parietal 


Fig.  2i. — Hypertrophy  and  Proliferation  of  Glandular  Elements. — ( From  a case  of  per- 
sistent hyperacidity — specimen  found  in  the  eye  of  the  tube  after  drawing  test-meal .)  X 500. 

or  oxyntic  cells  in  six  ducts  which  were  sectioned  very  nearly  down 
the  center  = 22-40  (see  Fig.  20). 

2.  Connective-tissue  Excess. — Proliferation  of  connective  tissue 
around  the  glands — glands  and  epithelial  cells  as  in  normal  con- 
dition. 

3.  Proliferation  of  Glands. — Under  this  class  we  have  in  the 
examination  of  nineteen  cases  been  impressed  with  the  probability 
that  there  are  three  types  of  this  condition  : 


HISTOLOGICAL  CONDITIONS  PRESENT. 


43 


Type  a. — Increase  of  gland-tubules,  but  normal  number  of 
border  cells.  In  this  sub-type  there  is  a proliferation  of  gland- 
tubules.  Under  the  same  field  of  microscope  there  will  be  more 
of  them  than  under  normal  conditions,  since  they  are  much  closer 
to  each  other,  but  the  number  of  central  and  oxyntic  cells  are 
from  18-42,  or  the  same  as  under  the  normal  condition. 


Fig.  22. — Atrophy  and  Vacuolization  of  Glandular  Elements— Mucoid  Degeneration 
of  Peptic  Cells — Increase  of  Interstitial  Connective  Tissue — Small  Round-celled 
Infiltration. — ( From  a case  of  chronic  alcoholic  gastritis.  Found  in  the  wash-water .) 
X 500. 


Type  b. — Increase  of  oxyntic  or  parietal  cells  with  normal 
number  of  gland-ducts.  Here  there  seems  to  be  no  proliferation 
of  the  gland-ducts.  The  connective  tissue  and  the  ducts  bear  the 
same  relation  as  in  class  1,  but  the  anilin-staining  oxyntic  cells 
maybe  so  increased  that  they  lie  in  juxtaposition,  giving  the  whole 
duct  the  appearance  of  a peptic  duct  of  the  dog;  the  number  may 
reach  seventy  in  one  duct.  The  oxyntic  cells  are  increased  in  size. 


144 


SIGNIFICANCE  OF  FRAGMENTS  OF  MUCOSA. 


Type  c. — Increase  of  the  number  of  ducts  in  which  the  number 
of  oxyntic  cells  appear  normal  in  size  and  number,  and,  in  the 
same  fragment  or  section,  portions  of  mucosa  in  which  the  ducts 
are  not  augmented,  but  the  oxyntic  cells  are  increased  in  number 
and  size;  this  third  type  is  a combination  of  types  a and  b.  When 
there  are  many  oxyntic  cells  above  the  normal,  the  entire  gland- 
duct  assumes  a tortuous  or  elongated  shape.  It  seldom  extends 
down  into  the  mucosa  in  the  same  plane;  therefore  it  is  very  rare 
that  a section  will  strike  down  the  middle  of  a duct.  Generally  the 
counts  in  sixteen  ducts  struck  fairly  along  the  central  canaliculus 
are  taken  as  an  average. 

4.  Incipient  Atrophy. — To  the  same  field,  under  the  micrometer, 
there  are  fewer  glands  present  than  normally  ; they  appear  shrunken 
and  smaller,  at  the  same  time  the  spaces  between  the  glands  are 
larger  than  normal  owing  to  an  increased  connective-tissue  forma- 
tion ; the  latter  is  thickly  invaded,  as  a rule,  with  small  round-cell 
infiltration.  The  next  type  is — 

5.  Atrophy. — In  complete  atrophy  there  are  only  remnants  of 
glands  left,  a few  degenerated  cells  lying  in  empty  circular  spaces 
where  glands  had  previously  existed ; there  is  also  a diffuse 
round-celled  infiltration  (see  Fig.  22). 

6.  Vacuolization. — Round  or  ovoid  vacuoles  exist  within  the 
glands  in  large  numbers,  being  the  result  of  mucoid  degeneration 
of  some  of  the  glandular  cells ; this  is  generally  associated  with 
connective-tissue  proliferation  (see  Fig.  22).  Vacuoles  are  present 
in  the  gland-cells  normally,  as  can  be  seen  in  the  drawings  of  Kupher 
and  Stohr.  We  have  also  seen  them  in  both  longitudinal  and  cross- 
section  of  the  gland-tubules,  but  rarely  more  than  two  or  three  to 
the  entire  duct.  It  is  conceivable  that  they  may  be  produced  by 
the  process  of  hardening  and  imbedding.  Some  of  the  fragments 
obtained  from  stomachs  may  show  characteristics  of  two  types. 

Deductions  from  Fifty  Cases. — (Hemmeter,  “ Ueber  die  His- 
tologie  der  Magendriisen,”  etc.;  Boas,  “Archiv  f.  Verdauungskrank- 
heiten,”  Bd.  iv,  p.  30).  In  fourteen  healthy  persons  the  mucosa 
fragments  were  normal  in  eleven;  proliferation  and  autodigestion 
marked  in  one,  which  showed  also  beginning  small  round-cell  in- 
filtration between  the  ducts  ; connective-tissue  increase  in  one.  In  a 
third  case  the  examination  showed  proliferation  in  one  fragment, 
and  a normal  condition  in  a second  found  in  the  same  wash-water. 

In  twenty-two  cases  of  hyperacidity  the  fragments  of  gastric 
mucosa  found  were  apparently  normal  in  four. 


HISTOLOGICAL  CONDITIONS  PRESENT. 


*45 


Atrophy  of  gland-tubules  and  connective-tissue  increase,  so  that 
there  were  fewer  glands, — but  in  these  few  there  were  contained  a 
larger  number  of  oxyntic  cells  than  normal, — in  two  cases. 

Proliferation  of  gland-ducts,  with  apparently  normal  oxyntic 
cells,  in  eight  cases. 

Proliferation  of  oxyntic  cells,  generally  without  marked  increase 
in  the  gland-tubules,  in  eight  cases. 

In  fourteen  cases  of  anacidity  or  subacidity  the  fragment  was  ap- 
parently normal  in  four  cases. 

.Proliferation  of  glands,  with  marked  small  round-cell  infiltration, 
was  found  once. 

Atrophy  in  some  form  was  found  in  the  fragments  from  the  nine 
remaining  cases. 

In  establishing  the  classification  of  euchlorhydria  and  hyperchlorhydria  we 
could  not  be  guided  exclusively  by  the  amount  of  free  HC1  found  after  the 
double  test-meal. 

Thus,  a young,  vigorous  farmer,  aged  twenty-five,  who  never  had  any  disease, 
showed  on  repeated  examination  an  amount  of  free  HC1  equal  to  6o°,  with  a 
total  acidity  of  8o°.  Ordinarily,  judging  simply  from  the  analysis,  such  a case 
would  be  diagnosed  as  hyperacidity,  according  to  the  principles  defined  in 
the  chapter  on  the  normal  amount  of  HC1 ; however,  these  cases  can  be  diag- 
nosed justly  and  accurately  when  considered  together  with  concomitant  signs 
and  symptoms  only.  Although  this  case  had  the  large  amount  of  free  HC1, 
there  was  no  starch  indigestion,  no  erythrodextrin,  no  pyrosis;  there  were  no 
symptoms  referable  to  the  stomach  at  all ; the  man  was  in  perfect  health. 

Another  case,  a neurasthenic  female  had  been  suffering  intensely  from  hy- 
peracidity and  occasional  gastroxynsis,  and  the  amount  of  free  HC1  was  never 
over  30°.  This  case  showed  hypermotility;  the  stomach,  as  a rule,  was  empty 
twenty-five  minutes  after  an  Ewald  test-meal ; with  our  intragastric  rubber  bag, 
in  connection  with  the  kymograph,  she  showed  very  frequent  and  sudden 
gastric  peristalsis  of  unusual  tonicity. 

Summary  of  results  from  examination  of  fragments  of  mucosa 
in  fifty  cases  : 

/ Perfectly  normal  in  eleven. 

(a)  Glandular  proliferations  in  one  ; (b)  normal 
in  one.  These  fragments  ( a and  b ) were  found 
in  same  wash-water. 

Connective-tissue  increase  in  two. 

Normal  in  four. 

Atrophy  in  two. 

Proliferation  of  gland-ducts,  but  normal  oxyntic 
cells  in  eight. 

Proliferation  or  hypertrophy  of  oxyntic  cells  in 
eight. 

f Normal  in  four. 

Proliferation  of  glands  in  one. 

^ Atrophy  in  nine. 


Fourteen  healthy  persons : 


Twenty-two  cases  of  Hyper- 
acidity : 


Fourteen  cases  of  Anacidity 
or  Subaciditv : 


146  SIGNIFICANCE  OF  FRAGMENTS  OF  MUCOSA. 

In  general  we  find  proliferation,  therefore,  present  in  two-thirds 
of  these  cases  of  hyperacidity,  and  atrophy  in  three-quarters  of 
these  cases  of  anacidity  or  subacidity.  Einhorn  ( loc . cit.)  does  not 
give  any  results  from  examination  of  perfectly  healthy  individuals, 
as  his  cases  of  euchlorhydria  seem  to  be  in  patients. 

Of  the  twelve  hyperacid  cases,  three,were  normal,  or  very  nearly 
so,  six  showed  proliferation,  and  three  showed  connective-tissue 
proliferation.  In  his  cases  of  anacidity,  or,  rather,  what  he  calls 
achylia  gastrica,  of  which  there  were  seven  cases,  there  was  atrophy 
three  times,  marked  vacuolization  once,  proliferation  once,  and 
normal  condition  twice. 

On  the  whole,  judging  from  Einhorn’s  results,  Cohnheim’s, 
Hayem’s,  and  our  own,  the  conclusions  seem  justifiable  that  pro- 
liferation of  glandular  elements  is  present  in  from  one-half  to  two- 
thirds  of  the  cases  of  hyperacidity ; and  atrophy  is  present  in  from 
one-half  to  two-thirds  of  the  cases  of  anacidity. 

Adolf  Schmidt  (“Virchow’s  Archiv,”  Bd.  cxliii,  S.  478)  asserts 
that  the  epithelium  of  the  surface  of  the  stomach  is  preserved 
better  than  the  gland-cells  in  inflammatory  conditions  of  the 
mucosa.  This,  he  says,  is  particularly  so  in  chronic  gastritis, 
which  forms  island-like  foci  in  stomachs  otherwise  not  much 
changed.  Our  experience,  and  that  of  W.  D.  Booker,  is  not  in 
accordance  with  this  observation  (see  Pathology  of  Simple,  Acute, 
and  Chronic  Gastritis  in  the  clinical  portion  of  this  work).  Although 
we  preserved  the  stomachs  by  injecting  them  immediately  after 
death  (within  twenty  minutes)  with  alcohol,  also  with  formalin  and 
sublimate,  so  that  autodigestion  was  at  once  checked,  our  sections 
showed  generally  a more  serious  destruction  of  the  surface  epithe- 
lium than  of  the  gland-cells.  At  times  both  are  so  much  altered 
that  it  is  impossible  to  say  which  is  most  or  least  affected.  It 
seems,  in  chronic  gastritis,  that  new  epithelium  will  be  re-formed 
quite  rapidly  where  the  old  has  been  lost  or  destroyed. 

In  cases  of  suspected  malignant  neoplasm  fragments  of  the 
growth  are  occasionally  found  and  are  of  importance  in  the  diag- 
nosis. In  carcinoma  of  the  cardia  or  the  esophagus  they  are 
most  frequently  found  in  the  lower  or  side  opening  of  the  tube,  as 
it  must  pass  through  or  over  the  growth  on  its  way  into  the 
stomach.  But  even  in  malignant  growths  of  other  parts  of  the 
stomach  patient  searching  in  the  sediment  of  the  wash-water  will 
sometimes  reward  the  clinician  by  the  discovery  of  tumor  frag- 
ments. Of  the  first  wash-water  in  the  morning,  about  50OC.C.  should 


HISTOLOGICAL  CONDITIONS  PRESENT. 


1 47 


be  permitted  to  settle  twelve  hours  in  a conical  glass  such  as  is 
used  for  the  settling  of  solid  urinary  constituents,  or  the  gastric 
contents  should  be  brought  to  settle  out  minute  particles  by  use 
of  the  centrifuge.  The  sediment  should  be  examined  under  a low 
power  (about  fifty  diameters).  The  centrifuge  is  preferable,  as 
long  standing  of  the  fluid  causes  putrefaction. 

Once  we  made  the  diagnosis  of  carcinoma  when  no  tumor  was 
evident,  from  repeatedly  finding  involuntary  muscle-fibers  when 
no  meat  had  been  eaten  for  six  days  after  thorough  lavage.  Four 
months  later,  at  the  autopsy,  it  proved  to  be  a broad,  flat  carcinoma 
of  the  posterior  wall.  The  method  of  recognition  of  neoplastic 
fragments  will  be  fully  considered  in  the  chapter  on  Carcinoma. 

The  drawing  of  a longitudinal  section  of  the  secreting  gland- 
tubules,  showing  beautifully  the  well-preserved  cylindrical  epithe- 
lium of  the  gastric  surface  and  well-differentiated  oxyntic  and 
chief  cells,  was  made  from  several  sections  of  a piece  of  mucosa  that 
was  torn  loose  by  the  stomach-tube,  inserted  by  a medical  student 
who  tried  to  aspirate,  by  means  of  the  pump,  a meal  that  had  dis- 
agreed with  him.  The  tearing  off  must  have  occurred  in  an  instant, 
as  there  were  no  signs  of  inflammation  in  the  sections.  The 
sections  were  stained  in  a variety  of  ways,  principally  in  the  eosin, 
hematoxylin,  Golgi,  and  Bismarck-brown  stains.  The  minute  com- 
munications of  the  oxyntic  or  parietal  cells  with  the  central  duct 
are  best  brought  out  by  the  Golgi  method  (see  frontispiece). 

The  drawings  of  fragments  found  in  the  wash-water,  illustrating 
glandular  proliferation,  with  glands  closely  packed  and  connective- 
tissue  diminished,  and  of  glandular  atrophy,  mucoid  degeneration, 
vacuolization,  and  small-cell  infiltration,  are  all  explained  by  the 
text  accompanying  the  illustrations.  We  have  seen  that  histologi- 
cal changes  approaching  or  actually  representing  pathological 
states  may  be  going  on  in  perfectly  healthy  stomachs.  Further- 
more, the  stomachs  of  diseased  patients  may,  on  serial  sections, 
show  a different  pathological  state  at  different  places  of  the  mucosa. 
Therefore  it  must  be  borne  in  mind  that,  although  the  findings  in 
hyperacidity  and  anacidity  appear  to  be  in  some  relation  to  the 
disease,  this  kind  of  investigation  must  not  be  relied  upon  as  rep- 
resenting in  a given  fragment  the  condition  of  the  entire  mucosa. 
It  represents  the  state  of  the  location  whence  it  sequestrated  ; that 
location  not  being  accurately  known,  generalizations  must  be 
made  with  caution. 

It  should  be  emphasized  that  the  most  important  conditions  in 


48 


CHEMISTRY  OF  GASTRIC  CONTENTS. 


these  fragments  are  not  the  number  of  gland-ducts  and  the  state  of 
the  connective  tissue,  but  the  relative  number  of  oxyntic  or  border 
and  chief  or  central  cells.  A fragment  may  show  a normal  or 
subnormal  number  of  gland-ducts,  and  at  the  same  time  these  may 
contain  an  abnormally  large  number  of  cells. 


CHAPTER  XV. 

THE  CHEMISTRY  OF  GASTRIC  DIGESTION. 

Occurrence  of  Secretions  in  the  Empty  Stomach. — Stimulations  to  Secre- 
tions of  Gastric  Juice. — Significance  of  Foam. — Preparation  of 
Gastric  Contents.  — Quantitative  Analysis.  — Methods.  — Standard 
or  Normal  Solutions.  — Indicators. — Titration.  — Apparatus.  * 

Most  authors  are  of  the  opinion  that  no  secretion  is  contained  in 
the  empty  stomach.  Schreiber  (“ Arch.  f.  exper.  Pathol,  u.  Phar.,” 
Bd.  xxiv,  S.  365  ; also,  “ Deutsche  med.  Wochenschr.,”  1894,  Nos. 
18  to  21),  however,  concludes  that  a secretion  is  found  also  in  the 
empty  stomach  ; that  is,  he  denies  a continuous  secretion  or  gastro- 
succorrhea  as  a disease  sui  generis,  and  claims  to  be  able  to  obtain 
60  c.c.  of  a secretion  possessing  good  digestive  power  from  a jejune, 
or  fasting,  stomach. 

Pick  (“  Prager  med.  Wochenschr.,”  1889,  No.  18),  who  obtained 
similar  results,  believed  that  the  secretion  was  set  up  by  the  stim- 
ulation of  the  tube.  Rosin  (“  Deutsche  med.  Wochenschr.,”  1888, 
No.  47),  A.  Hoffmann  (“Berliner  klin.  Wochenschr.,”  1889,  No. 
12),  and  Martius  (“  Deutsche  med.  Wochenschr.,”  1894,  p.  638) 
have  also  obtained  a digestive  secretion  from  the  fasting  stomach. 

Although  there  may  be  found  50  to  60  c.c.  of  a secretion 
possessing  digestive  powers  in  the  empty,  normal  stomachs  of 
perfectly  healthy  individuals,  this  does  not  prove  that  a continued 


* The  section  on  quantitative  chemical  analysis  of  gastric  contents  and  the  chapters  on 
the  condition  of  the  blood  and  urine  in  gastric  diseases  and  on  the  gases  of  the  stomach 
have  been  written  by  my  former  associate,  Dr.  Edward  L.  Whitney,  whose  experience 
as  demonstrator  of  clinical  pathology  has  admirably  fitted  him  for  the  concise  and  clear 
account  of  this  department.  It  gives  me  pleasure  to  express  my  thanks  to  him  for  h’s 
assistance. — (J.  C.  H.) 


GASTRIC  SECRETION  IN  THE  EMPTY  STOMACH.  1 49 

secretion  exists  normally  (Riegel,  “ Deutsche  med.  Wochenschr.,” 
1893,  p.  735).  Leo  (“  Krankheiten  d.  Bauchorgane,”  p.  54)  con- 
siders this  digestive  secretion  a residuum  of  the  last  previous 
meal,  and  seems  to  have  shown  conclusively  that  such  a residuum 
is  constantly  present  in  the  stomachs  of  infants  after  a night’s  sleep 
(see  Leo,  “ Berliner  klin.  Wochenschr.,”  1888,  No.  49).  For  the 
practical  objects  of  diagnosis  he  concludes  that  a secretion  of  50 
to  60  c.c.  of  digestive  fluid  found  in  a fasting  organ  must  not  be 
considered  pathological.  Only  when  the  amount  gained  reaches 
100  to  300  c.c.  does  it  indicate  hypersecretion,  which  is  often 
associated  with  hyperacidity  (Reichmann,  “ Berliner  klin.  Wochen- 
schr.,” 1887,  S.  12;  Bouveret  [ loc . rzV.] ; Debove,  and  Remond, 
“ Les  Maladies  de  l’Estomac  ”).  Riegel  and  Reichmann  do  not 
distinguish  sufficiently  between  so-called  continuous  secretion  of 
gastric  juice  with  a stomach  of  normal  capacity  and  normal  exit 
to  the  duodenum  and  continuous  secretion  which  appears  as  a 
concomitant  symptom  of  gastrectasia  with  probable  pyloric 
stenosis;  Einhorn  asserts  that,  with  more  accurate  differentiation 
between  these  states,  it  will  probably  be  found  that  the  normal 
stomach  in  a fasting  condition  contains  very  little,  if  any,  secretion. 
We  have  studied  a number  of  cases  whose  stomachs  were  of  natural 
size  and  where  there  was  no  disturbance,  but  which  contained  this 
secretion  early  in  the  morning  before  breakfast. 

J.  Schreiber  (“  Deutsche  med.  Wochenschr.,”  1894,  No.  53)  has 
experimented  upon  two  healthy  persons,  before  any  food  had  been 
taken,  and  found  gastric  juice  with  hydrochloric  acid  in  both.  The 
amount  of  secretion  thus  obtained  varied  from  10  to  22  c.c. 
Martius  (“  Deutsche  med.  Wochenschr.,”  1894,  No.  32)  and  Huber 
“ Korrespondenzblatt  f.  Schweizer  Aerzte,”  1894,  No.  49)  confirm 
Schreiber’s  results.  According  to  Ewald,  who  sums  up  the  liter- 
ature (in  Lubarsch  and  Ostertag’s  “ Ergebnisse  d.  spez.  Pathologie,” 
Bd.  hi,  S.  27)  and  gives  his  own  observations  in  a large  number 
of  cases,  this  problem  is  represented  in  the  following  manner:  In 
many  individuals  small  quantities  of  a digestive  secretion  contain- 
ing free  hydrochloric  acid  can  be  obtained  from  the  fasting,  or 
jejune,  stomach.  Sometimes  it  is  mixed  with  bile,  coloring  matter, 
and  duodenal  contents.  But  he  claims  that  the  stimulation  to  this 
secretion  has  been  furnished  by  swallowed  saliva  (Martius),  rem- 
nants of  food,  pharyngeal  secretion,  etc.,  and  that  the  state  of  things 
lies  between  a normal  and  an  abnormal  one,  and  that  there  is  no 
diseased  condition  of  the  gastric  mucosa. 


150 


MEANS  OF  OBTAINING  GASTRIC  SECRETION. 


In  the  case  of  typical  gastrosuccorrhea,  however,  there  is  a much 
increased  irritability  of  the  mucosa,  giving  rise  eventually  to  a pro- 
fuse secretion,  which,  when  found  in  empty  stomachs,  is  quanti 
tatively  more  considerable  than  that  found  in  normal  jejune  stom- 
achs. Huber  compares  it  to  a slow,  gradual  dying  away  of  secre- 
tory irritability  (“Abklingen  des  Sekretionsreizes  ”)  that  has  been 
set  up  by  the  ingesta  and  seems  to  linger  after  they  have  passed 
into  the  duodenum. 

In  order  to  obtain  gastric  secretion  a variety  of  methods  have 
been  suggested : 

By  chemical  stimulation,  according  to  Leube’s  method,  which 
consists  in  allowing  50  c.c.  of  a three  per  cent,  solution  of  sodium 
bicarbonate  to  flow  into  the  stomach.  After  twelve  minutes  this  is 
washed  out  again,  and  should  be  found  neutral.  By  thermic  stimu- 
lation, according  to  Jaworski’s  method,  consisting  of  the  introduc- 
tion of  100  c.c.  of  ice-water  and  washing  it  out  again  after  ten 
minutes,  when  it  should  contain  acid  and  pepsin.  These  methods, 
if  successful  at  all,  bring  out  the  gastric  juice  in  a most  diluted 
state,  and,  therefore,  give  no  adequate  means  of  determining  the 
secretion  by  chemical  analysis.  It  has  been  claimed  by  Einhorn 
(“New  York  Medical  Record,”  November  9,  1 889)  and  Allen  A. 
Jones  {ibid.,  1891)  in  this  country,  and  Hoffmann  (“  Berliner  klin. 
Wochenschr.,”  1889,  No.  13),  Ewald  ( loc . cit.),  and  Ziemssen,  in 
Germany,  that  the  gastric  secretion,  as  evinced  by  the  amount  of 
hydrochloric  acid,  could  be  increased  by  faradic  or  galvanic  stimu- 
lation. While  we  have  our  doubts  about  this  matter,  we  do  not 
wish  to  imply  that  electricity  is  not  a very  valuable  therapeutic 
agent  in  the  treatment  of  secretory  diseases;  we  could  not,  in  fact, 
dispense  with  it  as  an  auxiliary  to  treatment.  In  our  opinion,  the 
influence  of  electricity  on  secretion  is  doubtful. 

As  a means  of  obtaining  gastric  secretion,  this  method  is  certainly 
not  available.  The  normal  secretions  are  best  obtained  by  the 
natural  stimulation  of  one  of  the  test-meals,  as  stated  in  a previous 
chapter. 

Mathieu  and  Remond  (“  Societe  de  Biolog.,”  1890)  have  pub- 
lished a method  of  determining  the  total  quantity  of  stomach  con- 
tents by  finding  out  the  acidity  of  the  undiluted  contents  as  much 
as  can  be  drawn  ; then  that  of  the  contents  as  much  as  can  be 
gained  by  washing  out  the  stomach  with  a known  quantity  of  water, 
and  from  this  the  acidity  of  the  total  amount  of  contents  that  were 
originally  in  the  stomach  are  calculated.  Strauss  (“  Therapeutische 


PREPARATION  OF  GASTRIC  CONTENTS. 


151 


Monatshefte,”  Miirz,  1895)  has  simplified  this  procedure,  but  for 
the  practitioner  it  is  sufficient  to  know  the  amount  gained  by  the 
simple  methods  of  drawing  the  contents  by  expression  or  aspira- 
tion. Concerning  the  recognition  of  proteid  and  carbohydrate  in- 
digestion from  the  food-remnants,  it  should  be  added  that  this  is 
much  facilitated  by  the  double  test-meal  used  at  the  University  of 
Maryland  Hospital. 

In  gastrectasias  presence  of  foam  indicates  gas-fermentation. 
Gas  may  be  found  even  in  presence  of  normal  or  supernormal 
amount  of  hydrochloric  acid,  since  F.  Kuhn  (“  Zeitschr.  f.  klin. 
Med.,”  Bd.  xxi,  and  “ Deutsche  med.  Wochenschr.,”  1892,  No.  49) 
has  demonstrated  that  the  hydrochloric  acid  of  gastric  juice  has 
no  detrimental  effect  on  large  amounts  of  yeast.  Whenever  there 
is  stagnation  of  gastric  contents  this  gas-formation  can  occur. 

After  the  contents  of  the  stomach  are  withdrawn,  they  must  be 
prepared  for  and  submitted  to  chemical  examination.  The  contents 
may  be  beaten  up  thoroughly  to  make  a homogeneous  mixture, 
and  the  chemical  examinations  conducted  on  this  mixture ; or  this 
mixture  may  be  filtered  and  the  clear  filtrate  subjected  to  analysis. 
The  former  method  gives  more  accurate  results,  with  slightly 
higher  acidity,  than  the  latter  method,  which  has  the  advantage, 
however,  of  allowing  better  observation  of  color  changes  in  the 
solution  during  titration. 

Before  entering  upon  a discussion  of  the  chemical  methods  as 
applied  to  the  gastric  juice,  a short  description  of  the  methods, 
solutions,  and  apparatus  required  in  quantitative  analysis  will  be 
given. 

The  solutions  required  can  be  made  up,  and,  if  preserved  from 
the  influence  of  light  and  air,  kept  indefinitely. 

The  methods  used  in  quantitative  chemical  analysis  may  be 
divided  into  two  general  classes : Gravimetric  and  Volumetric.  The 
gravimetric  methods  consist  in  the  isolation  of  the  substance  or 
one  of  its  compounds,  which  is  weighed.  The  isolation  of  sub- 
stances in  a pure  state  often  requires  long  training  in  chemical 
methods,  and  if  only  a small  amount  of  the  substance  in  question  is 
present  it  may  be  very  difficult  to  separate  a weighable  amount. 
Many  substances  can  not  be  separated  from  mixtures  without  losing 
at  the  same  time  their  relation  to  other  substances  in  the  same  solu- 
tion. The  great  objection  to  the  gravimetric  methods,  however,  is 
the  large  amount  of  costly  apparatus  necessary,  and  the  length  of 
time  needed  for  the  manipulations. 


152 


STANDARD  SOLUTIONS. 


The  volumetric  methods  are  more  easily  performed.  In  these  the 
quantity  of  the  substance  under  examination  is  ascertained  by  a 
calculation  based  upon  a measured  quantity  of  a solution  of  a 
known  strength  required  to  perform  a certain  reaction  with  it. 

These  solutions,  called  standard  solutions,  are  of  two  kinds — 
normal  solutions  and  empirical  solutions. 

A normal  solution  is  one  which  contains  in  a liter  that  quantity  of 
the  active  reagent  expressed  in  grams  which  equals  the  sum  of  the 
atomic  weights  of  the  constituents  that  combine  with  one  atom  of 
hydrogen.  Thus  the  normal  solution  of  HC1  is  a liter  of  distilled 
water  containing  36.5  grams  c.p.  HC1  (H  = 1,  Cl  = 35-5)  in  solution. 

Decinormal  solutions,  N10,  are  one-tenth  the  strength  of  normal 
solutions. 

Centinormal  solutions,  N100,  are  one-hundredth  the  strength  of 
normal  solutions. 

Empirical  solutions  are  those  which  do  not  contain  an  exact 
atomic  proportion  of  the  reagent,  but  are  made  up  of  such  strength 
that  one  c.c.  is  equivalent  to  some  definite  weight  of  the  substance 
sought.  . 

Residual  titration,  or  back  titration,  consists  in  treating  the  sub- 
stance under  examination  with  standard  solution  in  excess  of  that 
known  to  be  required  ; the  excess  is  then  ascertained  by  residual 
titration  with  another  standard  solution. 

In  general,  titration  results  in  the  formation  of  a compound  that 
can  readily  be  distinguished  by  its  properties  from  those  substances 
present  in  either  solution. 

1.  It  may  form  a precipitate. 

2.  It  may  cause  the  complete  solution  of  some  precipitate. 

3.  A slight  excess  of  either  reagent  may  produce  some  visible 
change  in  some  constituent  of  the  solution,  or  a change  in  some 
substance  added  for  the  purpose  (indicators). 

4.  The  indicator  in  some  cases  can  not  be  added  to  the  solution, 
but  from  time  to  time  a few  drops  of  the  solution  are  added  to  the 
indicator  on  a watch-glass  at  the  side. 

Of  the  above,  the  normal  solution  is  the  most  used,  the  empirical 
solution  being  only  of  limited  application. 

It  would  seem  a simple  matter  to  make  up  a standard  solution 
which  would  be  perfectly  accurate,  but  in  practice  the  problem  re- 
quires experience.  Absolutely  pure  chemicals  are  not  easily  ob- 
tained, and  such  as  are  easily  obtained,  unmixed  with  other  mineral 
substances,  contain  a variable  amount  of  water,  and  are,  moreover, 


DECINORMAL  SOLUTIONS. 


153 


exposed  to  more  or  less  danger  of  contamination  from  the  impuri- 
ties of  the  air.  The  following  methods  of  obtaining  a tenth-normal 
solution  are  recommended  as  a basis  for  the  preparation  of  other 
solutions  : 

I.  Pure,  dry  oxalic  acid  is  obtained,  and  the  crystals  that  show  no 
sign  of  efflorescence  selected.  From  the  formula,  C2H204  -{-  2H20, 
it  is  seen  that  the  molecular  weight  is  126,  and  as  it  is  a dibasic 
acid  the  normal  solution  would  contain  one-half  of  this  (63  gm.) 
dissolved  in  distilled  water  and  made  up  to  one  liter  at  a temper- 
ature of  1 50  C.  As  a tenth-normal  (Ni0)  solution  is  required,  one- 
tenth  of  this,  or  6.3  gm.,  are  made  up  to  a liter  as  before,  and  used 
to  correct  the  solutions  employed  in  analysis.  It  must  be  noticed 
that  oxalic  acid  in  dilute  solution  soon  decomposes;  it  is,  therefore, 
to  be  freshly  prepared  as  required. 

To  prepare  an  equivalent  solution  of  caustic  soda  (decinormal 
NaOH)  about  five  gm.  of  caustic  soda  are  dissolved  in  about  900  c.c. 
of  distilled  water  and  well  mixed.  To  this  there  is  added  lime- 
water  or  baryta-water,  Ca(OH)2  or  Ba(OH)2,  as  long  as  a precipi- 
tate forms,  to  get  rid  of  carbonates  or  sulphates.  The  solution  is 
allowed  to  stand  until  the  impurities  have  settled.  Twenty-five 
c.c.  of  the  solution  are  then  measured  with  a pipette  into  a clean 
flask  or  beaker  and  titrated  with  the  above  solution  of  oxalic  acid, 
using  a few  drops  of  phenolphthalein  as  an  indicator,  until  the  red 
color  of  the  solution  just  disappears.  The  solution  is  then  diluted 
to  the  strength  of  a decinormal  solution. 

As  an  illustration  of  the  method  of  ascertaining  the  amount  of 
dilution  necessary  to  make  the  two  solutions  exactly  equivalent, 
we  will  suppose  that  the  25  c.c.  of  caustic  soda  solution  required 
28.3  c.c.  of  the  oxalic  acid  solution  to  cause  the  red  color  to  disap- 
pear. If  25  c.c.  of  the  caustic  soda  solution  neutralize  28.3  c.c.  of 
the  acid  solution,  then  the  amount  of  caustic  soda  solution  necessary 
to  neutralize  1000  c.c.  of  the  acid  solution  will  be  found  by  the  fol- 
lowing proportion  : 

28.3  : 25  : : iooo  : (X)  X = 883.4 

X = amount  of  caustic  soda  solution  necessary  for  1000  N10 
NaOH.  Dilute  883.4  c.c.  of  the  caustic  soda  to  1000  c.c.  with  dis- 
tilled water. 

After  diluting  the  solution  it  should  be  again  titrated  to  insure 
its  accuracy,  and,  if  properly  standardized,  it  will  change  from 
red  to  colorless,  and  vice  versa,  by  the  addition  of  a drop  or 


154 


INDICATORS. 


two  of  the  acid  or  alkaline  solutions,  respectively.  The  titration 
should  be  conducted  as  rapidly  as  possible  to  avoid  the  error  pro- 
duced by  absorption  of  C02  from  the  air,  and  the  solutions  kept  in 
well-stoppered  bottles  for  the  same  reason. 

2.  About  eight  gm.  of  pure,  dry  sodium  carbonate  are  heated  in  a 
platinum  crucible  for  ten  minutes  at  a dull-red  heat,  stirring  occa- 
sionally with  a platinum  wire.  After  heating,  it  is  powdered  in  a 
warm  mortar  and  allowed  to  cool  in  a desiccator.  When  cool,  5.3 
gm.  of  the  powder  are  weighed  rapidly,  washed  into  a flask  with 
hot  distilled  water,  and  made  up  to  a liter.  This  constitutes  a 
decinormal  solution  of  sodium  carbonate. 

A decinormal  solution  of  sulphuric  acid  is  prepared  in  the  follow- 
ing manner  : About  three  c.c.  of  the  pure  acid,  of  a specific  gravity 
of  1.840,  is  made  up  to  about  900  c.c. 

The  approximate  solution  is  standardized  against  the  sodium 
carbonate  solution  prepared  as  above,  using  a drop  or  two  of  a 
0.1  per  cent,  solution  of  methyl-orange  as  an  indicator.  Twenty- 
five  c.c.  of  the  acid  solution  is  titrated  with  the  decinormal  sodium 
carbonate  until  the  red  color  shown  by  this  indicator  in  acid  solu- 
tion turns  to  a light  yellow.  The  correction  of  the  approximate 
solution  is  made  from  a proportion  upon  exactly  the  same  principle 
as  in  the  former  case  (No.  1). 

To  correct  this  decinormal  solution  of  sulphuric  acid  for  very 
accurate  work,  the  following  method  is  recommended  : One  hun- 
dred c.q.  of  the  decinormal  solution  of  sulphuric  acid  is  alkalinized 
with  a strong  solution  of  pure  ammonia  (ammonium  hydrate).  The 
solution  is  evaporated  on  the  water-bath,  heated  to  105 0 C.  in  hot- 
air bath,  cooled,  and  weighed.  The  amount  of  sulphuric  acid  is 
calculated  from  the  amount  of  ammonium  sulphate  formed. 

Indicators. — An  indicator  is  a substance  used  in  volumetric  an- 
alysis, which  marks,  by  change  of  color  or  some  other  visible 
effect,  the  exact  point  at  which  a given  reaction  is  complete. 

Generally  the  indicator  is  added  to  jthe  substance  under  exami- 
nation, but  in  a few  cases  it  is  used  outside,  a drop  of  the  solution 
being  brought  in  contact  with  a drop  of  the  indicator. 

The  particular  uses  of  the  indicators  will  be  more  fully  explained 
in  their  proper  places,  under  the  quantitative  examination  of  the 
gastric  juice ; but  the  chief  ones  in  use  in  such  examinations  may 
be  briefly  mentioned : 

Tincture  of  litmus,  which  turns  red  in  acid  solution ; blue  in  an 


APPARATUS.  155 

alkaline  solution.  It  is  used  in  solution,  and  also  in  the  form  of 
test-papers.  (It  is  not  used  when  carbonates  are  present.) 

Phenolphthalein  solution,  a one  per  cent,  solution  of  phenol- 
phthalein  in  alcohol,  colorless  in  acid  solutions,  red  in  alkaline 
solutions.  It  is  not  reliable  for  alkaline  phosphates,  bicarbonates, 
or  ammonia. 

Methyl-orange  solution,  a 0.1  per  cent,  solution  of  methyl- 
orange  in  water,  turns  red  with  acids,  yellow  with  alkalies.  It  is 
not  affected  by  carbonic  acid,  and  is  valuable  for  titration  of  alka- 
line carbonates. 

The  other  indicators  and  their  uses  in  analysis  of  the  gastric 
juice  will  be  mentioned  later. 

Apparatus . — The  apparatus  needed  for  volumetric  work  is  com- 
paratively simple — burettes,  measuring-flasks,  measuring-cylinders, 
and  pipettes.  An  accurate  balance  is  required  in  all  chemical 
work,  delicate  to  a milligram  and  weighing  up  to,  say,  50  gm. 
Burettes  are  glass  tubes  graduated  to  tenths  of  a c.c.  and  holding 
from  25  to  100  c.c.  They  are  provided  at  the  lower  end  with  a 
rubber  tube  and  pinch-cock,  by  means  of  which  the  amount  of  the 
solution  can  be  accurately  regulated.  The  tube  is  graduated  upon 
its  outer  surface,  and  the  amount  of  the  solution  used  can  be  read 
off  from  this  graduation.  The  simplest  form  of  burette  is  the  one 
already  described,  known  as  Mohr’s,  of  which  various  modifications 
are  in  use. 

The  burette  should  be  placed  perfectly  perpendicular,  and  firmly 
fastened.  Fill  by  a funnel,  the  stem  resting  against  the  inner  sur- 
face of  the  burette  to  avoid  the  formation  of  bubbles.  Always  fill 
above  the  zero  mark ; gently  tap  the  burette  until  the  bubbles  dis- 
appear should  they  be  formed.  Then  run  out  a small  portion  (or 
down  to  the  zero  mark),  remembering  to  run  out  enough  to  re- 
move all  air-bubbles  from  the  bottom  of  the  burette. 

In  reading  the  results,  always  read  from  the  bottom  of  the 
meniscus  formed  by  the  rising  of  the  outer  borders  of  the  liquid 
along  the  sides  of  the  burette. 


156 


TESTS  FOR  PRESENCE  OF  FREE  ACIDS. 


CHAPTER  XVI. 

CHEMICAL  EXAMINATION  OF  GASTRIC  JUICE. 

Tests  for  Presence  of  Free  Acids.  — Tests  for  Free  Hydrochloric 
Acid.  — The  Dimethy l- Amido-Azo- Benzol  Test. — The  Resorcin 
Test. — Combined  Hydrochloric  Acid. — Lactic  Acid: 
Formation , Significance , Detection. 

Reaction. — The  reaction  of  the  gastric  juice,  obtained  by  means 
of  the  stomach-tube  or  otherwise,  after  the  administration  of  a test- 
meal,  is  always  acid  in  the  normal  individual.  The  reaction  is  best 
determined  by  dipping  into  the  juice  a piece  of  very  delicate  blue 
litmus-paper.  In  juice  of  acid  reaction  the  paper  immediately 
turns  red.  Very  rarely  is  the  reaction  alkaline,  this  being  found 
only  in  a few  cases  of  atrophy  of  the  gastric  mucosa,  occasionally 
in  acute  gastritis,  and  when,  for  some  reason,  a portion  of  the 
intestinal  contents  and  the  alkaline  bile  has  been  forced  through 
the  pylorus  in  sufficient  quantity  to  neutralize  the  acid  of  the 
stomach. 

In  severe  cases  of  gastric  atrophy  the  reaction  is  usually  acid, 
even  in  absence  of  fermentative  changes.  This  is  due  to  the 
presence  of  acid  salts,  such  as  acid  sodium  phosphate  (NaH2P04), 
and  of  traces  of  organic  acids,  which  occur  in  nearly  every  test- 
meal  in  quantities  sufficient  to  produce  an  acidity  of  from  six  to 
ten  degrees. 

Tests  for  Presence  of  Free  Acids. — A delicate  test  for  the 
presence  of  free  acids  is  found  in  Congo-red.  This  substance 
occurs  as  a fine  reddish-brown  powder,  dissolving  readily  in  water 
to  form  a clear  deep-red  solution,  which  changes  in  the  presence 
of  free  acids  to  a dark  blue.  It  may  be  used  in  two  ways  as  an 
indicator. 

1.  A solution  is  prepared  by  dissolving  one  gm.  of  the  powder 
in  ioo  c.c.  of  water,  and  adding  a drop  to  a few  c.c.  of  the  gastric 
juice.  If  the  juice  contains  even  a slight  trace  of  free  hydrochloric 
acid,  or  the  organic  acids  in  slightly  larger  quantities,  the  solution 
immediately  turns  a bright  blue. 

2.  A test-paper  may  be  prepared  by  soaking  bibulous  paper  in 
the  above  solution  of  the  dye  for  several  hours  and  then  carefully 


TESTS  FOR  FREE  HCl. 


157 


drying.  This  paper  is  simply  dipped  into  the  filtrate  or  into  the 
contents  before  filtration,  and  exhibits  the  same  color  reaction  as 
the  solution  mentioned  above,  and  has  the  additional  advantages  of 
being  more  convenient  and  exhibiting  as  readily  slight  changes  in 
color.  It  has  been  found,  also,  that  when  the  acidity  is  due  to 
organic  acids  and  not  to  free  hydrochloric  acid,  the  color  can  be 
made  to  disappear  by  warming  gently  over ’the  open  flame.  If  the 
acidity  is  due  to  hydrochloric  acid,  on  the  contrary,  the  dark-blue 
stain  on  the  paper  changes  to  a lighter  tint,  but  does  not  disappear 
except  when  strongly  heated. 

It  must  be  emphasized  that  this  color-change  from  red  to  blue 
does  not  occur  in  solutions  of  acid  salts  or  in  the  presence  of  com- 
bined hydrochloric  acid,  and  therefore  indicates  the  presence  of 
some  free  acid — inorganic  or  organic. 

Tests  for  Free  Hydrochloric  Acid. — Many  tests  have  been 
proposed  for  free  hydrochloric  acid,  the  following,  given  in  the 
order  of  their  accuracy  and  delicacy,  being  probably  the  most  re- 
liable : 


1.  Dimethyl-amido-azo-benzol 0.02  pro  1000 

2.  Phloroglucin-vanillin 0.05  “ 

3.  Resorcin 0.05  “ 


The  Dimethyl-Amido-Azo-Benzol  Test. — This  test,  recently 
introduced  by  Topfer,  is  probably  destined  to  replace  all  others  in 
the  clinical  laboratory,  both  on  account  of  its  simplicity  and  also 
on  account  of  its  ready  application  to  the  direct  quantitative  esti- 
mation of  the  amount  of  free  hydrochloric  acid  in  the  gastric  juice. 
This  indicator  occurs  in  the  form  of  a brown  powder,  readily  solu- 
ble in  alcohol,  only  slightly  soluble  in  water.  A few  drops  of  the 
alcoholic  solution,  added  to  a solution  of  hydrochloric  acid,  turns 
a bright  cherry-red,  increasing  in  intensity  as  the  strength  of  the 
acid  solution  is  increased.  In  the  absence  of  free  hydrochloric 
acid  or  other  mineral  acid  the  solution  turns  a bright  lemon- 
yellow. 

In  actual  practice  a 0.5  per  cent,  solution  of  the  substance  in 
alcohol  is  employed.  A few  drops  of  this  solution  are  added  to 
the  stomach  contents,  which  need  not  be  filtered  for  this  purpose, 
or  to  the  residue  left  in  the  receptacle  in  which  the  stomach  con- 
tents were  received.  If  free  hydrochloric  acid  is  present  the  cherry- 
red  color  develops  and  spreads  in  beautiful  rings  from  each  drop 
of  the  indicator,  usually  leaving  in  the  center  a clear,  yellow  area. 


58 


DIMETHYL-AMIDO-AZO-BENZOL. 


In  case  the  indication  is  doubtful,  the  following  modification  may 
be  employed : A small  porcelain  evaporating  dish  (or  white  butter 
plate)  is  thoroughly  rinsed  with  distilled  water  and  dried.  Upon 
one  side  of  the  dish  a few  drops  of  the  filtrate  are  placed,  and  upon 
the  opposite  side  a single  drop  of  the  indicator.  By  inclining  the 
dish  gently  the  two  solutions  may  be  made  to  mix,  and  at  the  line 
of  junction  the  cherry-red  color  may  be  seen,  the  white  background 
rendering  the  detection  of  the  tint  less  difficult. 

It  has  been  stated  by  Einhorn  and  others  that  this  test  is  liable 
to  mislead  in  cases  in  which  there  is  a large  amount  of  organic 
acidity.  It  is  true  that  in  the  presence  of  lactic  acid  amounting  to 
0.2  per  cent,  or  more  in  gastric  juice  this  test  yields  a red  color, 
resembling  that  due  to  inorganic  acids  ; but  the  objection  is  more 
theoretical  than  real,  as  the  presence  of  such  an  amount  of  organic 
acids  seldom  occurs  in  the  stomach,  and  in  the  presence  of  proteids, 
peptones,  mucin,  etc.,  still  stronger  solutions  of  the  organic  acids 
are  required  to  produce  the  characteristic  reaction. 

Furthermore,  the  quantitative  estimation  of  organic  acidity,  to  be 
described  presently,  will  show  the  necessity  of  employing  further 
tests  for  the  presence  of  free  hydrochloric  acid,  on  account  of  a 
specially  great  acidity  of  organic  acids,  which  does  not,  as  a rule, 
occur  in  a stomach  secreting  a normal  amount  of  hydrochloric  acid. 

The  Phloroglucin-vanillin  Test. — The  modification  of  this  test 
proposed  by  Boas  gives  the  most  satisfactory  results.  Two  gm. 
of  phloroglucin  and  one  gm.  of  vanillin  are  dissolved  in  ioo  gm. 
of  80  per  cent,  alcohol.  The  solution  must  be  kept  in  a dark- 
colored,  well-stoppered  bottle,  as  it  soon  decomposes  when  ex- 
posed to  the  light.  The  original  Giinzberg  formula  was  composed 
of  the  same  amount  of  the  ingredients  dissolved  in  30  c.c.of  abso- 
lute alcohol.  This  solution  still  more  readily  undergoes  decompo- 
sition, and  has  no  advantages  over  the  above  modification.  The 
solution  is  employed  in  the  following  manner:  Four  or  five  drops 
of  the  reagent  are  mixed  on  a small  porcelain  dish  or  small 
butter  plate  with  an  equal  amount  of  the  filtered  gastric  juice  or 
the  unfiltered  gastric  contents.  This  is  placed  on  a water-bath, 
kept  just  below  the  boiling  point,  and  evaporated  slowly.  If  free 
hydrochloric  acid  be  present  in  the  proportion  of  0.05  pro  thousand 
or  more,  a fine  rose  tint  will  develop  at  the  edge  of  the  drop  where 
the  mixture  is  dried. 

The  mixture  may  be  evaporated  over  a naked  flame  with  the 
same  results,  provided  the  temperature  is  not  raised  above  the 


RESORCIN  TEST  FOR  FREE  HCl. 


159 


boiling  point.  If  too  much  heat  is  applied,  a brown  or  brownish- 
red  color  may  develop,  which  resembles  the  color  produced  where 
free  hydrochloric  acid  is  absent.  The  rose  color  produced  by  this 
reagent  comes  only  from  free  mineral  acids ; organic  acids,  acid 
salts,  combined  hydrochloric  acid,  peptone,  and  albumose  produce 
only  a brown  or  yellowish  discoloration. 

The  Resorcin  Test. — The  solution  consists  of  five  gm.  of 
resorcin  (resublimed),  and  three  gm.  of  cane  sugar  dissolved  in 
100  c.c.  of  94  per  cent,  alcohol.  Six  drops  of  the  filtered  gas- 
tric juice  and  three  drops  of  the  solution  are  mixed  on  a porcelain 
plate  and  slowly  evaporated  as  in  the  phloroglucin-vanillin  (Giinz- 
berg)  test.  Care  here  must  also  be  employed  that  too  much  heat  is 
not  applied,  as  heating  too  strongly  simply  yields  a brown  or  black 
deposit.  If  the  operations  be  properly  conducted  and  free  hydro- 
chloric acid  be  present,  a fine  vermilion  line  forms  at  the  edge 
of  the  drops,  following  down  the  edge  of  the  solution  as  evapora- 
tion proceeds,  while  the  color  at  the  periphery  gradually  fades, 
disappearing  entirely  after  a short  time,  leaving  a reddish-brown 
stain.  This  test  has  the  same  degree  of  delicacy  as  the  phloro- 
glucin-vanillin test  and  the  advantage  of  much  greater  stability, 
retaining  its  delicacy  for  months,  while  the  latter  lasts  only  a few 
weeks. 

Many  other  tests  might  be  mentioned,  some  of  them  much  less 
delicate,  among  them  Tropaeolin  00,  Mohr’s  reagent,  methyl-violet, 
and  emerald-green,  but  the  three  described  will  be  found  the  most 
reliable  and  easily  applied. 

Combined  Hydrochloric  Acid. — If  albuminous  bodies  are 
treated  with  a weak  solution  of  hydrochloric  acid,  it  is  found 
that  a certain  amount  of  the  hydrochloric  acid  combines  with 
them  to  form  compounds  which  do  not  give  the  reactions  of 
free  hydrochloric  acid.  In  other  words,  certain  affinities  of  the 
albuminous  substance  must  be  saturated  before  hydrochloric  acid 
appears  in  the  free  state.  In  the  stomach  the  same  reaction  must 
take  place,  probably  to  a greater  extent,  due  to  the  more  com- 
plicated chemical  processes  through  which  these  substances 
pass.  This  is  shown  by  the  fact  that  even  after  a simple  test-meal 
a certain  amount  of  time  elapses  before  the  presence  of  free  hydro- 
chloric acid  can  be  demonstrated.  In  the  Ewald  meal  from  twenty 
to  forty  minutes  elapse  before  free  hydrochloric  acid  can  be  dem- 
onstrated in  the  normal  individual,  while  in  the  more  complex 
meals  considerably  more  time  is  required.  This  form  of  hydro- 


l6o  LACTIC  ACID  FORMATION,  ETC. 

chloric  acid  is  important,  inasmuch  as  it  constitutes  a part  of  the 
physiological  hydrochloric  acid,  and  stomach  digestion  will  pro- 
ceed in  a fairly  normal  manner,  if  enough  hydrochloric  acid  is 
secreted  to  saturate  these  affinities,  while  not  enough  is  secreted  to 
form  the  excess  or  reserve  supply  called  free  hydrochloric  acid. 
It  is  evident,  therefore,  that  if  free  hydrochloric  acid  be  present,  all 
these  affinities  must  be  saturated,  while  in  its  absence  some 
hydrochloric  acid,  enough  to  more  or  less  saturate  these  affinities, 
may  have  been  secreted.  The  entire  absence  of  hydrochloric  acid, 
both  free  and  combined,  if  more  than  temporary,  is  a serious 
condition,  indicating  an  atrophy  of  the  gastric  mucosa,  a severe 
gastric  catarrh,  achylia  gastrica,  or,  perhaps,  cancer.  From  these 
considerations  it  will  be  seen  how  important  the  determination  of  the 
combined  hydrochloric  acid  is,- in  all  conditions  of  anacidity.  The 
estimation  and  quantitative  determination  of  the  combined  hydro- 
chloric acid  will  be  deferred  to  the  paragraphs  devoted  to  the  quan- 
titative determination  of  hydrochloric  acid. 

The  amount  of  pure  hydrochloric  acid  necessary  to  combine 
with  ioo  gm.  (or  ioo  c.c.)  of  the  various  food-stufifs  will  be  given 
in  the  chapter  on  the  Therapy  of  HC1. 

Lactic  Acid:  Formation,  Significance,  Detection. — It  was 
formerly  supposed  that  lactic  acid  was  secreted  by  the  stomach, 
but  by  the  more  accurate  investigations  of  later  years  it  has  been 
shown  beyond  doubt  that  lactic  acid  in  the  gastric  contents  is  either 
introduced  as  such  in  the  food  or  is  the  product  of  abnormal  fer- 
mentative changes  in  the  food  after  ingestion. 

Lactic  acid  may  be  introduced  in  food  either  as  sarcolactic  acid 
from  meat  or  fermentation  lactic  acid  found  in  bread  and  other 
starchy  foods.  Lactic  acid  may  be  formed  after  the  food  is  ingested, 
in  cases  of  carcinoma  of  the  stomach,  and  probably  also  in  small 
amounts  in  other  conditions,  of  subacidity  or  anacidity  associated 
with  deficient  motility. 

In  the  great  majority  of  cases  of  carcinoma  of  the  stomach 
lactic  acid  is  present  in  considerable  amounts,  except  in  those  cases 
in  which  the  motility  is  not  impaired.  In  such  cases  only  a small 
amount  of  lactic  acid  can  usually  be  demonstrated  ; sometimes 
it  is  absent.  There  are  cases  of  carcinoma  of  the  fundus  or 
body  of  the  stomach  in  which  the  motility  is  so  good  that  at  the 
end  of  one  hour  no  remains  of  the  test-meal  can  be  regained. 

Traces  of  lactic  acid  can  usually  be  detected  for  some  time 
after  the  administration  of  the  Ewald  breakfast  or  similar  meals, 


RECOGNITION  OF  LACTIC  ACID.  1 6 1 

though  at  the  height  of  digestion  the  usual  tests  are  negative,  due 
either  to  the  absorption  of  the  lactic  acid,  or  the  interference  of  free 
hydrochloric  acid,  or  the  products  of  digestion  with  the  delicacy 
of  the  tests.*  In  cases  in  which  it  is  desirable  to  prove  the  forma- 
tion of  lactic  acid  within  the  stomach,  it  is  necessary  to  employ 
some  meal  which  is  entirely  free  from  lactic  acid. 

Such  a meal  has  been  proposed  by  Boas,  consisting  of  oatmeal- 
gruel  to  which  only  a little  salt  has  been  added.  The  stomach  is 
washed  out  on  the  evening  preceding  the  administration  of  the 
meal  until  no  food-particles  can  be  found,  the  gruel  given  in  the 
morning,  and  the  contents  removed  one  hour  after. 

Only  rarely,  under  such  conditions,  is  any  notable  amount  of 
lactic  acid  to  be  demonstrated  except  in  cases  of  carcinoma  of  the 
stomach.  The  easiest  clinical  test  for  the  presence  of  lactic  acid  is 
that  of  Uffelmann.  Ten  c.c.  of  a four  per  cent,  solution  of  carbolic 
acid  are  mixed  with  twenty  c.c.  of  water,  and  a drop  of  a strong 
solution  of  ferric  chlorid  added.  A beautiful  amethyst-blue  color 
is  produced,  which  turns  a canary-yellow  when  treated  with  a solu- 
tion of  lactic  acid  or  gastric  juice  containing  lactic  acid.  The  delicacy 
of  this  test  is  interfered  with  by  the  presence  of  free  hydrochloric 
acid  and  peptones.  Glucose,  acid  phosphates,  citric  acid,  and 
alcohol  give  a reaction  resembling  that  of  lactic  acid,  butyric  acid 
giving  a much  lighter  tint.  In  case  of  doubt,  a modification  that 
has  given  good  results  is  the  following:  Five  or  ten  c.c.  of  the 
filtered  gastric  juice  are  treated  with  ten  times  their  volume  of  ether, 
free  from  alcohol,  and  then  shaken  in  a stoppered  separating  funnel 
for  fifteen  or  twenty  minutes  and  allowed  to  stand  till  the  layers 
have  separated.  The  ethereal  solution  is  allowed  to  evaporate,  the 
residue  dissolved  in  five  or  ten  c.c.  of  water,  and  the  solution  tested 
for  lactic  acid  as  above.  While  this  test  is  not  a very  delicate  one, 
lactic  acid,  when  present  in  considerable  amounts,  gives  a more 
decided  reaction  than  any  of  the  substances  mentioned  as  having  a 
similar  reaction,  and  it  is  a good  test  for  clinical  purposes. 

Boas’  method  is  to  be  employed  in  doubtful  cases.  This  method 
is  based  upon  the  fact  that  when  lactic  acid  is  treated  with  strong 
oxidizing  agents,  formic  acid  and  acetic  aldehyd  are  formed  : 

C3H603  = CH3COH  + HCOOH. 


* Sticker  (“  Munch,  med.  Wochenschr. 1896,  No.  26)  has  shown  that  passage  of 
carbohydrates  through  the  mouth  is  followed,  without  exception,  by  the  formation  of 
more  or  less  lactic  acid. 


62 


DETECTION  OF  LACTIC  ACID. 


Acetic  aldehyd  may  be  easily  recognized  by  its  action  on  Ness- 
ler’s  reagent,  or  upon  an  alkaline  solution  of  iodin  in  iodid  of 
potassium.  Nessler’s  reagent  is  prepared  in  the  following  manner: 

One  hundred  c.c.  of  a four  per  cent,  solution  of  iodid  of  potas- 
sium are  warmed,  and  while  warm  treated  with  iodid  of  mercury 
until  a small  amount  remains  undissolved.  After  cooling,  40  c.c. 
of  water  are  added.  Two  parts  of  this  solution  are  then  treated 
with  three  parts  of  a strong  solution  of  caustic  potash  ; any  precipi- 
tate which  may  form  is  filtered  off  and  the  reagent  kept  in  a well- 
stoppered  bottle. 

The  solution  of  iodin  is  prepared  by  mixing  a solution  of  iodin 
in  iodid  of  potassium  with  caustic  potash  or  potassium  carbonate. 

Method. — The  filtered  gastric  juice  is  tested  for  the  presence  of 
free  acids  as  above,  and,  if  present,  10  or  20  c.c.  are  treated  with  an 
excess  of  barium  carbonate.  If  no  free  acids  are  present,  this  is  not 
necessary.  The  solution  is  now  evaporated  to  a syrup  on  the 
water-bath  to  drive  off  the  fatty  acids.  The  syrup  is  treated  with 
a few  drops  of  phosphoric  acid  and  brought  to  a boiling  point  to 
expel  carbon  dioxid.  After  cooling  it  is  extracted  with  100  c.c.  of 
ether  free  from  alcohol  by  shaking  for  half  an  hour.  After  stand- 
ing for  a short  time  to  allow  separation  to  take  place,  the  ethereal 
layer  is  drawn  off  and  evaporated  (avoiding  a flame),  the  residue 
taken  up  in  45  c.c.  of  water,  shaken,  and  filtered.  The  filtrate  is 
treated  in  an  Erlemeyer  flask  with  5 c.c.  of  strong  sulphuric  acid 
and  as  much  black  oxid  of  manganese  as  will  lie  on  the  point  of  a 
knife-blade.  The  flask  is  closed  with  a perforated  stopper,  in 
which  is  placed  a bent  glass  tube,  the  long  arm  passing  into  a 
cylinder  filled  with  10  or  15  c.c.  of  Nessler’s  reagent  or  alkaline 
iodin  solution  prepared  as  described.  Carefully  heat  the  flask,  and 
if  lactic  acid  is  present  aldehyd  will  distil  over,  forming  aldehyd 
mercury,  yellowish  red  in  color,  if  Nessler’s  reagent  is  used,  and 
yellowish  crystals  of  iodoform,  which  may  be  recognized  by  their 
odor,  if  the  alkaline  solution  of  iodin  is  employed. 

Butyric  acid  can  usually  be  determined  by  its  odor  alone, 
which  is  that  of  rancid  butter.  In  case  of  doubt,  10  c.c.  of  the 
gastric  juice  are  extracted  with  50  c.c.  of  ether,  the  ethereal  solu- 
tion evaporated,  and  the  residue  taken  up  with  water.  The  odor  is 
more  evident  in  this  concentrated  aqueous  solution.  A small 
amount  of  calcium  chlorid  causes  the  separation  of  an  oily  layer 
of  butyric  acid  ; strong  mineral  acids  also  separate  the  oily  layer 
or  drops  of  the  acid. 


QUANTITATIVE  ANALYSIS  OF  THE  STOMACH  ACIDS.  1 63 

Acetic  acid  may  also  be  detected  by  its  odor. 

Ten  c.c.  of  the  gastric  juice  are  extracted  with  ether,  the  ether 
evaporated,  the  residue  taken  up  with  a small  amount  of  water, 
accurately  neutralized  with  caustic  soda  solution,  and  mixed  with 
a few  drops  of  a very  dilute  solution  of  ferric  chlorid.  In  the 
presence  of  acetic  acid  this  gives  a dark-red  color. 

The  ethereal  residue  after  evaporation  is  taken  up  with  a small 
amount  of  strong  sulphuric  acid  and  alcohol.  If  acetic  acid  is 
present,  the  fragrant  odor  of  ethyl  acetate  is  easily  detected. 

Fatty  acids  do  not  occur  normally  in  the  stomach  contents. 
Butyric  acid  may  be  formed  when  a large  amount  of  milk  or  carbo- 
hydrates have  been  ingested,  usually  associated  with  an  excess 
of  lactic  acid.  It  has  been  shown  also  that  butyric  acid  can  be 
formed  from  lactic  acid. 

Acetic  acid,  on  the  contrary,  is  a product  of  alcohol,  and  may  be 
formed  from  alcohol  ingested  or  from  alcohol  produced  by  the  ac- 
tion of  yeast  upon  the  sugar  contained  in  the  stomach  contents. 
Hence  it  follows  that  it  is  necessary  to  exclude  alcoholism  before 
significance  is  attached  to  the  presence  of  acetic  acid  in  the  stomach 
contents.  If,  in  the  case  of  acetic  acid,  alcoholism  be  excluded, 
and,  in  the  case  of  butyric  acid,  the  ingestion  of  butter  or  fats  in 
general  be  excluded,  the  presence  of  these  acids  has  the  same  sig- 
nificance as  the  occurrence  of  lactic  acid — viz.,  stenosis  of  the 
pylorus  with  dilatation  and  fermentation. 


CHAPTER  XVII. 

QUANTITATIVE  ANALYSIS  OF  THE  STOMACH  ACIDS. 

Numerous  methods  have  been  devised  for  the  estimation  of  the 
amount  of  free  hydrochloric  acid  present  in  the  gastric  juice.  The 
most  convenient  method  of  estimation  for  clinical  purposes  is  that 
of  Topfer,  which  at  the  same  time  estimates  the  acidity  due  to 
organic  acids  and  acid  salts,  and  that  due  to  the  combined  hydro- 
chloric acid. 

Topfer’s  Method. — Three  indicators  are  used  in  this  method: 

1.  A 0.5  per  cent,  alcoholic  solution  of  dimethyl-amido-azo- 
benzol. 


64 


topfer’s  method. 


2.  A one  per  cent,  aqueous  solution  of  alizarin  (alizarin  mono- 
sulphonate  of  sodium). 

3.  A one  per  cent,  alcoholic  solution  of  phenolphthalein. 

1.  As  has  been  mentioned  under  the  head  of  tests  for  free  hydro- 
chloric acid,  dimethyl-amido-azo-benzol  reacts  to  very  faint  traces 
of  mineral  acids,  particularly  hydrochloric,  but  to  organic  acids 
only  when  present  in  very  large  amounts,  and  not  at  all  to  com- 
bined hydrochloric  acid  or  acid  salts.  It  will  be  seen  that  by  this 
indicator  we  can  easily  find  the  amount  of  free  hydrochloric  acid. 
Topfer’s  method  gives  results  as  reliable  as  those  of  the  improved 
Sjoqvist’s  or  Braun’s  method,  according  to  Paul  Hari  (“Arch.  f. 
Verdauungskrankheiten,”  Bd.  it,  S.  332). 

Ten  c.c.  of  the  filtered  gastric  juice  are  measured  into  a small, 
clean  flask,  and  a few  drops  of  dimethyl-amido-azo-benzol  added. 
The  solution  turns  a bright  red  in  the  presence  of  free  hydrochloric 
acid.  The  solution  is  now  titrated  with  a decinormal  solution  of 
caustic  soda  (prepared  as  above)  until  the  red  color  of  the  solution 
changes  to  a clear  yellow. 

2.  Into  a second  beaker  or  flask  ten  c.c.  of  the  gastric  juice  are 
measured,  a few  drops  of  the  alizarin  solution  added,  and  the  solu- 
tion titrated  with  the  decinormal  solution  of  caustic  soda  until  the 
solution  turns  to  a clear  violet  color. 

As  this  tint  is  difficult  for  the  unpractised  eye  to  recognize, 
Topfer  recommends  the  following  preliminary  tests: 

(a)  To  five  c.c.  of  distilled  water  add  two  or  three  drops  of  the 
alizarin  solution.  A clear  yellow  color  results. 

(1 b ) To  five  c.c.  of  a one  per  cent,  solution  of  disodium  phosphate 
add  the  alizarin  solution  as  above.  A reddish  color  with  a slight 
tinge  of  violet  results. 

(c)  Five  c.c.  of  a one  per  cent,  solution  of  sodium  carbonate 
when  treated  with  alizarin,  as  above,  give  a clear  violet  tint,  which 
is  the  tint  to  be  reached  in  the  titration.  Until  the  eye  becomes 
accustomed  to  the  reaction,  it  is  well  to  prepare  this  solution  as  a 
guide  in  the  titration. 

3.  To  a third  portion  (ten  c.c.)  of  the  filtered  gastric  juice  two  or 
three  drops  of  phenolphthalein  solution  are  added  and  the  solution 
titrated  with  the  decinormal  solution  of  caustic  soda.  After  a cer- 
tain amount  of  the  solution  has  been  added,  a light-rose  color 
develops,  which  is  not,  however,  the  end  of  the  reaction.  It  will 
be  noticed  that  as  the  drop  of  caustic  soda  solution  falls  into  the 
solution  a dark-red  color  is  produced  at  the  point  of  contact, 


topfer’s  method. 


165 


fading  into  rose  color  on  agitation.  The  titration  must  be  carried 
on  until  the  entire  solution  has  reached  this  color  and  no  line  of 
separation  can  be  made  out  on  adding  a drop  of  the  caustic  soda 
solution. 

There  are  two  ways  of  stating  the  result  of  the  titrations.  The 
simplest  method  is  to  state  the  number  of  c.c.  of  the  caustic  soda 
solution  which  would  be  necessary  to  neutralize  100  c.c.  of  the 
gastric  juice  as  that  number  of  degrees  of  acidity.  For  example, 
the  number  of  c.c.  of  the  caustic  soda  solution  necessary  to  neu- 
tralize ten  c.c.  of  the  gastric  juice,  using  dimethyl-amido-azo-benzol 
as  an  indicator,  is  2.3  c.c.  One  hundred  c.c.  would  then  require 
ten  times  that,  the  amount  of  acidity  being  stated  as  23  degrees 
= 23  c.c. 

The  second  method  of  stating  the  results  is  to  give  the  amount 
of  acid  per  thousand  in  terms  of  hydrochloric  acid.  As  each  c.c. 
of  the  solution  of  caustic  soda  will  neutralize  0.00365  gm.  of  pure 
hydrochloric  acid,  the  above  example  would  show  0.8395  gm.  of 
hydrochloric  acid  per  thousand,  or  0.08395  per  cent. 

As  an  example  of  the  calculations  employed  in  Topfer’s  method, 
let  us  suppose  that  in  the  titration  (1)  with  dimethyl-amido-azo- 
benzol  as  an  indicator,  3.5  c.c.  of  caustic  soda  solution  were  em- 
ployed, (2)  with  alizarin  4.9  c.c.  of  the  caustic  soda  solution  were 
required,  and  (3)  with  phenolphthalein  7.5  c.c.  of  caustic  soda  solu- 
tion were  required  to  produce  the  proper  tint,  using  in  each  case 
ten  c.c.  of  the  stomach  contents. 

1.  As  dimethyl-amido-azo-benzol  reacts  only  with  free  hydro- 
chloric acid,  the  acidity  referable  to  this  is  35  degrees,  or  o.  12775 
per  cent. 

2.  Alizarin  shows  the  tint  of  an  alkaline  reaction  when  the  free 
hydrochloric  acid,  organic  acids,  and  acid  salts  have  been  neutral- 
ized, combined  hydrochloric  acid  having  no  effect  upon  it.  Hence 
it  follows  that  by  subtracting  the  amount  of  free  hydrochloric  acid 
from  the  acidity  found  by  alizarin,  the  amount  of  acidity  due  to 
organic  acids  and  acid  salts  will  be  found ; in  this  case  49 — 35  = 
14  degrees,  or  0.05 1 1 per  cent. 

3.  Phenolphthalein  turns  to  a dark-red  color  when  all  the  acidi- 
ties of  the  solution  have  been  saturated,  including  the  combined 
hydrochloric  acid.  The  amount  of  combined  hydrochloric  acid 
may  be  found  by  subtracting  the  acidity  found  by  alizarin  from  that 
found  by  phenolphthalein;  in  this  case  75  — 49  = 26  degrees,  or 
0.0949  per  cent. 


l66  METHOD  OF  MARTIUS  AND  LUTTKE. 

Method  of  Martius  and  Luttke. — By  this  method  the  amount 
of  physiological  hydrochloric  acid,  the  free  and  combined  hydro- 
chloric acid,  are  found,  as  well  as  the  total  chlorin  of  the  gastric 
juice,  by  determination  of  the  amount  of  chlorin.  The  method  is 
based  upon  the  fact  that  by  moderate  incineration  the  free  hydro- 
chloric acid  can  be  driven  off,  while  the  chlorin  in  combination 
with  the  inorganic  bases  is  not  affected. 

For  this  method  the  following  solutions  are  required: 

1.  A decinormal  solution  of  hydrochloric  acid,  which  can  be 
prepared  by  standardizing  against  the  decinormal  caustic  soda  solu- 
tion as  described  in  a former  chapter. 

2.  A decinormal  solution  of  nitrate  of  silver,  containing  25  per 
cent,  of  pure  nitric  acid.  This  solution  is  approximately  made  up 
by  dissolving  17  gm.  of  pure  crystallized  nitrate  of  silver  in  900  c.c. 
of  a 25  per  cent,  solution  of  nitric  acid,  and  adding  50  c.c.  of  the 
liquor  ferri  sulphur  oxydati  of  the  German  Pharmacopeia  (the 
liquor  ferri  oxysulphatis  [“  National  Formulary  ”]  will  serve  the 
same  purpose).  The  solution  is  then  standardized  against  the  solu- 
tion of  hydrochloric  acid  and  diluted  to  the  proper  volume.  Each 
c.c.  of  the  solution  is  equivalent  to  0.00365  gm.  of  pure  hydro- 
chloric acid. 

3.  A decinormal  solution  of  ammonium  sulphocyanate.  Eight 
gm.  of  the  pure  salt  are  dissolved  in  900  c.c.  of  distilled  water  and 
titrated  against  the  decinormal  solution  of  silver  nitrate.  After 
ascertaining  the  strength  of  this  solution  it  is  diluted  so  that  it 
is  exactly  equivalent  to  the  decinormal  solution  of  nitrate  of 
silver. 

Method. — 1.  To  determine  the  total  amount  of  chlorin  present  in 
the  gastric  juice,  10  c.c.  of  the  stomach  contents,  after  thorough 
mixing,  are  measured  into  a small  cylinder  graduated  to  100  c.c., 
and  treated  with  20  c.c.  of  the  solution  of  nitrate  of  silver.  The 
mixture  is  thoroughly  shaken  and  allowed  to  stand  for  ten  minutes. 
The  mixture  is  then  diluted  to  100  c.c.,  once  more  agitated,  and 
filtered  through  a dry  filter  into  a dry  flask.  Fifty  c.c.  of  the  filtrate 
are  then  titrated  with  the  decinormal  solution  of  ammonium  sul- 
phocyanate until  a permanent  red  color  appears.  Multiply  the 
number  of  c.c.  of  ammonium  sulphocyanate  by  2,  as  only  half 
the  filtrate  was  taken,  and  subtract  from  the  number  of  c.c.  of 
nitrate  of  silver  added  (20);  the  result  will  be  the  number  of  c.c. 
of  the  nitrate  of  silver  solution  precipitated  by  the  total  chlorin  of 
the  gastric  juice  and  correspond  to  the  same  number  of  c.c.  of  deci- 


LEO’S  METHOD.  1 67 

normal  solution  of  hydrochloric  acid,  the  whole  amount  of  chlorin 
being  expressed  in  terms  of  hydrochloric  acid. 

2.  To  determine  the  amount  of  chlorin  in  combination  with  in- 
organic bases. 

Ten  c.c.  of  the  filtered  gastric  juice,  or  of  the  well-mixed  stomach 
contents,  are  evaporated  to  dryness  in  a platinum  or  porcelain  cru- 
cible, over  a water-bath  or  on  a plate  of  asbestos,  to  avoid  loss  from 
sputtering.  The  incineration  is  carried  only  to  the  point  when  the 
residue  ceases  to  burn  with  a luminous  flame.  After  cooling,  the 
residue  is  treated  with  distilled  water  up  to  about  ioo  c.c.,  or  until 
the  filtrate  comes  away  free  from  chlorids,  which  may  be  shown 
by  treating  with  a drop  of  silver  nitrate.  If  the  filtrate  remains 
perfectly  clear  after  the  addition  of  a drop  of  nitrate  of  silver,  the 
residue  is  free  from  chlorids.  To  the  clear  filtrate  is  now  added 
ten  c.c.  of  the  - decinormal  solution  of  nitrate  of  silver,  and  the 
excess  titrated  by  means  of  the  decinormal  solution  of  ammo- 
nium sulphocyanate  as  before.  The  amount  of  ammonium  sulpho- 
cyanate  solution  subtracted  from  the  amount  of  the  silver  solution 
(ten  c.c.)  gives  the  amount  of  silver  precipitated  by  the  chlorids  re- 
maining after  incineration  in  combination  with  the  inorganic  bases. 
By  subtracting  the  result  of  the  second  process  from  that  of  the 
first,  the  amount  of  free  and  combined  hydrochloric  acid  is  de- 
termined. 

Modifications. — I.  By  titrating  with  decinormal  caustic  soda  solu- 
tion, using  dimethyl-amido-azo-benzol  as  an  indicator,  we  obtain 
the  amount  of  free  hydrochloric  acid ; this  subtracted  from  the 
sum  of  the  free  and  combined  hydrochloric  acid  together,  as  arrived 
at  by  the  method  No.  2 on  previous  page,  will  give  the  amount  of 
combined  hydrochloric  acid. 

2.  By  determining  the  total  acidity  with  phenolphthalein  and  sub- 
tracting from  it  the  amount  of  free  and  combined  hydrochloric  acid, 
we  can  estimate  the  acidity  due  to  organic  acids  and  acid  salts. 

3.  The  amount  of  organic  acid  present  may  be  estimated  in 
terms  of  hydrochloric  acid  by  the  method  of  Hehner-Seeman  (to 
be  described  later).  This  result  deducted  from  the  result  of  the 
preceding  modification  gives  the  amount  of  acidity  due  to  acid  salts. 

Leo’s  Method. — Leo  bases  his  method  upon  the  fact  that  when 
calcium  carbonate  is  added  in  a fine  powder  to  the  gastric  juice  the 
free  and  combined  hydrochloric  acid  combine  with  the  calcium  car- 
bonate to  form  calcium  chlorid,  a neutral  salt,  while  the  acid  salts 
are  not  affected.  During  the  reaction,  however,  the  calcium  chlorid 


68 


QUANTITATIVE  ESTIMATION  OF  LACTIC  ACID. 


reacts  with  the  phosphates  to  form  acid  calcium  phosphate  (mono- 
calcium phosphate,  CaHP04).  As  this  requires  double  the  amount 
of  caustic  soda  solution  to  neutralize  that  would  be  required  for 
the  acid  sodium  phosphate,  it  is  necessary  to  add  each  time  an 
excess  of  calcium  chlorid  solution  before  titration. 

Method . — Ten  c.c.  of  the  gastric  juice  are  shaken  up  with  50  c.c. 
of  ether  to  remove  organic  acids.  The  residue  after  drawing  off 
the  ethereal  layer  is  treated  with  five  c.c.  of  a concentrated  solu- 
tion of  calcium  chlorid  and  titrated  with  the  decinormal  solution 
of  caustic  soda,  using  phenolphthalein  as  an  indicator.  This  deter- 
mines the  acidity  due  to  free  and  combined  hydrochloric  acid  and 
to  acid  salts.  A second  portion  of  fifteen  c.c.  is  treated  with  a 
small  amount  of  pure,  dry  calcium  carbonate,  the  mixture  stirred 
and  immediately  filtered  through  a dry  filter.  The  carbon  dioxid 
is  expelled  from  the  filtrate  by  passing  a current  of  air  through  it. 
Ten  c.c.  of  the  filtrate  are  then  treated  with  five  c.c.  of  the  saturated 
solution  of  calcium  chlorid  and  titrated  as  above.  The  acidity 
found  is  due  to  the  acid  phosphates.  By  subtracting  the  result 
found  in  the  second  titration  from  that  of  the  first,  the  amount  of 
free  and  combined  hydrochloric  acid  is  determined. 

Boas’  Method. — This  method  is  an  easily  applied  test  for  free 
hydrochloric  acid,  which  gives  fairly  accurate  results  in  the  absence 
of  organic  acids  or  when  they  are  present  only  in  traces.  Ten  c.c. 
of  the  filtered  gastric  juice  are  titrated  with  decinormal  caustic  soda 
solution  until  a small  amount  (a  drop)  removed  by  a platinum  loop 
fails  to  change  the  tint  of  Congo  paper.  Instead  of  using  the  paper 
as  an  indicator  outside,  a small  bit  of  the  Congo  paper  may  be 
dropped  into  the  solution  and  the  titration  conducted  slowly,  with 
constant  shaking,  until  the  paper  regains  its  original  red  color. 
This  test,  however,  can  not  be  employed  in  the  presence  of  any 
considerable  amount  of  free  organic  acids. 

Lactic  Acid— Quantitative  Estimation. — A simple  clinical  test 
for  lactic  acid  has  been  devised  by  Strauss  (“  Berliner  klin.  Woch.,” 
1895,  No.  37).  A separating  funnel  is  graduated  to  five  c.c.  below 
and  twenty-five  c.c.  above.  The  funnel  is  filled  to  the  five  c.c. 
mark  with  gastric  juice  and  ether  added  to  the  twenty-five  c.c. 
mark.  The  funnel  is  corked  and  well  shaken,  and  after  standing 
for  a short  time  to  allow  the  fluids  to  separate,  the  liquids  are  run 
out  to  the  five  c.c.  mark.  Distilled  water  is  added  to  the  twenty- 
five  c.c.  mark  and  the  mixture  treated  with  two  drops  of  a solution 
of  the  officinal  tincture  of  the  chlorid  of  iron,  diluted  1 : 10.  On 


QUANTITATIVE  ESTIMATION  OF  LACTIC  ACID. 


169 


25  c.c. 


-5  c.c. 


shaking  the  mixture  a greenish-yellow  color  is  produced  if  lactic 
acid  is  present  in  the  proportion  of  I per  1000  or  more.  If  present 
in  the  proportion  of  from  0.5  to  I per  1000, 
only  a pale-green  color  is  produced. 

Boas’  Method. — This  method  of  esti- 
mating the  amount  of  lactic  acid  depends 
upon  its  oxidation  into  aldehyd  and  the 
estimation  of  the  latter  by  means  of  a 
standard  solution  of  iodin. 

Solutions  required  : 1.  A decinormal 

solution  of  iodin  is  prepared  by  dissolving 
twenty-five  gm.  of  potassium  iodid  in  about 
200  c.c  of  water,  and  dissolving  in  this  12.6 
gm.  of  resublimed  iodin.  The  solution  is 
diluted  with  distilled  water  to  1000  c.c.,  and 
requires  no  correction. 

2.  A decinormal  solution  of  sodium  arse- 
nite  : Dissolve  16.5  gm.  of  sodium  arsenite 
in  about  900  c.c.  of  distilled  water.  It  is 
then  titrated  against  the  decinormal  solution 
of  iodin  and  diluted  so  that  the  two  solu- 
tions are  equivalent. 

3.  Hydrochloric  acid  (sp.  gr.  1018). 

4.  Normal  solution  of  potassium  hydrate 
(56  gm.  in  1000  c.c.). 

Method  : Ten  or  twenty  c.c.  of  the  filtered 
gastric  juice  are  tested  for  the  presence  of 

free  acid ; if  present,  a small  amount  of  barium  carbonate  is  added 
(if  free  acid  be  absent,  this  addition  is  unnecessary)  and  evaporated 
to  a syrup.  A few  drops  of  phosphoric  acid  are  added  and  the 
solution  boiled  slightly  to  expel  carbon  dioxid. 

Allow  the  syrup  to  cool  ; extract  with  100  c.c.  of  ether  free  from 
alcohol ; after  the  two  fluids  have  separated  draw  off  the  ethereal 
solution  ; evaporate ; take  up  the  residue  in  forty-five  c.c.  of  water, 
and  filter.  The  filtrate  is  treated  in  an  Erlemeyer  flask  with  five  c.c. 
of  sulphuric  acid  and  a small  amount  of  manganese  dioxid.  The 
flask  is  closed  by  a two-holed  rubber  stopper,  one  aperture  being 
closed  by  a glass  tube  and  rubber  tubing  clamped  off,  the  other 
opening  receiving  a bent  glass  tube  leading  to  the  distilling  appa- 
ratus. The  distillate  is  received  in  a large  flask  well  stoppered. 
The  mixture  is  distilled  at  a gentle  heat  until  about  four-fifths  of 


Fig.  23.— Strauss’  Mixing 
Funnel  for  Lactic  Acid 
Determinations, 


1^0  ANALYSIS  OF  THE  STOMACH  CONTENTS. 

the  fluid  has  passed  over.  The  distillate  is  then  treated  with  twenty 
c.c.  of  the  decinormal  solution  of  iodin  and  the  same  amount 
(twenty  c.c.)  of  the  normal  potassium  hydrate  solution,  thoroughly 
shaken  and  allowed  to  stand  for  a few  minutes  in  the  flask.  Twenty 
c.c.  of  hydrochloric  acid  and  an  excess  of  sodium  bicarbonate  in 
powder  are  then  added,  and  the  excess  of  iodin  determined  by 
titration  with  the  solution  of  sodium  arsenite.  The  sodium  arsenite 
is  added  until  the  solution  is  decolorized;  fresh  starch  solution  and 
the  iodin  solution  are  then  added  until  the  blue  color  becomes  per- 
manent. Each  c.c.  of  the  iodin  solution  in  excess  of  the  sodium 
arsenite  solution  is  equivalent  to  0.003388  gm.  of  lactic  acid. 

Quantitative  Estimation  of  Fatty  Acids. — Leo  (“  Centralblatt 
f.  d.  med.  Wissenschaften,”  1889)  has  recommended  the  following 
method:  The  total  acidity  of  the  gastric  juice  is  first  accurately 
determined.  Ten  c.c.  are  boiled  until  the  vapor  given  off  has  no 
longer  an  acid  reaction.  The  residue  is  then  titrated  with  Tor 
normal  NaOH,  using  phenolphthalein  as  an  indicator.  The  loss 
in  the  total  acidity  gives  the  amount  of  the  fatty  acids.  This 
method  does  not  give  accurate  results,  as  some  HC1  is  given  off 
in  the  boiling  process.  By  determining  the  amount  of  HC1  before 
and  after  the  boiling,  the  amount  lost  is  determined  and  correction 
can  be  made,  greatly  increasing  the  accuracy  of  the  method  (Adler). 

Total  Organic  Acids. — The  total  organic  acids  are  best  esti- 
mated by  the  method  of  Hehner-Seeman,  called,  by  Leube,  Braun’s 
method. 

Ten  c.c.  of  the  gastric  juice  are  accurately  neutralized  with  a 
decinormal  solution  of  caustic  soda,  using  phenolphthalein  as  an 
indicator.  This  solution  is  then  evaporated  to  dryness,  carefully 
avoiding  sputtering,  and  incinerated  as  long  as  the  residue  burns 
with  a luminous  flame.  After  cooling  the  residue  is  extracted 
with  boiling  distilled  water,  filtered,  and  the  amount  of  sodium  car- 
bonate formed  determined  by  titration  with  a decinormal  solution 
of  hydrochloric  acid.  As  the  presence  of  free  carbon  dioxid  in- 
terferes somewhat  with  the  delicacy  of  the  reaction  when  phenol- 
phthalein is  used  as  an  indicator,  the  following  modification  has 
given  better  results : After  the  incinerated  mass  has  been  extracted 
with  boiling  water  and  filtered,  a known  excess  of  the  decinormal 
solution  of  hydrochloric  acid  is  added,  the  solution  boiled  to  expel 
any  carbon  dioxid  in  solution,  and  the  excess  of  acid  determined 
by  back  titration  with  a decinormal  solution  of  caustic  soda. 

This  method  is  based  upon  the  fact  that  when  salts  of  the 


SALIVA. 


171 

organic  acids  with  the  alkalies  are  incinerated  at  a low  heat  the 
carbonates  of  the  alkalies  are  formed  with  the  liberation  of  water 
and  carbon  dioxid.  This  method  is  simple.  Martius  and  Liittke 
speak  favorably  of  it,  and  the  author  has  confirmed  its  accuracy  by 
control  analyses  with  other  methods. 


CHAPTER  XVIII. 

DIGESTIVE  FERMENTS.— PRODUCTS  OF  DIGESTION.— 
TESTS  FOR  SAME. 

Saliva. — The  saliva  as  found  in  the  mouth  is  the  mixed  secre- 
tions of  all  the  salivary  glands.  It  may  be  readily  obtained  for 
testing  by  requesting  the  individual  under  examination  to  chew  a 
piece  of  soft  rubber  or  other  insoluble 'substance,  to  stimulate  the 
secretion,  and  as  it  forms  it  is  placed  in  a clean  receptacle.  It  is 
a clear,  slightly  opalescent  fluid,  of  a mucoid  consistency,  having  a 
specific  gravity  of  from  1002  to  1006.  Under  normal  conditions  it 
has  a slight  alkaline  reaction,  its  alkalinity  averaging  in  man  0.08 
per  cent.,  expressed  as  sodium  carbonate  (Chittenden). 

Its  active  constituent,  ptyalin,  acts  most  readily  upon  boiled 
starch,  raw  starch  being  protected  from  its  action  by  the  coating  of 
cellulose  surrounding  each  granule.  Its  action  is  entirely  amylo- 
lytic,  as  it  has  no  action  upon  other  food-products. 

Its  action  upon  starch  may  be  demonstrated  in  the  following 
simple  manner:  A few  c.c.  of  boiled  starch-paste  are  treated  in  a 
test-tube  with  a small  amount  of  saliva.  A few  drops  removed  and 
treated  on  a testing-plate  with  a drop  of  iodin  solution  give  the 
characteristic  blue  color  of  starch.  After  a moment  or  two  a few 
drops  removed  will  show  a violet  color,  and  by  treating  a portion 
at  intervals  the  color  changes  gradually  to  a deep  reddish  brown, 
and  finally  disappears.  Different  products  of  the  action  of  the  fer- 
ment are  found  at  different  stages  of  digestion.  The  violet  color 
first  found  is  a color  which  results  from  a mixture  of  erythrodex- 
trin  and  starch  when  treated  with  iodin.  Later  the  color  becomes 
reddish  brown,  due  to  the  change  of  the  starch  entirely  into  dex- 
trins  and  sugar.  When  digestion  has  gone  on  until  the  solution 
gives  no  color  whatever  with  iodin,  the  solution  still  contains  some 
form  of  dextrin  (achroodextrin),  as  may  be  shown  by  the  addition 


1 72 


TESTS  FOR  PTYALIN. 


of  alcohol,  which  throws  down  a profuse  white  precipitate.  It  may 
be  shown,  also,  that  the  solution  contains  sugar  by  treating  a small 
amount  of  the  mixture  with  Fehling’s  solution.  This  sugar,  ac- 
cording to  the  investigations  of  Nasse,  von  Mehring,  and  Musculus, 
is  not  dextrose,  as  formerly  taught,  but  maltose. 

The  action  of  ptyalin  is  most  energetic  at  the  temperature  of  the 
body.  It  acts  best  in  a neutral  medium,  though  a small  trace  of 
alkali  has  little  or  no  effect  upon  it.  Its  activity  is  stimulated  by 
the  addition  of  enough  acid  to  combine  with  its  proteid  constit- 
uents. A minute  trace  of  acid  still  allows  the  action  to  continue, 
but  for  practical  purposes  we  may  say  that  the  addition  of  free 
acids,  in  such  quantities  as  are  found  in  the  gastric  juice,  not  only 
stops  its  action,  but  possibly  destroys  the  ferment,  so  that  after 
neutralization  it  is  no  longer  able  to  digest  starch. 

In  the  stomach  the  action  of  the  ptyalin  probably  continues 
until  the  presence  of  free  acid  destroys  the  ferment.  As  no  free 
acid  can  normally  be  demonstrated  in  the  stomach  until  the  lapse 
of  fifteen  or  twenty  minutes,  the  greater  portion  of  the  starch  is 
transformed  into  sugar  and  achroodextrin.  Under  normal  condi- 
tions, then,  we  should  find,  in  the  gastric  juice  removed  for  exami- 
nation, sugar,  achroodextrin,  and  a faint  trace  of  erythrodextrin. 
The  presence  of  a marked  reaction  of  erythrodextrin  may  be 
taken  as  valuable  presumptive  evidence  of  hyperacidity,  its  ab- 
sence indicating  either  normal  acidity  or  subacidity. 

Only  in  rare  instances  has  absence  of  ptyalin  from  the  saliva 
been  seen. 

There  are  some  unexplained  cases  in  which,  with  a normal  or 
diminished  acidity,  the  digestion  of  starches  is  very  poor,  as  is 
shown  by  the  marked  reaction  of  erythrodextrin  and  the  small  per- 
centage of  sugar  found  by  quantitative  test.  The  amylolytic  power 
of  the  salivary  excretion  ought  always  to  be  examined  in  such  cases. 

Pepsin. — The  proteolytic  ferment  of  the  gastric  juice  is  active 
only  in  an  acid  medium,  and  is  destroyed  by  very  dilute  solutions 
of  the  alkaline  carbonates.  Pepsin  is  probably  not  secreted  as  such, 
its  precursor  being  pepsinogen  or  propepsin,  which  is  transformed 
by  weak  acids  into  the  active  ferment,  pepsin.  While  hydrochloric 
acid  acts  best  in  thus  transforming  pepsinogen  into  pepsin,  other 
acids  to  a lesser  degree  can  perform  the  office.  Pepsin,  like  the 
other  ferments,  has  the  property  of  changing  an  almost  unlimited 
amount  of  proteids,  providing  the  products  of  its  action  are  removed 
when  formed,  and  the  temperature  kept  at  a favorable  point,  as  it 


TESTS  FOR  PEPSIN.  1 73 

appears  to  act  by  its  presence,  not  being  itself  destroyed  or  changed 
by  the  reaction. 

While  it  has  never  been  isolated  in  a pure  state,  we  know  that  a 
product  can  be  obtained  by  complex  chemical  methods  which,  while 
intensely  proteolytic,  exhibits  none  of  the  reactions  of  proteids  ; so 
that  the  ferment,  whatever  its  nature,  is  probably  not  a proteid. 

The  amount  of  acid  necessary  for  the  most  vigorous  action  of 
pepsin  varies  with  the  form  of  proteids  employed.  For  example, 
pepsin  acts  best  on  fibrin  when  the  acidity  is  about  I : 1000,  while 
coagulated  egg-albumen  is  digested  most  rapidly  when  the  acidity 
amounts  to  two  or  three  per  thousand  of  hydrochloric  acid. 

Test. — Three  test-tubes  or  small  wine-glasses  are  taken,  and  a 
small,  thin  slice  of  boiled  egg-albumen  placed  in  each.  To  the  first 
is  added  three  c.c.  of  the  gastric  juice  ; to  the  second,  three  c.c.  of 
the  gastric  juice  to  which  hydrochloric  acid  has  been  added  in  suffi- 
cient quantity  to  bring  the  acidity  to  two  or  three  per  thousand  ; the 
third  is  acidulated  as  in  number  two  and  a few  grains  of  pepsin 
added.  The  three  tubes  or  glasses  are  now  placed  in  the  incubator, 
at  a temperature  of  40°  C.,  and  allowed  to  remain  for  three  hours. 

If  at  the  end  of  this  time  all  three  tubes  show  digestion  by  the  solu- 
tion of  the  egg-albumen,  the  specimen  contained  pepsin  ; if  numbers 
two  and  three  only  show  digestion,  the  contents  contained  pepsino- 
gen but  no  pepsin  ; while  if  only  the  third  tube  or  glass  shows  traces 
of  digestion,  the  specimen  contained  neither  pepsin  nor  pepsinogen. 

Pepsinogen. — This  substance  is  supposed  to  be  secreted  by  the 
cells  of  the  gastric  mucosa,  and  to  be  changed  into  pepsin  by  the 
action  of  the  hydrochloric  acid  of  the  gastric  juice.  This  action 
has  been  differently  explained  by  various  experimenters,  the  most 
plausible  theory  being  that  a combination  of  the  two  takes  place 
with  the  formation  of  pepsin — hydrochloric  acid. 

In  the  absence  of  hydrochloric  acid,  this  body,  pepsinogen,  may 
be  present  in  normal  amount,  and  require  only  the  addition  of  a 
sufficient  quantity  of  hydrochloric  acid  to  bring  the  gastric  juice 
to  a normal  acidity  to  render  the  stomach  contents  active. 

In  the  absence  of  free  hydrochloric  acid  we  may  test  for  the 
presence  of  this  substance  by  acidulating  with  hydrochloric  acid,  as 
in  number  two  of  the  pepsin  test,  adding  a small  bit  of  boiled  egg- 
albumen  and  placing  in  the  thermostat  at  a temperature  of  40°  C. 
for  three  hours,  at  the  end  of  this  time  noting  the  presence  or  ab- 
sence of  signs  of  digestion. 

The  test  proposed  by  Hammerschlag  for  the  peptonizing  power 


174 


DETECTION  OF  RENNIN. 


of  the  gastric  juice  has  been  highly  recommended  in  the  recent 
works  on  gastric  diseases.  It  is  carried  out  in  the  following 
manner : A solution  of  about  one  per  cent,  of  albumen  containing 
0.4  per  cent,  free  hydrochloric  acid  is  prepared,  and  ten  c.c.  added 
to  each  of  two  tubes.  To  one,  the  control-tube,  five  c.c.  of  dis- 
tilled water,  to  the  other  five  c.c.  of  the  gastric  juice,  are  added,  and 
both  tubes  set  in  the  incubator  for  one  hour  at  body-temperature. 
At  the  end  of  this  time  the  amount  of  albumen  in  each  tube  is 
estimated  by  the  Esbach  albuminometer,  the  difference  between 
the  two  tubes  showing  the  amount  of  digested  albumen. 

Two  objections  may  be  brought  against  this  method  : (1)  The 
Esbach  albuminometer  is  by  no  means  an  accurate  method  of  esti- 
mating the  amount  of  albumen ; (2)  peptones  are,  in  part  if  not 
completely,  precipitated  by  picric  acid  in  the  cold. 

Boas,  following  out  the  observations  of  Brficke  (“  Vorlesungen 
fiber  Physiologie,”  p.311,  1884:  Quantitative  Determination  of 
Pepsin,  etc.),  employs  a comparative  test  which  in  doubtful  cases  may 
yield  valuable  information.  Properly  labeled  tubes  are  prepared, 
and  in  them  are  placed  measured  quantities  of  gastric  juice  diluted 
with  a solution  of  hydrochloric  acid  of  the  normal  strength  of  the 
gastric  juice  (two  or  three  per  1000),  so  that  the  tubes  contain  the 
gastric  juice  in  dilutions  of  1 : 10  and  1 : 20.  To  each  tube  a small 
flake  of  egg-white  or  fibrin  is  added  and  put  in  a thermostat  at  the 
temperature  of  the  body.  From  the  amount  of  dilution  at  which 
digestion  ceases,  an  idea  may  be  gained  of  the  amount  of  pepsin 
or  pepsinogen  which  any  gastric  juice  contains.  For  comparison, 
similar  tubes  may  be  prepared  of  normal  gastric  juice,  and  the 
digestive  power  of  the  two  compared. 

Chymosin  or  Rennin  and  Rennin  Zymogen. — In  addition  to 
pepsin,  the  gastric  juice  also  contains  a ferment,  or  its  zymogen, 
whose  special  property  appears  to  be  the  precipitation  of  casein 
from  milk.  As  in  the  transformation  of  pepsinogen  into  pepsin 
hydrochloric  acid  is  required,  so  rennin  zymogen  in  the  gastric 
juice  is  not  transformed  into  rennin  except  in  the  presence  of 
hydrochloric  acid.  Certain  neutral  salts  of  lime,  such  as  calcium 
chlorid,  however,  have  the  power  of  transforming  rennin  zymogen 
into  rennin,  even  in  neutral  or  slightly  alkaline  solutions. 

The  following  tests  for  the  presence  of  rennin  and  its  zymogen 
have  been  devised  by  Boas  : 

Rennin. — Five  c.c.  of  the  gastric  juice  are  exactly  neutralized 
with  a decinormal  solution  of  caustic  soda,  five  c.c.  of  neutral  milk 


TEST  FOR  RENNIN  ZYMOGEN.  175 

added,  and  the  mixture,  after  being  well  shaken,  is  placed  in  an 
incubator  at  the  body-temperature. 

If  rennin  be  present,  the  casein  will  form  a firm  coagulum  in  from 
ten  to  fifteen  minutes. 

A relative  quantitative  estimation  of  the  rennin  ferment  may  be 
performed  by  the  following  method  : 

The  gastric  juice  is  accurately  neutralized  and  portions  of  this 
diluted  with  distilled  water,  in  known  proportions,  i : io,  I : 20,  etc. 
To  five  c.c.  of  each  of  these  dilutions  five  c.c.  of  neutral  milk  are 
added,  and  the  tubes  placed  in  the  thermostat  at  the  body-temper- 
ature for  fifteen  minutes.  At  the  end  of  this  time  the  tubes  are 
removed  and  the  dilution  at  which  no  coagulation  takes  place  is 
noted.  In  stating  the  dilution  note  must  be  taken  of  the  fluid 
added  in  neutralizing. 

Rennin  Zymogen. — Five  c.c.  of  the  gastric  juice  are  rendered 
faintly  alkaline  by  the  addition  of  a decinormal  solution  of  caustic 
soda  ; one  c.c.  of  a one  per  cent,  solution  of  calcium  chlorid  and 
five  c.c.  of  neutral  milk  are  added.  The  tube  is  placed  in  the  ther- 
mostat, and  after  fifteen  minutes  should  show  a firm  cake  of  casein 
if  rennin  zymogen  be  present. 

Quantitative. — The  gastric  juice  is  rendered  faintly  alkaline  by 
adding  a decinormal  solution  of  caustic  soda  and  dilutions  pre- 
pared, i : io,  i : 20,  etc.,  estimating  in  the  dilution  the  amount  of 
fluid  added  in  alkalinizing.  Five  c.c.  of  each  of  these  dilutions 
are  placed  in  test-tubes  with  five  c.c.  of  neutralhmilk  and  one  c.c.  of 
a one  per  cent,  solution  of  calcium  chlorid.  These  are  placed  in 
a thermostat  at  the  body-temperature,  and  at  the  end  of  fifteen 
minutes  the  dilution  at  which  the  enzyme  fails  to  act  is  noted. 
From  the  observations  of  Boas  and  others  it  appears  that  the 
secretion  of  the  ferments  and  the  pro-enzymes  is  less  affected  by 
the  minor  disturbances  which  may  cause  a temporary  arrest  of  the 
acid  secretion  of  the  stomach.  Decrease  in  the  activity  of  the 
ferments,  on  the  other  hand,  is  usually  the  result  of  some  organic 
change  in  the  gastric  mucosa. 

By  experiment  upon  normal  individuals  it  has  been  found  that 
rennin  is  active  in  dilutions  of  from  i : 30  to  1 : 40,  and  rennin 
zymogen  in  dilutions  varying  from  1 : 100  to  1 : 150.  It  has  been 
found  that,  even  in  the  absence  of  free  hydrochloric  acid,  the  fer- 
ments may  be  active  up  to  the  limit  observed  in  normal  individuals, 
and  that  in  such  cases  the  condition  of  anacidity  was  a temporary 
matter,  due  to  some  mental  or  circulatory  disturbance,  the  acid  re- 
appearing when  the  cause  of  the  disturbance  was  removed. 


I76  PRODUCTS  OF  PEPSIN  DIGESTION. 

On  the  other  hand,  in  cases  of  anacidity  in  which  the  rennin 
zymogen  was  active  only  in  the  stronger  dilutions,  1 .*5,  1 : 10, 
etc.,  the  anacidity  is  due  to  some  organic  change  in  the  gastric 
mucosa  from  which  recovery  is  usually  rare. 

It  will  be  seen  from  these  considerations  of  what  importance  a 
quantitative  investigation  of  the  gastric  ferments  is  from  the  prog- 
nostic standpoint. 

Action  of  Pepsin  on  Proteids. — The  action  of  pepsin  upon 
proteids  only  takes  place  to  a slight  extent  in  a neutral  solution. 
Faust  (“  Zur  Kentniss  des  Pferdeblutserumalbumins,”  u.  s.  w. ; 
“Archiv  f.  experiment.  Pathol,  u.  Pharmakol.,”  Bd.  xli)  has  shown 
that  crystallized  serum-albumin,  when  treated  with  a neutralized 
extract  of  the  gastric  mucous  membrane,  gives  off  to  the  fluid  a 
small  amount  of  a highly  nitrogenous  neutral  body,  possibly  a 
cyanamid.  In  acid  solution  the  action  is  a very  complex  one  and 
not  as  yet  fully  understood.  The  first  observable  result  of  the 
action  of  a hydrochloric  acid  solution  of  pepsin  upon  a coagulated 
albumen,  such  as  egg-white,  is  apparently  a partially  mechanical 
change.  The  egg-white  swells  up,  its  edges  become  rounder,  and 
it  becomes  clearer  and  more  glassy  in  appearance.  The  egg-white 
then  begins  to  dissolve,  as  is  shown  by  the  presence  in  the  solution 
of  a substance  precipitated  by  neutralization,  which  may  be  called 
syntonin,  or  acid-albumin.  This  action  takes  place  also  in  acid 
solutions  to  which  pepsin  has  not  been  added.  The  next  step  is 
one  in  which  the  pepsin  plays  an  important  part.  The  syntonin  or 
acid-albumin  is  changed  first  into  the  primary  albumoses,  proto- 
and  hetero-albumose.  These  undergo  further  change  and  become 
deutero-albumoses,  and,  finally,  peptones.  These  substances  may 
be  distinguished  from  each  other  by  the  following  reactions : 

[a)  Native  albumins  may  be  removed  from  the  solution,  if  pres- 
ent, by  rendering  the  stomach  contents  faintly  acid,  if  not  already 
so,  and  boiling.  The  precipitate  will  consist  of  the  native  proteids, 
viz.,  albumin  and  globulin. 

(£)  The  solution  is  carefully  neutralized  by  the  addition  of  a 
weak  caustic  soda  solution.  The  precipitate  will  consist  of  syntonin 
or  acid-albumin.  The  neutralization  must  be  exact,  as  the  precip- 
itate is  dissolved  by  an  excess  of  acid  or  alkali  to  form  acid-albu- 
min or  alkali-albumin,  respectively. 

( c ) The  filtrate  from  which  the  albumin  and  acid-albumin  has 
been  removed  is  now  saturated  with  magnesium  sulphate  and  fil- 
tered. The  precipitate,  which  consists  of  the  primary  albumoses, 
proto-  and  hetero-albumoses,  is  dissolved  in  water,  placed  in  a 


SEPARATION  OF  ALBUMOSES. 


1 7 7 


dialyzer,  and  the  salts  removed  by  dialysis.  As  hetero-albumose 
is  insoluble  in  pure  water,  it  is  precipitated  by  the  removal  of  the 
salts,  as  in  a dialyzer.  The  proto-albumose  remains  in  solution,  as 
it  is  soluble  in  water,  and  may  be  tested  for  by  acidulating  with 
nitric  acid  in  the  cold,  the  precipitate  redissolving  on  heating. 

(d)  Deutero-albumose,  or  secondary  albumose,  is  detected  in  the 
following  manner:  A sufficient  quantity  of  the  gastric  juice  is  freed 
from  albumen  and  acid-albumin,  according  to  (a)  and  (< b ).  The 
filtrate  is  saturated  with  powdered  ammonium  sulphate  and  the 
precipitate  which  forms,  consisting  both  of  primary  and  secondary 
albumoses,  is  filtered  off,  and  washed  thoroughly  with  a saturated 
solution  of  ammonium  sulphate. 

The  precipitate  is  redissolved  in  the  least  amount  of  water  pos- 
sible, faintly  acidulated  with  acetic  acid  and  saturated  with  common 
salt,  which  precipitates  the  primary  albumoses,  leaving  the  deutero- 
albumose,  or  secondary  albumose,  in  solution.  After  filtration  the 
secondary  albumose  may  be  detected  by  saturating  again  with 
ammonium  sulphate  any  precipitate  which  may  form  consisting  of 
deutero-albumose.  It  may  be  detected  also  by  adding  a consider- 
able amount  of  common  salt  to  its  solution  and  acidulating  with 
nitric  acid.  A precipitate  will  form  in  the  presence  of  deutero- 
albumose,  redissolved  on  heating. 

(< e ) Peptone  may  be  detected  by  precipitating  all  the  other  pro- 
teids  by  saturating  with  ammonium  sulphate  and  filtering.  The 
filtrate  contains  the  peptone,  which  may  be  tested  for  by  the  biuret 
reaction.  The  filtrate  is  treated  with  an  excess  of  caustic  alkali 
and  a few  drops  of  a very  dilute  solution  of  copper  sulphate.  If 
peptones  are  present  in  the  solution  a pink  or  rose-red  color 
appears. 

Under  some  circumstances  the  precipitation  of  the  albumoses  by 
ammonium  sulphate  is  incomplete,  and  in  these  cases  the  method 
given  by  Muller  (“  Zeit.  f.  phys.  Chemie,”  Bd.  xxvi,  S.  48)  gives 
good  results. 

The  stomach  contents  are  treated  with  an  equal  volume  of  a 
thirty  percent,  solution  of  ferric  chlorid,  nearly  neutralized  by  the 
addition  of  a solution  of  caustic  soda  and  filtered.  The  filtrate  is 
treated  with  a small  amount  of  zinc  carbonate,  well  shaken  and 
again  filtered.  The  filtrate  is  clear  and  colorless,  and  may  now  be 
tested  by  the  biuret  reaction  as  given  above. 


7§ 


GASTROSCOPY. 


CHAPTER  XIX. 

GASTROSCOPY. 

Although  the  method  and  instruments  for  directly  inspecting 
the  interior  of  the  stomach  are  by  no  means  perfect,  the  author  has 
considered  it  practical  to  insert  this  account  of  the  procedure 
because  of  its  undoubted  future  development  as  a diagnostic 
aid. 

The  first  one  to  use  a gastroscope  was  Mikulicz  (“  Ueber  Gas- 
troskopie  u.  Oesophagoskopie,”  “Wien.  med.  Presse,”  1 88 1 , No. 
43  ; also  “ Wien.  med.  Wochenschr.,”  1883,  Nos.  23  and  24).  The 
instrument  used  was  made  by  Leiter,  of  Wien,  and  was  curved  at 
an  obtuse  angle.  The  following  account  of  the  technic  and  value 
of  the  method  is  quoted  from  Rosenheim  (loc.  cit .) : 

“ Gastroscopy  is  founded  on  the  fact  discovered  by  this  author, 
that  in  the  majority  of  cases  (eighty  percent.)  it  is  possible  to  in- 
troduce, without  special  difficulty,  a straight,  rigid  tube,  twelve  mm. 
in  diameter,  the  patient  having  first  been  placed  in  the  dorsal  posi- 
tion. It  is  possible  to  introduce  such  a tube  far  into  the  stomach, 
often  as  far  as  the  navel,  and  eventually  below  the  same.  The 
establishment  of  this  fact  first  furnished  him  with  a foundation 
on  which  gastroscopy  could  be  developed,  after  he  had  come  to 
the  conclusion  that  an  optical  apparatus,  to  be  suitable  for  the 
stomach,  must  be  straight  as  in  the  cystoscope  ” (Rosenheim, 
“ Gastroskopie,”  “ Berlin,  klin.  Wochenschr.,”  1896,  No.  13). 

Apart  from  complications  that  are  due  to  tumors,  exudations, 
enlargement  of  the  liver,  etc;  (that  is,  to  the  pathological-anatomical 
conditions),  apart  also  from  congenital  anomalies  (abnormally  con- 
torted course  of  the  esophagus  or  abnormal  contraction),  two  facts 
are  to  be  considered  in  the  light  of  an  impediment  to  a successful 
probing  by  means  of  introducing  a rigid  tube  into  the  stomach  : In 
the  first  place,  the  bend  to  the  left,  or  spiral  twist,  which  the 
esophagus  shows  so  frequently  in  its  subphrenic  part;  and,  secondly, 
the  occurrence  of  spasm  at  the  lower  physiological  contraction  of 
the  organ.  With  continued  practice  it  becomes  apparent  that  the 
anatomical  obstruction,  caused  by  the  change  in  the  direction  of 
the  esophagus,  may  usually  be  overcome  if  the  instrument  is  intro- 
duced from  the  right  angle  of  the  mouth,  preferably  while  the 
head  is  turned  slightly  to  the  right,  laterally. 


DESCRIPTION  OF  GASTROSCOPE. 


179 


The  obstruction  before  the  cardia,  caused  by  spasm  of  the 
muscles  of  the  esophagus,  can  not  be 
eliminated  mechanically  ; here  the  man- 
ner of  introducing  the  tube  makes  no 
difference,  and  soothing  the  patient, 
persistence,  and  adaptation  can  alone 
lead  to  the  desired  result.  Local 
anesthesia  is  useless.  How  much  the 
occurrence  of  the  spasm  is  due  to 
the  psychic  condition  of  the  patient 
was  shown  by  numerous  observations 
with  invalids,  particularly  neurasthenic 
persons,  who  were  timid  and  restive 
when  the  probe  was  first  introduced, 
and  with  whom  it  was  impossible  to 
penetrate  to  the  stomach  ; while  later, 
after  they  had  become  familiar  with  the 
proceeding,  this  was  easily  accomplished. 

It  is  necessary  to  keep  in  mind,  also, 
that  the  spasm  appears  more  frequently 
with  persons  who  are  suffering  with  an 
ulcer  or  carcinoma  near  the  cardia. 

Description  of  the  Instrument. — 

(See  Fig.  24.)  The  gastroscope  is  a 
straight  metal  instrument,  68  cm.  in 
length,  12  mm.  in  diameter,  consisting 
of  three  concentric  systems  of  tubes, 
and  terminating  in  a larger  head  piece 
for  the  different  conduits.  The  inner 
tube  (1)  forms  an  optical  apparatus, 
the  ocular  of  which  is  situated  at  0, 
and  a rectangular  prism,  P,  is  located 
in  front  of  its  objective  lenses.  The 
visual  angle  of  the  telescope  (otherwise 
constructed  according  to  the  principle 
which  has  been  approved  in  the  cysto- 
scope,  viz.,  as  a terrestrial  telescope) 
amounts  to  6o°,  so  that  it  is  possible  to 
inspect  an  area  five  cm.  in  diameter  at  a 
distance  of  five  cm.  from  the  object. 

The  center  of  the  portion  in  view  lies 


i8o 


GASTROSCOPY. 


vertically  over  the  small  side  (cathetus)  of  the  rectangular  prism 
which  receives  the  image.  In  order  to  inspect  a surface  the 
center  of  which  does  not  lie  at  right  angles  over  the  cathetus, 
the  rectangular  prism  may  be  replaced  by  an  acute  angular 
prism  ; by  this  means  those  surfaces  also  can  be  examined  that 
are  situated  above,  which  can  be  only  partially  viewed  by  means 
of  a rectangular  prism.  The  absolute  necessity  of  inspecting 
parts  of  the  stomach  which  appear  at  varying  heights — for  instance, 
the  region  of  the  pylorus — explains  this  arrangement. 

The  optical  apparatus  is  inclosed  by  a tube  (3)  that  is  closed 
at  the  lower  end  by  a head-piece,  A , carrying  a tip  of  rubber,  G. 
Just  above  the  tip  there  is  an  aperture,  Ef  which  is  closed  by  a 
glass  window,  behind  which  there  is  situated  an  incandescent  lamp, 
as  shown  in  5.  At  the  upper  and  lower  ends  of  the  lamp  the 
metal  contacts  that  conduct  the  current  are  fastened.  Above  the 
window  there  is  a second  aperture,  B,  in  which  the  prism  is  adjusted, 
and  inside  of  which  it  may  even  be  moved  up  or  down.  In  the 
tube  (3)  there  are  four  canals  separated  from  one  another.  Two 
of  these  canals,  which  end  at  C and  D , serve  to  conduct  water 
through  the  instrument  and  around  the  lamp,  to  prevent  excessive 
heating  of  the  tubes  caused  by  the  incandescent  lamp.  The  third 
canal  is  used  to  receive  the  wires  that  conduct  the  current  to  the 
lamp;  while  the  fourth  canal,  which  begins  at  / and  opens  at  the 
lower  end  of  the  instrument  behind  the  window,  E,  is  used  to 
introduce  air,  which  must  be  pumped  into  the  stomach,  by  means 
of  a blast,  to  distend  its  walls.  Toward  the  top  the  thin  tube 
terminates  in  a larger  head-piece  that  establishes  tlffe  connection 
of  the  canals  with  the  different  conduits  for  water,  air,  and  elec- 
tricity. 

Figure  24  (1)  shows  the  sliding  tube,  a tube  with  a centimeter 
scale,  that  can  be  shoved  over  the  instrument  (3)  and  easily  re- 
volved on  the  same.  It  has  an  aperture  at  E corresponding  to  the 
aperture  B,  and,  by  being  turned  180  degrees,  it  serves  to  cover 
this  aperture,  as  well  as  the  prism  lying  behind  the  same,  so  as  to 
prevent  the  optical  apparatus  from  being  soiled  by  mucus  while 
the  instrument  is  being  introduced.  If  the  external  tube  is  so 
adjusted  that  the  aperture  B is  closed,  and  if,  to  further  protect  the 
optical  apparatus,  the  latter  is  turned  180  degrees  so  that  the 
exposed  surface  of  the  prism  faces  the  side  of  the  tube,  then  the 
prism  enjoys  a double  protection,  and  in  consequence  the  instru- 
ment can  not  be  soiled  while  being  introduced.  Small  metal  knobs 


DESCRIPTION  OF  GASTROSCOPE. 


1 8 1 


are  attached  to  the  top  of  all  three  tubes,  to  enable  us  to  control 
from  the  outside  their  position  in  the  stomach  ; when  these  stand 
in  a straight  line  the  observer  knows  that  the  prism  is  not  covered 
by  the  revolving  tube,  but  faces  the  cavity  of  the  stomach  through 
the  aperture.  The  electric  current  -f-  and  — is  introduced  at 
the  points  of  contact  by  means  of  a movable  cable  that  is  equipped 
with  an  interrupter.  The  intensity  of  the  electric  current  is  six- 
teen volts.  In  conducting  water  through  the  apparatus  a stand 
carrying  an  irrigator  is  used.  The  two  rubber  tubes  conduct  the 
water  through  the  instrument.  By  means  of  a cock  the  flow  of 
the  water  can  be  interrupted.  Another  tube  carries  the  water 
that  has  passed  through  the  instrument  into  the  wrater-bucket. 
To  cool  the  instrument  it  is  advisable  to  use,  not  cold  water,  but 
water  of  about  40°  C.,  in  order  that  the  lenses  of  the  optical 
apparatus  and  the  surfaces  of  the  prism  may  not  be  covered  with 
a film  of  moisture  caused  by  sudden  condensation.  The  stand 
carries  the  accumulator  (storage  battery)  used  to  furnish  the  elec- 
tricity ; this  is  supplied  with  a rheostat  for  regulating  the  current, 
and  also  with  an  interrupter. 


It  is  absolutely  necessary  in  every  case  to  convince  ourselves, 
before  carrying  out  the  gastroscopic  investigation,  that  the  way 
from  the  teeth,  as  far  as  the  great  curvature,  is  really  unobstructed, 
and  no  special  difficulties  are  offered  to  the  passage  of  a straight 
rigid  tube  while  the  patient  occupies  the  dorsal  position.  This  test 
should  never  be  neglected.  At  the  same  time  the  procedure 
should  be  carried  out  with  the  greatest  caution. 

Rosenheim  employs  for  this  purpose  a hollow  steel  probe  seventy 
cm.  long,  and  having  the  diameter  of  the  gastroscope  (12  mm.),  or 
a smaller  one,  ending  likewise  below  in  a rubber  appendage,  in  the 
side  of  which  there  is  a small  aperture  provided  with  a blast ; the 
parts  can  be  screwed  off  to  facilitate  cleansing;  a centimeter  scale 
is  engraved  on  the  sides.  This  probe  is  introduced  in  the  dorsal 
position,  preferably  from  the  right  corner  of  the  mouth;  after 
measurements  along  the  back  have  been  made  to  determine  the 
distance  of  the  cardia  from  the  teeth,  and  after  having  applied  a 
four  per  cent,  solution  of  cocaine  to  the  pharynx,  the  patient  is 
directed  to  breathe  quietly  and  deeply,  and  to  lift  his  right  hand 
on  feeling  a pain  in  the  region  of  the  stomach  or  above  the  same. 
If  the  patient  shows  pain,  the  procedure  must  cease  at  once.  If 
resistance  is  felt,  a moment  of  rest  intervenes,  or  eventually  the 


I 82 


PROCEDURE  OF  GASTROSCOPY. 


instrument  is  retracted  a little,  only  to  try  again  whether  the  resist- 
ance yields  under  gentle  pressure,  the  reaction  on  the  part  of  the 
patient  meanwhile  determining  the  degree  of  energy  that  is  to  be 
employed  in  this  manipulation.  The  absolute  law  in  probing  is  to 
avoid  all  strong  pressure,  otherwise  lesions  of  the  membrane,  even 
perforation  of  the  esophagus  or  stomach,  may  be  the  consequence. 
After  the  diaphragm  has  been  passed,  air  is  pumped  into  the 
stomach  and  we  determine  how  far  the  instrument  is  able  to  pene- 
trate into  the  inflated  organ. 

The  correct  guiding  of  the  instrument  from  the  right  corner  of 
the  mouth  plays  an  important  part  in  the  success  of  introducing 
the  instrument  in  the  majority  of  cases. 

If  we  wish  to  get  our  bearings  and  inform  ourselves  by  means 
of  the  telescope  about  the  vast  cavity  of  the  stomach,  it  is  prefer- 
able to  start  from  the  normal  position  just  described  : The  point 
of  the  instrument  far  down  at  the  great  curvature,  the  window 
turned  to  the  front.  In  this  position  the  front  wall  of  the  stomach 
approaches  the  eye  closely,  within  from  two  to  three  cm.,  so  that  we 
see  it  magnified.  A hasty  glance  suffices  to  recognize  the  condition 
of  the  mucous  membrane  here,  and  we  then  immediately  change 
the  position  of  the  instrument  by  revolving  it  slowly  to  the  right 
so  that  the  prism  faces  the  pylorus.  This  part  of  the  stomach  and 
the  adjoining  portion  of  the  small  curvature  vary  in  their  distance 
from  the  prism  in  various  cases.  The  distance  is  from  six  to  twelve 
cm.,  and  the  image  which  we  receive  of  this  section  is,  therefore, 
usually  somewhat  reduced  in  size  (to  about  one-half).  We  now 
are  examining  a part  of  the  organ  that,  from  a practical  point  of 
view,  is  perhaps  the  most  important,  since  ulcers  and  cancers  are  so 
frequently  located  there.  We  exert  ourselves  now,  starting  from 
the  opening  of  the  pylorus,  to  investigate  systematically  the  whole 
hollow  cone,  situated  to  the  right.  This  part  does  not  escape  us, 
as  a rule,  if  we  move  the  tube  gradually  from  the  great  curvature 
upward  while  revolving  the  apparatus  generally  in  both  directions. 
After  we  have  found  the  orifice  of  the  stomach,  as  a fixed  point,  it 
is  not  difficult  to  espy  from  the  same  the  neighboring  section  of 
the  small  curvature,  at  least,  and  something  of  the  rear  wall.  The 
higher  the  portio  pylorica  lies  behind  the  liver,  the  more  it  (as  is 
normal)  bends  away  to  the  rear  on  the  right,  the  more  difficult  it  is 
to  inspect,  while  a low  position  greatly  facilitates  our  investigation. 

In  the  former  case  (for  which  we  may  be  somewhat  prepared  by 
the  preceding  inflation  of  the  stomach)  the  optical  apparatus  pro- 


THE  ESOPHAGOSCOPE. 


183 


vided  with  an  acute-angled  prism  is  recommended.  It  is  possible 
to  recognize  how  .different  the  distance  is  between  the  prism  and 
the  pylorus  during  the  normal  position  of  this  segment  of  the 
organ  and  during  dislocation  of  the  same.  In  the  former  case  the 
distance  is  more  considerable  ; we  must  withdraw  the  instrument 
farther,  to  bring  at  least  a part  of  the  portio  pylorica  within  the 


Fig.  25. 

1.  Esophagoscope.  2.  Obturator.  3.  Esophageal  forceps.  4.  Esophageal  applicator. 
{Rosenheim.*) 


angle  of  the  prism  ; and  if  the  point  of  the  instrument  diverges  a 
little  farther  to  the  left  from  the  vertebral  column,  this  approach  to 
the  cardia  avails  nothing ; under  all  circumstances  we  receive  only 
an  image  of  the  part  beneath  the  orifice  of  the  stomach.  During 

* Our  thanks  are  due  to  Professor  Theod.  Rosenheim  (Berlin)  for  presentation  of  these 
illustrations. 


84 


GASTROSCOPY. 


these  manipulations  we  are  in  danger  of  being  surprised  by  an 
obscuring  of  the  field  of  vision, since  we  are  compelled  to  approach 
closely  the  descending  part  of  the  small  curvature  adjoining  the 
cardia.  These  disturbances  are  avoided  if  we  take  a view  of  the 
pyloric  portion  from  a deeper  point,  a thing  which  can  be  conve- 
niently effected  by  the  employment  of  an  acute-angled  prism  in  the 
apparatus;  the  center  of  the  circle,  which  we  then  survey,  no 
longer  stands  perpendicularly  over  the  prism.  We  no  longer  re- 
ceive the  image  from  a region  at  the  same  level  with  the  prism,  but 
from  one  a little  higher. 

If  the  pyloric  portion  is  dislocated  to  the  lower  margin  of  the 
liver,  or  deeper,  the  rectangular  prism  opposite  the  same  can  easily 
be  adjusted  without  needing  a correction. 

After  inspecting  the  pyloric  portion  we  approach  the  great  curva- 
ture with  the  point  of  the  gastroscope,  and  turn  the  instrument  to 
the  left  by  180  degrees;  while  slowly  withdrawing  the  instrument, 
we  next  inspect  the  part  of  the  fundus  and  cardiac  portion  that 
belong  to  the  left  half  of  the  body.  The  investigation  is  now  com- 
pleted ; the  illumination  is  discontinued,  the  revolving  tube  is 
pushed  in  front  of  the  window,  the  blast  is  removed  in  order  that 
the  gases  may  quickly  escape  ; only  after  this  is  the  instrument 
withdrawn.  Rosenheim  has  devised  a gastroscope  more  recently 
in  which  the  stream  of  water  for  the  cooling  of  the  electric  lamp  is 
dispensed  with  ; the  lamp  is  only  flashed  now  and  then,  and  not 
kept  incandescent  continuously.  The  latter  instrument  is  thinner 
and  only  ten  mm.  in  diameter. 

Conclusion. — (i)  Not  all  parts  of  the  interior  of  the  stomach 
can  be  inspected.  Portions  of  the  greater  curvature — of  the  pos- 
terior wall,  the  immediate  neighborhood  of  the  cardia — are  not 
visible.  It  can  not  be  practised  on  all  individuals. 

(2)  All  suspected  cases  of  ulcer  must  be  excluded  if  recent  pain 
and  hemorrhages  have  occurred.  Ulcers  at  pylorus  are  less  liable 
to  be  injured  than  those  near  the  cardia. 

(3)  Rosenheim  suggests  that  gastroscopy  may  be  employed  for 
the  early  diagnosis  of  carcinoma  and  its  differentiation  from  ulcer. 
It  is  an  inconvenient  procedure  and  very  difficult  of  execution, 
and  not  free  from  danger. 


PART  SECOND. 


THERAPY  AND  MATERIA  MEDICA  OF  STOMACH 
DISEASES. 


CHAPTER  I. 

THE  PRINCIPLES  OF  DIETETIC  TREATMENT  OF 
GASTRIC  DISEASES. 

In  the  chapter  on  the  Physiology  of  Digestion  we  have  briefly 
considered  the  various  food-substances,  their  nutritious  and  innu- 
tritious  constituents,  the  amounts  of  each,  requisite  to  maintain  a 
healthy  organism,  and  their  caloric  values,  etc.  It  is  one  of  the 
far-reaching  deserts  of  the  great  Father  of  Medicine  to  have  first 
methodically  developed  dietetics  for  the  sick  as  a special  discipline 
and  an  integral  part  of  therapy. 

In  his  classical  dissertation  on  the  conduct  of  febrile  diseases 
(Hippocrates,  “ De  victus  ratione  in  morbis  acutis  ”),  in  his  aphor- 
isms, and  in  many  other  treatises,  he  emphasizes  the  great  impor- 
tance of  careful  regulation  of  nutrition  for  patients.  His  principles, 
based  upon  analytical  experience,  are  stated  with  unsurpassable 
precision.  His  dietetics  are  free  from  speculation,  and  regard  the 
nature  and  stage  of  the  disease,  the  constitution,  age,  and  habits  of 
the  patient ; above  all,  they  show  what  is  in  our  days  termed  an  in- 
dividualizing principle.  It  would  seem  probable  that  a therapeutic 
aid  that  had  been  logically  considered  at  the  very  dawn  of  medical 
knowledge,  and  by  such  an  able  mind,  would  at  the  present  time  be 
one  of  the  most  highly  developed  in  medicine,  particularly  when 
one  reflects  upon  the  declaration  of  Donders  (“Die  Nahrungsstoffe 
des  Menschen,”  Crefeld,  1853):  “Whoever  works  at  the  develop- 
ment of  our  knowledge  on  food-substances  is  working  on  a broad 
basis  for  the  development  of  mankind.”  Fortunately  for  us,  many 
bright  intellects  have  already  applied  themselves  to  this  work,  and 

13  185 


86 


DIETETIC  TREATMENT  OF  GASTRIC  DISEASES. 


our  knowledge  has  been  enriched  by  treasures  of  valuable  informa- 
tion. But  the  well-advised  special  student  can  not  fail  to  recognize 
that  we  have  only  entered  a vast  territory,  and  that  the  greater  part 
of  it  remains  to  be  explored.  Even  the  small  portion  which  by 
hard  toiling  is  clearly  our  own  is,  we  regret  to  say,  far  from  being 
the  common  property  of  the  profession — at  least,  it  does  not  seem 
to  be  taken  advantage  of ; the  profession  at  large  failing  to 
realize  that  a logical  and  individualizing  diet  is  a more  potent 
therapeutic  factor  than  medicine. 

The  results  so  far  obtained  show  great  domains  of  research  and 
inquiry  yet  to  be  explored  for  truth  bearing  on  dietetics.  And 
many  of  our  present  results  demand  reconsideration  for  correct 
interpretation.  Various  eminently  fitted  observers  disagree  on 
vital  dietetic  questions,  because  the  special  point  of  view  from 
which  each  one’s  research  (“  Fragestellung  ”)  was  undertaken  was 
not  identical,  sometimes  not  defined  with  precision.  Sometimes 
the  intricacy  of  the  question  to  be  solved  did  not  permit  of  direct 
methods  of  investigation,  and  indirect  methods  had  to  be  em- 
ployed. 

The  scales  of  digestibility  of  various  foods,  as  devised  by  Leube 
and  Penzoldt,  for  instance,  were  arrived  at  by  determination  of  the 
time  which  the  stomach  required  to  discharge  these  foods  into  the 
duodenum.  Evidently  the  term  “digestibility”  means  the  rate  of 
solution  of  the  various  food-substances  by  the  constituents  of  the 
gastric  juice,  or  of  the  intestinal  juices,  as  the  case  may  be.  Diges- 
tibility, therefore,  has  reference  mostly  to  secretion,  but  the  rate  of 
the  gastric  expulsion  of  chyme  is  a problem  of  motility. 

To  be  of  easy  digestibility  food-substances  must — 

1.  Offer  only  a slight  resistance  to  the  digestive  juices — i.  e.y 
they  must  be  of  easy  solubility. 

2.  They  must  not  impede  or  accelerate  peristalsis. 

3.  They  must  not  excessively  irritate  the  digestive  organs, 
either  mechanically  or  chemically. 

4.  They  must  not  increase  the  processes  of  fermentation  or 
putrefaction. 

5.  The  greater  portions  of  the  substance  must  be  absorbable 
either  in  the  stomach  or  intestines. 

To  say  that  veal  in  amounts  of  100  gm.  leaves  the  stomach  in 
one  to  two  hours  does  not  imply  that  it  is  digestible,  for  the  same 
may  be  said  of  sawdust  (from  actual  experiment  of  a colleague, 
made  upon  himself).  By  our  method  of  duodenal  intubation  we 


CRITERION  OF  DIGESTIBILITY. 


!87 


succeeded  in  regaining  from  the  duodenum  56.4  per  cent,  of  a 
weighed  amount  of  ingested  veal  two  hours  and  fifteen  minutes 
after,  it  had  been  eaten.  The  veal  was  weighed  and  was  easily 
recognizable  ; besides,  nothing  else  had  been  eaten  at  the  time. 
The  celerity  with  which  a food  disappears  from  the  stomach,  there- 
fore, is  not  so  much  an  indication  of  its  digestibility  as  it  is  of  the 
gastric  motor  power. 

A more  correct  way  to  determine  the  digestibility  of  various 
foods — one  which  we  have  systematically  experimented  with  on  a 
number  of  volunteers  from  our  classes  who  had  a normal  digestion 
— is  to  find  out  how  much  by  weight  of  a known  amount  of  in- 
gested food  is  converted  into  peptone  or  dextrose  and  maltose,  as 
the  case  may  be,  in  a given  time — for  instance,  one  hour  or  thirty 
minutes. 

In  a large  number  of  these  experiments  we  aspirated  some  of  the 
weighed  test-meals  from  the  duodenum  (method  of  the  author, 
Boas’  “Archives  for  Digestive  Diseases,”  vol.  11).  For  approxi- 
mately accurate  results  it  is  sufficient  to  weigh  the  insoluble  residue 
of  the  particular  food  that  is  drawn  out  of  the  stomach.  It  is 
necessary  to  have  those  experiments  which  are  to  serve  as  crucial 
tests  of  digestibility  made  with  comparatively  pure  proteids,  such 
as  meat  and  egg,  and  pure  carbohydrates,  such  as  rice.  The  amount 
of  water  used  in  the  cooking  and  the  amount  ingested  must  be 
known,  and  can  be  found  out  by  evaporating  control  samples  to 
dryness. 

It  may  thus  be  learned  how  much  proteid  is  rendered  soluble  by 
the  pepsin  hydrochloric  acid,  how  much  casein  is  digested,  or  how 
much  of  starch  is  converted  into  dextrose  and  maltose  in  the  fifteen 
to  forty-five  minutes,  or  any  desired  period  during  which  the  par- 
ticular ferments  are  permitted  to  act.  The  results  can  naturally 
not  be  absolutely  correct,  but  only  relatively  so ; at  least,  they  are 
more  nearly  correct  than  the  conditions  of  the  experiment  will 
allow  the  results  of  Leube  and  Penzoldt  to  be. 

The  absolute  amount  of  food  need  not  be  regained  ; all  that  is  re- 
quired for  a comparative  study  is  to  learn  in  a given  sample — say, 
thirty  c.c. — the  proportion  of  soluble  and  insoluble  chyme.  Dex- 
trose present  can  be  determined  by  titration,  as  we  have  shown  else- 
where ; and  from  the  reactions  of  the  various  transition  products 
from  proteid  to  peptone  the  amount  of  the  latter  can  also  be 
approximately  known,  particularly  if  the  amount  of  solid  residue 
of  proteid  that  can  be  regained  is  learned  first. 


1 88 


DIETETIC  TREATMENT  OF  GASTRIC  DISEASES. 


It  is  an  interesting  fact  that  the  results  of  these  tests  of  digesti- 
bility performed  directly  on  the  normal  stomach  can  be  confirmed 
by  control  analysis,  made  with  animals  (making  allowance  for  the 
increased  secretion  of  HC1  in  dogs),  and  by  analysis  made  with 
artificial  digestive  mixtures  in  the  incubator.  In  the  chapter  on 
Digestion  by  Pepsin  it  has  been  explained  why  the  exact  gastric 
digestion  can  not  be  imitated  in  a test-tube,  mainly  because  the 
formation  of  peptone  in  the  stomach  remains  at  a certain  percent- 
age  by  the  absorption  of  peptones  over  that  amount.  As  soon  as 
the  amount  of  peptone  exceeds  a certain  percentage  it  retards, 
and  may  even  suspend,  proteolysis.  The  retardation  of  proteolysis 
which  occurs  in  hyperacidity  may  be  explained  in  this  way — i.  e., 
more  peptone  is  formed  in  a given  time  than  normally,  and  as  it 
can  not  be  absorbed  as  rapidly  as  it  is  formed,  it  inhibits  further 
proteolysis  by  its  presence  ; besides,  the  stomach  attempts  to  main- 
tain a fairly  constant  degree  of  concentration  of  contents  by  removal 
of  chyme  into  the  duodenum. 

Notwithstanding  all  these  differences,  test-tube  or  artificial  diges- 
tion experiments  are  very  valuable  for  comparative  studies  in 
digestibility,  particularly  when  deductions  are  made  in  combination 
with  test-meals  on  the  normal  and  diseased  human  stomach.  In 
the  stomach,  we  must  bear  in  mind,  there  is  a carbohydrate  and  a 
proteid  digestion  ; we  can,  however,  rarely  give  food  exclusively 
from  the  standpoint  of  gastric  digestion,  for  Leube  and  Penzoldt’s 
tables  show  that  the  greater  portion  of  the  digestive  work  is  exe- 
cuted in  the  intestine. 

Our  results,  so  far  as  we  can  judge  at  present,  agree  with  the 
main  ones  of  these  observers.  Leube  studied  the  duration  of  reten- 
tion of  various  foods  in  the  stomachs  of  diseased  patients,  and 
Penzoldt  in  the  stomachs  of  healthy  individuals  (that  is,  before  they 
were  expelled  in  the  duodenum).  We  have  confirmed  their  princi- 
ples by  experiments,  ascertaining  the  amounts  of  proteid  and  carbo- 
hydrates converted  into  a soluble  form  in  a given  time  in  normal 
and  pathological  stomachs.  These  experiments  were  supported  by 
tests  made  with  artificial  digestive  mixtures  and  on  dogs. 

The  explanation  of  the  agreement  of  these  various  methods  of 
testing  digestibility  is  probably  the  fact  that  food-substances  which 
are  most  rapidly  and  thoroughly  converted  into  a soluble  form 
are  also  most  easily  expelled  into  the  intestines.  Easily  soluble 
proteids,  though  solid,  are  readily  converted  into  a liquid  or  at 
least  semisolid  form,  in  which  they  are  readily  propelled  onward. 


ADAPTATION  OF  DIET. 


I 89 

Proteid  soluble  with  difficulty  is  retained  longer,  because  the  pre- 
antral  sphincter  has,  to  a degree,  a selective  action,  and  will  not 
readily  permit  the  passage  of  solid  food.  The  matters  of  solu- 
tion and  rate  of  propulsion  of  foods  are,  then,  the  factors  which 
are  intimately  correlated  and  largely  go  to  make  up  the  quality  of 
digestibility.  The  definition  of  a digestible  food,  then,  is  one  that 
makes  relatively  small  demands  upon  the  secretory  and  motor 
functions  of  the  stomach,  which  is  readily  absorbed  and  produces 
no  subjective  complaints  or  feeling  of  discomfort. 

From  a pathological  point  of  view,  however,  the  conception  of 
digestibility  is  a variable  one.  Foods  that  maybe  easily  digestible 
for  a gastric-ulcer  patient  may  be  very  indigestible  for  a case  of 
atrophic  gastritis  or  of  cancer.  Leube  and  Penzoldt’s  method  of 
estimating  gastric  digestibility  by  the  rate  at  which  various  foods 
are  expelled  into  the  duodenum,  gives  a relatively  correct  indica- 
tion for  the  sound  normal  organ,  because  secretory  and  motor 
functions  are  equally  taxed  as  they  go  hand  in  hand. 

The  results  can  not  be  unconditionally  applied  to  abnormal  states 
where  one  or  the  other  function,  or  both,  are  disturbed,  sometimes 
in  opposite  directions,  secretion  increased,  motility  diminished,  or 
vice  versa.  There  are  conditions  in  which  gastric  digestion  is  com- 
pletely destroyed  and  must  be  replaced  by  the  intestinal  function. 
There  are  states  of  absolute  and  permanent  loss  of  gastric  secre- 
tion (achylia),  in  which  the  propulsion  of  food  from  the  stomach 
is  not  delayed.  Now,  one  can  not  speak  of  gastric  digestibility  in 
these  cases,  because  there  is  very  little,  if  any;  but  such  cases  may 
have  a perfect  intestinal  digestion,  so  that  the  distinction  between 
“ gastric  ” and  “ intestinal  digestibility  ” is  important. 

The  diet  of  patients  must  be  varied  and  adapted  to  the  con- 
dition of  the  gastric  secretion,  motility,  and  absorption ; but  it 
must  also — and  this  is  generally  overlooked — be  adapted  to  the 
sensibility  of  the  stomach.  The  neuroses  of  sensation,  considered 
in  the  clinical  portion  of  this  work,  offer  a fertile  field  of  work  to 
the  thoughtful  dietarian.  An  abnormally  increased  feeling  of 
hunger,  in  which  this  intensely  heightened  sensation  can  hardly  be 
appeased  by  food  and  absence  of  the  feeling  of  satiation, — bulimia 
and  akoria, — as  well  as  absence  of  hunger,  in  which  the  appetite  is 
very  readily  appeased,  can  in  many  cases  be  successfully  treated 
by  diet. 

By  treating  bulimia  dietetically,  we  do  not  mean  to  suggest 
unlimited  ingestion  of  food,  but  rather  a painstaking  investigation 


I9O  DIETETIC  TREATMENT  OF  GASTRIC  DISEASES. 

of  the  cause,  which  may  be  an  unduly  large  stomach  or  conval- 
escence from  infectious  disease  (typhoid).  We  do  not  class  the 
increased  desire  for  food  observed  in  men  performing  exceptional 
physical  work,  in  women  during  pregnancy  and  lactation,  as  well 
as  in  rapidly  growing  children,  as  bulimia.  This  augmentation  of 
hunger  is  due  to  a greater  requirement  of  food,  because  the  organ- 
ism has  greater  expenses  in  supplying  material  for  growth  or 
energy.  Many  forms,  perhaps  sixty  per  cent.,  of  bulimia  cases  are 
due  either  to  hyperesthesia,  hyperacidity,  or  hypermotility.  If 
these  are  causes,  the  treatment  given  under  these  diseases  should 
be  administered  (clinical  part).  The  meals  should  be  allowed  every 
two  or  three  hours,  and  consist  largely  of  such  proteids  as  have  a 
great  combining  affinity  for  HC1.  These  are  given  under  Flei- 
scher’s list  of  the  HC1  binding  power  of  foods.  But  if  an  irritative 
state  of  the  glandular  layer  can  be  ascertained,  the  diet  should  be 
largely  amylaceous.  If  the  motility  be  exaggerated  with  the  hyper- 
acidity, it  is  well  to  direct  the  patient  to  drink  frequently  of  cold 
alkaline  waters,  such  as  the  Saratoga  Vichy,  or  the  alkaline  effer- 
vescent water  recommended  by  Jaworski  (see  clinical  part),  particu- 
larly when  the  stomach  is  empty. 

Anorexia , in  its  severe  forms,  is  most  often  due  to  organic 
changes  in  the  gastric  walls.  In  the  nervous  forms  it  is  often 
benefited  by  a course  of  forced  feeding  with  the  stomach-tube. 
Persistent  anorexia  in  highly  neuropathic  individuals  had,  in  fact, 
best  be  treated  this  way  as  soon  as  the  patients  positively  refuse 
food,  because  a complete  cure  can  frequently  be  accomplished  by 
gavage  alone.  The  feeding  through  the  tube  has  a moral  and 
educational  effect  not  to  be  underestimated.  In  my  experience  as 
physician-in-charge  of  Bay  View  Asylum,  many  cases  were  observed 
to  resume  taking  their  meals  with  good  appetite  as  soon  as  they 
became  convinced  that  forced  feeding  would  be  insisted  upon.  But 
aside  from  this  moral  effect  there  is  also  a physiological  one  : this 
consists  in  the  supplying  of  a stimulant  to  the  stomach  in  the 
form  of  food.  Nourishment  is  the  proper  stimulant  to  secretion, 
and  if  it  is  wanting  for  a long  time  the  functions  of  the  stomach 
soon  become  arrested,  and  with  them  the  appetite.  The  nutritive 
stimulant  to  the  gastric  mucosa  is  food;  it  causes  a filling  of  the 
blood-  and  lymph-vessels,  thus  indirectly  bringing  about  a better 
nutrition  of  the  histological  elements  of  the  mucosa  and  a resump- 
tion of  HC1  formation  with  ferments,  which  in  anorexia  is,  as  a rule, 
suppressed.  In  fact,  as  appetite  causes  eating  in  the  healthy,  so 


EFFECT  OF  ABSORPTION  ON  SELECTION  OF  DIET.  I9I 

eating  will  cause  appetite  in  these  cases  of  anorexia.  In  mild  cases 
of  anorexia  a sensation  of  hunger  is  frequently  started  up  by  salty 
and  “ piquante  ” articles,  such  as  caviar,  sardelles,  herrings,  etc.,  and 
at  the  same  time  small  doses  of  alcohol  with  bitter  tonics,  such  as  the 
Angostura  bitters,  are  advisable.  The  extractive  substances  in 
fresh  meats  (bouillon)  are  stimulants  to  appetite  (Pawlow).  Lavage 
with  solutions  of  chlorid  of  sodium  or  a .04  per  thousand  HC1  is 
most  effective.  The  most  essential  condition  to  a proper  dietetic 
treatment  is,  of  course,  that  the  patient  should  have  appetite.  A 
great  point  is  gained  if  he  can  be  made  to  take  food  with  pleasure. 
For  the  management  of  those  cases  with  anorexia  we  must  refer  to 
the  article  on  this  subject. 

The  author  agrees  with  Sir  William  H.  Broadbent  (“  Brit.  Med. 
Jour.,”  vol.  11,  1893,  p.  1268)  when  he  says:  “ In  all  cases  in  which 
the  cause  has  been  overfeeding  or  improper  food,  or  food  taken  at 
a wrong  time,  an  extremely  strict  and  meager  diet  for  a few  days 
will  be  the  best  treatment.  No  advantage  is  gained,  however, 
from  a low  diet  in  neurotic  cases. 

“ The  object  we  set  before  ourselves  must  be,  not  to  level  down 
the  diet  to  the  digestive  capabilities  of  the  stomach,  but  to  level  up 
the  digestion  till  it  can  deal  efficiently  with  the  amount  of  food  for 
the  due  support  of  the  nervous  system.  No  hard  and  fast  rule 
can  be  laid  down.  Speaking  generally,  such  a (neurotic)  patient 
will  digest  food  which  he  relishes  better,  even  if  it  have  the  repu- 
tation of  being  indigestible,  than  the  most  digestible  and  scientific- 
ally prepared  food  which  he  eats  by  order,  and  dislikes.  A very 
common  experience  is  that  he  is  tempted  by  a good  dinner,  eats 
largely  and  indiscriminately,  and  then,  instead  of  a bad  night  and 
great  discomfort,  which  he  thinks  he  has  deserved,  he  sleeps  well 
and  feels  all  the  better  for  his  indiscretion.” 

A very  important  point  will  be  to  disabuse  the  patient’s  mind  of 
the  idea  that  pain  after  meals  necessarily  indicates  that  the  food 
has  been  unsuitable.  One  day,  and  under  one  set  of  circumstances, 
anything  will  agree  ; on  another  day,  under  different  circumstances, 
nothing  is  digested.  Directions  must  be  given  not  to  eat  when 
exhausted  or  excited  or  anxious,  not  to  jump  from  meals  and  rush 
off  to  work  of  any  kind,  and  to  eat  very  slowly. 

The  state  of  the  gastric  absorption  has  to  be  considered  in  the 
selection  of  a diet.  In  most  text-books  this  factor  of  dietetics  is 
entirely  neglected.  In  the  light  of  the  most  modern  knowledge  on 
absorption,  that  furnished  by  the  work  of  von  Mehring,  according 


I92  DIETETIC  TREATMENT  OF  GASTRIC  DISEASES. 

to  which  it  is  almost  limited  to  cane-,  grape-,  and  milk-sugar, 
maltose,  dextrin,  alcohol,  and  peptone,  while  water  is  not  at  all 
absorbed  (see  Absorption),  it  is  not  at  once  evident  why  the  state 
of  absorption  should  be  considered  in  selecting  a diet.  Von 
Mehring’s  results,  however,  seem  to  point  the  way  in  selecting 
peptones,  maltose,  dextrin,  alcohol,  etc.,  where  we  must  depend 
on  rapid  diffusion  of  nutritious  material,  and  also  in  avoiding 
water,  or  foods  containing  water,  where  the  gastric  walls  are  weak, 
because  it  is  not  absorbed  and  overdistends  by  its  weight.  Not 
only  this,  but  simultaneously  with  resorption  a more  or  less  active 
excretion  of  water  occurs  into  the  stomach.  The  amount  of  this 
excretion  of  water  increases  or  diminishes  with  the  quantity  of 
substances  resorbed  or  taken  up.  Certain  gastric  diseases  con- 
nected with  much  fermentation  are  supposed  to  be  in  etiological 
relation  with  tonic  muscular  spasms — forms  of  tetany  of  gastric 
origin.  Bouveret  and  Devic  (“  Rech.  clin.  et  experim.  sur  la 
tetanie  d’origine  gastrique,”  “Revue  de  Med.,”  1892,  xn,  p.  48) 
assert  that  alcohol  is  instrumental  in  favoring  the  formation  of  an 
intragastric  diffusable  toxin  in  dilations  and  hypersecretive  states, 
and  that  these  poisons  bring  about  the  spasms.  Fleiner  (loc.  cit.) 
and  Kussmaul  recommend  that  no  alcohol  in  any  form  be  given  in 
dilatations  with  pyloric  stenosis,  where  naturally  the  absorption  of 
the  alcohol  must  be  very  much  retarded.  The  latter  authors  do 
not  accept  the  toxic  origin  of  the  spasms,  but  suggest  that  the 
alcohol  causes  a tremendous  excretion  of  water  into  the  stomach, 
thus  robbing  the  organism  of  a requisite  amount, — a tetany,  there- 
fore, due  to  drying  of  muscles  and  nerves  ; both  views  are  merely 
hypotheses.  The  practical  deduction  is  that  where  the  absorption 
has  been  found  defective  by  tests,  alcohol  had  best  be  avoided. 

•Boas  recommends  that  explicit  written  directions  be  given  to 
each  patient  after  the  diagnosis  has  been  made,  concerning — 

1.  Exact  time  of  meals. 

2.  An  exhaustive  account  of  articles  of  diet  and  luxury  that 
are  allowed.* 

3.  An  exact  statement  of  the  weights  and  measurements  of  the 
foods  and  beverages. 

4.  Brief  instructions  on  the  preparation  of  the  food,  temperature 
of  drinks,  seasoning,  etc. 

5.  Special  account  of  foods  that  are  forbidden. 

* Dr.  E.  R.  Schreiner  has  devised  a useful  diet-list  by  which  the  physician  is  enabled 
to  rapidly  fulfil  this  desideratum.  (Published  by  P.  Blakiston’s  Son  & Co.,  Phila.). 


PREPARATION  OF  FOOD. 


193 


The  time  for  the  ingestion  of  food  is  an  essential  factor  in 
dietetics,  particularly  with  our  American  business  men,  with  whom 
it  is  a common  practice  to  sacrifice  meal  hours  to  business.  The 
hours  for  meals  should  be  religiously  observed  by  gastric  sufferers, 
and  the  hours  for  stomach-rest  or  fasting  also.  Hyperacidity  and 
forms  of  nervous  dyspepsias  occasionally  require  small  meals 
frequently  repeated ; the  same  is  true  of  some  types  of  atonic  and 
stenotic  gastrectasias,  where  the  chyme  still  reaches  the  duodenum 
but  with  difficulty. 

Other  stomach  diseases  require  long  pauses  of  rest  between  the 
meals,  and  it  is  not  always  possible  to  state  a priori  how  much 
digestive  work  and  how  much  rest  any  particularly  diseased  stomach 
may  require.  It  is  only  after  a prolonged  study  of  the  various 
gastric  functions  that  the  physician  can  give  correct  instruction  in 
chronic  cases  (see  chapter  on  the  Use  and  Abuse  of  Rest,  etc.). 

There  is  much  need  for  enlarging  the  dietetic  menu  of  dys- 
peptics; nothing  should  be  forbidden,  except  there  are  actual  facts 
founded  on  experiment,  the  nature  of  the  disease,  or  the  idio- 
syncrasies of  the  case  proving  it  to  be  harmful.  Our  experience 
is  that  when  the  menu  is  too  limited  a certain  disgust  for  the 
diet  eventually  becomes  manifest,  resulting  either  in  temporary 
anorexia  or  a disregard  of  the  directions  and  indulgence  in  for- 
bidden foods. 

Directions  as  to  preparations  of  the  food  are  sometimes  neces- 
sary. Here  the  physician  must  be  able  to  indicate,  for  instance  in 
an-  or  subacidity  or  atrophic  gastritis,  that  the  meats  should  be  finely 
scraped  or  cut,  then  cooked  in  a steam  broiler,  with  a liberal  season- 
ing of  pepper  and  salt.  In  hyperacidity,  gastroxynsis,  gastritis 
acida,  and  the  convalescence  from  gastric  ulcer,  all  seasoning  except 
a little  salt  must  be  avoided;  wherever  there  is  excess  of  HC1  the 
meats  should  also  be  finely  divided  before  cooking.  The  amounts 
of  paprika,  red  and  black  pepper,  mustard,  horse-radish,  lemon, 
vinegar,  and  ginger,  that  can  be  allowed  in  cases  of  absolute  sup- 
pression of  secretion  (as  these  materials  have  some  effect  in  stimu- 
lating secretion),  must  be  stated. 

The  preparation  of  soups  and  gravies,  the  amounts  and  kinds  of 
fats  and  sugars  to  be  used  in  the  cooking,  are  points  of  importance. 
For  a more  detailed  account  of  these  indispensable  methods  and 
directions  for  preparations  of  food,  reference  must  be  had  to  works 
on  Dietetics, — vide  Gilman  Thompson,  Munk  and  Ufifelmann,  Wiel 
(“  Tisch  fur  Magenkranke  ”),  Boas  (“  Diat  u.  Wegweiser  f.  Magen- 


194 


DIETETIC  TREATMENT  OF  GASTRIC  DISEASES. 


kranke  ”),  Woltering  (“  Diatetisches  Handbuch  ”),  Yeo  (“  Food  and 
Diet  ”),  Penzoldt  (vol.  iv  of  the  “ Handbuch  f.  spezielle  Therapie  ”), 
Honigmann  (“  Zeitschr.  f.  Krankenpflege,”  1894,  No.  8),  Wegele 
(“  Diatetische  Behandl.  d.  Magen-  u.  Darmkrankh.”),  Leyden 
(“  Ernahrungstherapie  u.  Diatetik Moritz  (“  Die  Krankenernah- 
rung,”  Universal-Lexikon  der  Kochkunst,  2 vols.,  published  by 
J.  J.  Weber,  Leipzig).* 

The  Diet  as  Influenced  by  the  State  of  the  Secretion.— The 

anomalies  of  secretion  are:  (1)  Hyperacidity,  (2)  Sub-  and  Ana- 
cidity,  which  form  one  group  of  gastric  neuroses.  In  another 
group  we  may  classify  hypersecretion  (of  normal  gastric  juice  in 
which  the  HC1  is  not  increased  or  diminished).  This  is  the 
“ Magensaftfluss  ” of  Reichmann,  the  gastrosuccorrhea  chronica  or 
periodica,  of  which  Schreiber  holds  that  it  is  not  a disease  sui 
generis.  We  class  the  so-called  “ gastroxynsis  ” of  Rossbach  with 
the  hypersecretions,  because  it  impresses  us  to  be  a gastric  neuro- 
sis with  excessive  secretion  and  hemicrania,  and  is  hardly  entitled 
to  be  classed  as  a distinct  and  separate  disease. 

As  far  as  diet  is  concerned,3  the  hypersecretions  do  not 
exactly  coincide  with  the  hyperacidity  in  the  treatment.  For  the 
augmented  gastric  juice  in  the  super-  or  hypersecretions  may  be 
a passive  act  on  the  part  of  the  glands, — their  activity  may  be  kept 
up  by  retained  food.  But  in  hyperacidity  the  excessively  high 
percentage  of  HC1  is  an  active  process,  an  irritative  state  of  the 
mucosa  in  which  it  responds  with  excessive  formation  of  acid  to 
all  food  stimuli.  In  the  hypersecretions  the  diet  should  be  selected 
with  regard  to  favoring  rapid  gastric  evacuation.  In  hyperacidity 
there  is  no  better  treatment  than  rest.  These  are  states  in  which 
there  is  an  accelerated  digestion  of  albuminous  and  proteid  foods, 
and  a retardation  of  carbohydrate  digestion,  which  is  caused  by 
an  inhibition  of  the  inverting  action  of  the  diastase  of  the  saliva, 
the  ptyalin  by  the  excessive  amount  of  HC1.  The  same  is  true  of  the 
pancreas  diastase.  Boas  has  shown  (loc.  cit.)  that  a neutralization 
of  the  chyme  will  restore  the  diastatic  action,  but  we  have  assured 
ourselves  that  if  the  gastric  acidity  has  once  reached  0.3  per  cent, 
the  action  of  the  ptyalin  can  not  again  be  so  perfectly  restored  by 
neutralization  with  sodium  carbonate  as  it  was  before.  In  other 
words,  excessive  hyperacidity  permanently  damages  the  ptyalin. 


* A Complete  Encyclopsedia  on  the  Art  of  Cooking,  Preserving,  Table  Ethics, 
Menus,  etc. 


DIET  IN  HYPERACIDITY  AND  HYPERSECRETION.  1 95 

It  may  resume  some  inverting  action  after  neutralization,  but  it  is 
not  equal  to  that  evinced  during  the  first  forty-five  minutes  of 
normal  gastric  digestion.  An  intensely  acid  gastric  juice  will  pro- 
duce a deleterious  effect  on  the  bile  by  precipitating  from  it  a sub- 
stance up  to  the  present  time  not  isolated,  by  which  the  bile  aids  in 
partial  digestion  of  the  fats.  In  a similar  way  the  secretion  of  the 
pancreas  is  prevented  from  performing  its  work,  because  it  can  do 
so  only  in  an  alkaline  or  faintly  acid  medium.  There  are  three 
organic  diseases  which  dietetically  come  under  this  group  of  ex- 
cessive acidity  or  secretion ; these  are  ulcer,  gastritis  acida,  and 
ulcus  carcinomatosum.  Concerning  the  dietetic  treatment  of  hy- 
peracidities, uniformity  of  opinion  does  not  exist.  As  a general 
rule,  it  can  be  stated  that  in  the  simple  forms  a bland,  unirritating 
diet,  which  at  the  same  time  binds  as  much  hydrochloric  acid  as 
possible,  should  be  prescribed.  We  favor  a diet  that  does  not  irritate 
the  mucosa  any  more  than  is  absolutely  necessary.  There  are  two 
indications  : (i)  An  etiological  one,  directed  to  the  condition  of 
the  mucosa  and  demanding  rest  for  the  irritative  state  present ; 
(2)  a symptomatic  one,  directed  to  neutralization  of  the  excess 
of  HC1  by  diet  having  the  greatest  HCl-binding  affinity.  These 
two  indications  are  to  some  extent  opposed  to  one  another.  The 
etiological  indication  necessitates  avoidance  of  albuminous  food, 
for  in  our  experience  proteid  and  albuminous  foods  produce  an 
increased  secretion  of  HC1.  The  second  or  symptomatic  indication 
calls  for  a large  ingestion  of  albumen  to  combine  with  the  HC1. 
In  case  of  ulcer  the  food  must  be  the  least  irritating,  the  mildest 
that  our  menu  contains.  Not  the  total  quantity  of  acid  secreted 
constitutes  hyperacidity,  but  the  amount  secreted  in  excess  of  what 
is  required  for  combining  with  the  proteids.  For  instance,  a case 
may  show  hyperacidity  after  a simple  Ewald  test-breakfast  of  a roll 
and  a glass  of  water,  because  the  acid  secreted  meets  with  nothing 
to  combine  with  and  remains  free,  while  the  same  case  may  show 
very  little  excess  or  normal  acidity  after  the  first  of  our  double 
test-meals,  as  employed  at  the  University  of  Maryland,  consisting 
of  beefsteak,  eggs,  rice,  milk,  and  bread,  because  the  acid,  in  this  in- 
stance, at  once  enters  into  combination.  The  more  abundant 
secretion  of  HC1  is  more  completely  used  up  when  the  meals  con- 
sist of  a preponderance  of  proteid  food  than  when  they  con- 
sist of  carbohydrates.  Therefore,  the  dietetics  of  these  cases,  as 
usually  recommended,  include  the  red  meats,  venison,  game, 
turkey,  eggs,  chocolate,  etc.,  liberally,  a certain  limitation  of  carbo- 


I96  DIETETIC  TREATMENT  OF  GASTRIC  DISEASES. 

hydrates,  and  the  alkaline  carbonated  waters.  In  hyperacidity 
and  supersecretion  spices  are  to  be  forbidden,  and  only  so  much 
salt  as  is  indispensable  to  make  the  food  palatable.  All  acids,  such 
as  vinegar  or  lemon-juice,  in  the  food  simply  aggravate  the 
trouble. 

There  are  undoubtedly  different  kinds  of  hyperacidities.  We 
feel  justified  in  distinguishing  two  classes:  (1)  Those  in  which 
there  is  a preponderance  of  nervous  symptoms  and  fragments  of 
the  mucosa  show  no  increase  in  the  number  of  gland-tubules  or  in 
the  oxyntic  or  acid  cells  ; these  cases  are,  then,  of  a purely  neurotic 
type. 

(2)  Secondly,  those  in  which  there  is  an  increase  in  the  number 
of  gland-tubules  or  in  the  oxyntic  cells.  A simple  neurotic  case 
may  eventually  lead  to  increase  of  oxyntic  cells,  by  the  greater 
demand  for  acid  secretion.  There  is  no  hard  and  fast  line  to  sepa- 
rate these  classes,  but  they  demand  somewhat  different  treatment 
for  reasons  stated  further  on.  A number  of  competent  observers 
have  recommended  an  exclusion  of  proteid  and  an  increase  of  the 
carbohydrate  foods  in  hyperacidity. 

For,  although  proteid  foods  combine  with  more  HC1  than  any 
other,  they  are  also  the  greatest  stimulants  to  the  secretion  of  acid. 
See  Dujardin-Beaumetz  (“Traitement  des  maladies  de  l’estomac  ”) 
and  von  Sohlern  (“  Berlin,  klin.  Wochenschr.,”  xci,  Nos.  20  and  21)  ; 
Fleiner  (“  Volkmann’s  klin.  Vortr.,”  No.  103) ; Rummo  (“  Terapia 
clin.,”  1892,  Nos.  10,  II,  12);  v.  Jaksch  (“  Zeitschr.  f.  klin.  Med.,” 
Bd.  xvii,  1896).  These  writers  argue  that  carbohydrate  food  is 
not  so  irritating  and  calls  forth  much  less  secretion  of  HC1. 
W.  Roux  (“  Entwicklungsmechanik  der  Organismen,”  1895)  states 
that  increased  activity  heightens  the  specific  force  of  the  organs, 
while  diminished  activity  lowers  it.  The  existence  of  the  cells  of 
the  organism  depends  upon  their  work  ; those  that  work  most  are 
nourished  best  and  grow  strongest.  In  other  words,  the  elements 
in  any  tissue  that  are  incited  to  greatest  activity  and  function  will 
gain  supremacy  over  others  and  increase  in  strength  and  numbers. 
The  deductions  are  not  purely  theoretical,  for  not  only  do  we  find 
proliferation  of  acid  cells  in  hyperchlorhydria  to  be  present  in  from 
fifty  to  seventy-five  per  cent,  of  the  cases,  but  in  animals  with  a high 
acidity  of  HC1  (dog,  fox,  wolf,  etc.,  carnivora)  there  is  a tremendous 
multiplication  of  acid  cells.  It  seems  logical,  therefore,  that  there 
are  cases  in  which  the  hyperacidity  may,  in  the  long  run,  be  kept 
up  by  a proteid  diet,  although  for  the  time  being  this  diet  may 


HYPERACIDITY  TREATED  BY  AMYLACEOUS  DIET.  1 97 

render  the  acidity  less  by  combining  with  the  free  HC1.  Ex- 
perience teaches  that  the  most  annoying  symptoms,  the  gastralgia 
and  pyrosis,  are  promptly  relieved  by  the  proteid  diet,  and  we  shall 
indorse  the  latter  as  most  eminently  proper  in  selected  cases. 
When,  however,  the  symptoms  are  relieved  only  very  briefly,  par- 
ticularly when  the  ratio  of  the  ethereal  to  the  preformed  sulphates 
in  the  urine  is  found  to  become  very  high  under  a rich  albuminous 
diet,  and  the  indican  increases,  we  advise  a diet  rich  in  carbohy- 
drates and  fats.  The  author  has  analyzed  the  gastric  contents  of 
two  men  who  were  vegetarians  by  principle,  the  average  amount 
of  free  HC1  in  one  being  12.5  after  an  Ewald  test  breakfast;  in  the 
other  the  average  amount  of  free  HC1  was  10.6.  In  a Japanese 
student  who  had  lived,  according  to  his  own  statement,  almost 
exclusively  on  rice,  milk,  sugar,  and  a kind  of  Japanese  bread,  the 
average  amount  of  free  HCi  after  an  Ewald  test  breakfast  was  14.6. 
See  Chas.  E.  Simon,  on  “ The  Relation  of  Indican  to  Gastric 
Diseases”  (“  Amer.  Jour.  Med.  Sciences,”  August,  1895).  This 
can  be  filled  by  all  breads  and  articles  made  from  flour,  rice,  peas, 
beans,  potatoes,  the  cereals,  oatmeal,  and  rich  milk  and  butter. 
It  is  true  that  in  some  forms  of  hyperacidity  these  substances  can 
be  found  sometimes  six  hours  after  they  are  ingested,  unchanged  in 
the  stomach  ; but  here  the  motility  is  seriously  at  fault.  As  alkalies 
must  be  given  even  with  a proteid  diet,  they  should,  in  case  the 
food  consists  largely  of  carbohydrates  and  fats,  be  given  imme- 
diately after  meals  and,  if  need  be,  combined  with  ptyalin  or  diastase 
to  hasten  amylolysis.  It  is  frequently  observed,  that  the  amount 
of  free  HCI  becomes  less  and  less,  and  the  alkalies  and  artificial 
ferments  may  be  dispensed  with  if  the  amylaceous  diet  is  persisted 
in.  This  diet  we  suggest  particularly  after  the  albuminous  diet 
has  failed,  for  there  are  cases  of  hyperacidity  which  are  undoubt- 
edly maintained  by  an  exclusive  proteid  diet.  It  must  not  be  over- 
looked that  such  a thing  as  a pure  carbohydrate  diet  does  not 
exist,  because  all  articles  of  this  class  contain  protein,  and  some  very 
considerable  quantities  of  it ; peas,  beans,  and  lentils,  for  example, 
contain  more  protein  in  the  percentage  composition  than  pork, 
beef,  ham,  or  fish.  It  is  not  a total  exclusion,  but  simply  a re- 
duction of  proteid  that  is  practically  recommended.  According  to 
Pawlow  (“  Die  Arbeit  der  Verdauungsdriisen,”  p.  187),  fats  and 
oils  inhibit  the  secretion  of  HCI  by  the  gastric  mucosa.  We  have 
tested  this  on  ten  normal  persons  and  ten  cases  of  hyperacidity 
and  could  confirm  the  observation,  so  that  we  now  recommend 


I98  DIETETIC  TREATMENT  OF  GASTRIC  DISEASES. 

butter  and  olive  oil  in  as  large  quantities  as  can  be  expediently 
eaten,  for  cases  of  hyperacidity.  Strauss,  of  Berlin,  has  found  that 
sugars  as  in  candies  reduce  the  secretion  of  HC1. 

All  cases  of  hyperacidity  require  a certain  amount  of  carbohy- 
drates. It  is  a matter  of  experience  that  proteid  diet  alone  will 
not  permanently  satisfy  their  cravings.  Flour  and  the  many  arti- 
cles prepared  from  it  are  not  readily  converted  into  dextrin  in  an 
excessively  acid  medium.  It  is  expedient,  therefore,  to  recommend 
dextrinized  flours,  such  as  Avenacia,  Maggi,  and  Kufifeke’s  flour. 
The  American  product,  “ Horlick’s  Food,”  is  a flour  in  which  the 
wheat  starch  has  been  almost  entirely  converted  into  dextrin  by  malt 
diastase.  It  has  a high  caloric  value,  and  its  price  is  sufficiently 
moderate  for  humbler  practice  when  artificial  flours  seem  indi- 
cated. 

Regarding  the  preparation  of  carbohydrates,  we  refer  to  the 
special  lists  given  in  the  text  under  the  various  diseases,  and  to 
Wegele’s  “ Diatetische  Kiiche.”  In  the  hyperacidity  of  ulcer  the 
diet  must  be  of  the  least  irritating  quality,  and  the  coarse-fibered 
meats — beef,  mutton,  lamb,  veal,  venison — are  not  to  be  allowed, 
even  during  the  periods  of  convalescence,  and  when  they  are 
finally  conceded,  they  should  all  be  reduced  to  a pulpy  (scraped) 
form. 

In  sub-  or  anacidity,  when  the  motor  function  is  good,  the  prob- 
lem of  diet  is  not  so  complicated,  because  the  deficient  HC1  can 
be  supplied  if  it  is  found  necessary,  and  the  intactness  of  the  peris- 
talsis insures  a good  intestinal  digestion.  ^ As  the  motility  is  the 
only  safeguard  against  malnutrition,  great  care  should  be  taken  to 
avoid  injuring  it  by  overloading  the  organ.  Small  meals  frequently 
repeated  are  indicated,  consisting  of  very  tender  meat  (in  fine  sub- 
division), soft,  tender  vegetables,  such  as  finely  chopped  spinach, 
cauliflower,  ends  of  asparagus,  puree  of  potatoes,  peas,  beans,  len- 
tils. \ The  fats,  which  are  best  given  in  form  of  rich  cream  and  good 
butter,  have  a high  caloric  value.  Unfortunately,  they  depress 
the  already  deficient  secretion  of  HC1  still  more  in  subacidity. 
They  must  be  forbidden  as  soon  as  it  is  discovered  that  they  cause 
gastric  irritation  by  formation  of  fatty  acids.  The  diet  must  vary 
according  to  the  cause  of  the  sub-  or  anacidity.  If  it  can  be 
ascertained  that  there  is  no  injury  of  the  glandular  apparatus,  but 
simply  an  inhibition  of  secretion,  the  salty  and  spicy  articles,  even 
pepper  and  ginger,  may  be  advised. 

Such  sub-  or  anacidities  are  improved  by  taking  caviar,  sardelles, 


DIETETIC  PREPARATIONS  OF  BEEF. 


I99 


small  pickled  herrings,  or  anchovies,  before  meals,  because  salt  is  an 
approved  stimulant  to  secretion.  In  these  cases  HC1  is  not  only 
supplied  because  of  its  deficiency,  but  also  because  it  is  actually 
curative  in  hastening  the  resumption  of  secretion.  If,  however, 
the  absence  of  HC1  and  ferments  is  due  to  results  of  inflammation 
still  going  on,  all  spices  and  unnecessary  salt  and  foods  containing 
them  must  be  forbidden,  since  they  may  act  as  irritants.  Although 
HC1  is  absent,  it  will  be  found  best  not  to  administer  it  when  it  causes 
symptoms  of  gastric  distress.  In  these  cases,  where  the  mucosa 
is  extremely  sensitive  and  an  atrophic  gastritis  exists,  gastric  diges- 
tion had  best  be  converted  into  an  alkaline  proteolysis  and  amylo- 
lysis  by  supplying  pancreatin.  According  to  recent  experiments 
(Rachford,  “Amer.  Jour,  of  Physiol.,”  vol.  11)  sodium  bicarbonate 
retards  pancreatic  digestion,  and  hence  its  addition  to  pancreatin  is 
not  called  for.  In  these  extreme  cases  of  sub-  or  anacidity  it  is 
sometimes  found  that  hydrochloric  acid  gives  pain  and  even  causes 
emesis.  Meats  that  are  given  in  anacidity  must  not  be  too  fresh, 
but  properly  seasoned  and  very  tender ; they  must  be  thoroughly 
cooked  in  a steam  broiler  until  they  almost  fall  apart  into  the  primi- 
tive muscle-bundles.  A practical  way  is  to  rub,  cut,  or  scrape  the 
meat  prior  to  cooking  it.  Finally,  if  in  addition  to  the  anacidity 
one  has  reason  to  believe  that  duodenal  digestion  is  also  disturbed 
(from  chronic  duodenitis,  occlusion  of  the  pancreatic  or  bile-duct, 
or  from  catarrh,  or  carcinoma  of  the  duodenum,  pancreas,  gall- 
bladder, or  liver),  then  the  administration  of  meat-powders  and  beef 
peptones  is  in  order.  These  substances,  which  are  really  albumoses, 
though  capable  of  satisfying  the  requirements  of  metabolism,  are 
not  palatable  and  are  relatively  expensive.  The  peptones  most 
frequently  used  in  Germany  are  those  of  Kemmerich,  Denayer, 
and  Maggi.  Ewald  and  Gumlich  (“  Berlin,  klin.  Wochenschr.,” 
1890,  No.  44)  have  investigated  the  qualities  of  a “ peptone  beer,” 
and  found  it  quite  nutritious.  Boas  speaks  favorably  of  the 
American  product  “ Mosquera  ” Julia  Beef  Meal.  Professor  R. 
H.  Chittenden  (in  a report  to  the  Philadelphia  County  Medical 
Society,  May,  1891)  has  given  the  results  of  his  analysis  of 
American  beef  products,  which  are  found  in  the  following  table  : 


200 


DIETETIC  TREATMENT  OF  GASTRIC  DISEASES. 


PERCENTAGE  COMPOSITION  OF  BEEF  PRODUCTS,  ANALYZED  1891. 


Constituents. 

Liebig’s  Extract 
of  Beef. 

Armour’s  Ex- 
tract of  Beef. 

Valentine’s 
Meat  Juice. 

Wyeth’s 
Beef  Juice. 

Bovinine. 

Murdock’s 
Liquid  Food. 

1 

Johnston’s 
Fluid  Beef. 

Arlington 
Chemical  Co.’s 
Beef  Peptonoids. 

Mosquera 
Beef  Meal. 

Water  (at  1 io°  C.), 

20.06 

14.03 

60.31 

57-88 

81.09 

83-99 

39-58 

6.80 

6.68 

Solid  matter  (at 
no0  C.),  . . . 

79-94 

85-97 

39.69 

42. 12 

18.91 

16.01 

60.42 

93.20 

93-32 

Soluble  in  water,  . 

50.40 

48.14 

31.26 

Insoluble  in  water, 

0 

0 

0 

O 

0 

0 

10.02 

45.06 

62.06 

Inorganic  constitu- 
ents, .... 

24.04 

28.29 

II.30 

17-52 

1.02 

0.66 

13-52 

5.08 

4-23 

Phosphoric  acid 
(P205),  .... 

9-13 

7.28 

4.00 

3-94 

0.03 

0.09 

3-91 

I.40 

I.71 

Fat,  ether  extrac- 
tives,   

0.91 

I.27 

0.78 

0.85 

1.49 

0.27 

1.29 

2-95 

13.60 

Soluble  in  80  per 
cent,  alcohol,  . 

55.72 

67.92 

29.15 

35-o8 

34-io 

Total  nitrogen, 

9-52 

8.80 

2.68 

3-25 

2.43 

2.29 

7.38 

4.42 

12.36 

Nitrogen  of  insolu- 
ble matter,  . . 

1.46 

3-25 

7-65 

Insoluble  proteid 
matter,  . . . 

9.12 

20.30 

47.81 

Soluble  albumin 
coagulable  by 
heat,  . . . . 

0.06 

0.68 

o-55 

0.47 

13.98 

14.29 

0 

O 

0 

Soluble  albumoses, 

0 

0 

0 

0 

0 

0 

0 

5-44 

11.09 

Peptone,  ... 

0 

0 

0 

0 

0 

0 

0 

1.87 

18.34 

Total  proteid  mat- 
ter available  as 
nutriment,  . . 

0.06 

0.68 

0-55 

0.47 

13.98 

14.29 

9.12 

27.61 

77.24 

Nutritive  value  as 
compared  with 
fresh  lean  beef 
(lean  beef— 100), 

0.30 

3-50 

2.80 

2.40 

72.40 

74.00 

47.20 

14  30 

4CO.00 

Armour  & Company,  of  Chicago,  manufacture  a valuable  product 
which  is  called  “ Vigoral,”  containing  sixty-eight  per  cent,  albumi- 
noids. It  is  a saturated  solution,  or  rather  suspension,  of  pure 
powdered  beef  in  beef  extract.  These  substances  readily  decom- 
pose and  should  be  tested  as  to  their  freshness.  So  the  table  of 
Chittenden’s  comparisons  is  valuable  only  to  show  the  superiority 
of  foods  containing  the  beef  in  powder  or  insoluble  form,  to  the 
extracts,  which  represent  only  the  soluble  salts  of  the  beef  and 
very  little  of  the  nitrogenous  constituents — rarely  more  than  eight 
per  cent. 

The  Mosquera  beef  meal  is  a product  that  undoubtedly  has  an 
exceptionally  high  nutritive  value,  the  total  proteid  matter  avail- 
able as  nutriment  being  77.24  per  cent.  It  also  contains  13.60 


DIETETICS  OF  ATONY  AND  DILATATION. 


201 


per  cent,  fat,  1 1.09  per  cent,  soluble  albumoses,  and  18.34  per  cent, 
of  peptone.  With  Chittenden’s  authority  for  this  analysis,  and  our 
own  experience  as  to  its  easy  digestibility  and  perfect  absorption, 
this  product  commands  an  important  place  in  our  dietary  for  sub- 
or  anacidity  and  gastric  atrophy,  particularly  when  associated  with 
intestinal  disease.  The  juice  of  the  pineapple  contains  a proteo- 
lytic ferment,  thus  adapting  this  fruit  for  the  treatment  of  cases 
where  no  gastric  juice  is  secreted.  For  its  digestive  effect  only  the 
juice  of  the  fresh  fruit  should  be  swallowed,  and  the  fiber  removed 
from  the  mouth.  By  boiling  the  pineapple  the  proteolytic  ferment 
is  destroyed. 

When  atony  or  pronounced  dilatation  accompany  any  gastric 
disease,  particularly  those  already  referred  to,  the  dietetic  manage- 
ment is  most  important.  Weakening  and  loss  of  motility  are 
among  the  most  serious  affections  of  the  organ,  and  in  the  gravity 
of  their  consequences  outweigh  any  disturbance  of  secretion. 
Motor  insufficiency  may  supervene  upon  any  gastric  disease.  As 
a rule,  the  chronic  affections  rarely  become  manifest  until  the 
motility  is  disturbed;  that  is,  until  the  muscular  tonus  relaxes. 
Many  times  a co-existing  secretory  or  organic  disease  is  the  cause 
of  the  dilatation ; for  instance,  it  is  generally  admitted  that  hyper- 
acidity can  produce  spasm  of  the  pyloric  sphincter,  which  the 
gastric  peristalsis  will  be  unable  to  overcome. 

In  the  section  on  Motor  Insufficiency,  in  the  third  (clinical)  part 
of  this  work,  the  etiology  of  this  affection  will  be  fully  considered. 
When  ingesta  remain  in  the  stomach  longer  than  normally,  fermen- 
tation, gas-formation,  and  distention  eventually  supervene,  causing 
stasis  in  the  muscular  layer  and  dilatation  (Naunyn,  “ Deutsches 
Arch.  f.  klin.  Med.,”  1882,  Bd.  xxxi).  In  dilatation  proper — the 
deciding  sign  of  which  is  presence  of  ingesta  in  the  stomach  in  the 
morning  after  a test-meal  taken  twelve  hours  previously — we  must, 
from  a dietetic  as  well  as  from  a therapeutic  standpoint,  distinguish 
between  the  myasthenic,  atonic  form  due  to  simple  relaxation  of 
the  muscularis,  and  the  obstructive  form  due  to  pyloric  or  duodenal 
stenosis. 

In  the  first  variety  dietetic  and  other  treatment  may  effect  a cure. 
In  the  stenotic  types  little  beyond  transient  improvement  must  be 
expected,  except  when  the  obstacle  (cicatrix,  carcinoma,  hyper- 
trophied pylorus,  gall-stones,  peritoneal  adhesions,  etc.)  can  be 
removed  permanently  or  temporarily,  or  where  a new  route  can  be 
devised  for  the  passage  of  the  chyme.  Here  abdominal  surgery 
14 


202 


DIETETIC  TREATMENT  OF  GASTRIC  DISEASES. 


asserts  itself,  and  gastro-enterostomy  has  thus  far  produced  the 
best  results.  (See  chapter  on  Operative  Treatment  of  Gastric 
Diseases.) 

The  dietetic  management  of  dilatation  will  have  regard  not  only 
to  the  injured  muscular  tonus,  but  also  to  the  secretory  or  organic 
disease  with  which  it  may  be  associated.  For  example,  if  it  is 
associated  with  chronic  gastritis,  the  diet  must  be  that  for  this  dis- 
ease and  dilatation ; and  if  it  is  combined  with  hyperacidity,  the 
diet  is  the  one  devised  for  this  trouble  and  dilatation.  As  the 
fundamental  thing  in  dilatation  is  to  prevent  burdening  of  the 
muscularis,  the  diet  must  be  as  light  in  weight  as  possible,  and  espe- 
cially, as  far  as  practicable,  exclude  liquids,  for  these  are  not  only 
all  heavy,  but  are  not  at  all  absorbed  from  the  stomach  (excepting 
alcohol).  The  requisite  amount  of  water  is  best  given  by  high 
sigmoid  enemata  : y2  of  a liter,  slightly  warmed,  two  or  three  times 
a day.  In  this  manner  a water  impoverishment  can  be  prevented 
(see  Wegele,  “ Die  atonische  Magenerweiterung  u.  ihre  Behand- 
lung”).  An  absolutely  dry  diet  was  suggested  by  van  Swieten, 
Chomel  (“  Les  Dyspepsies,”  Paris,  1857),  and  Fossagrives,  but  its 
strict  execution,  as  was  developed  by  Schroth,  is  impracticable, 
since  fully  developed  dilatations  require  months,  even  years,  of 
strict  dieting,  which,  if  followed  out  on  these  lines,  would  inevitably 
produce  dangerous  drying  ,out  of  the  organs  (Kussmaul,  “ Zur 
Behandl.  d.  Magenerweit.,”  “ Deutsch.  Arch.  f.  klin.  Med.,”  Bd.  vi). 

Although  it  is  not  a dietetic  therapy,  yet  lavage  must  be  men- 
tioned here.  If  large  masses  of  decomposed  food  are  vomited, 
the  stomach-tube  is  indispensable.  Milk  diet,  used  exclusively, 
aggravates  the  symptoms  without  exception.  Should  the  vomit 
or  test-meals  reveal  that  carbohydrates  habitually  disagree  and 
ferment,  an  exclusive  beef-  or  meat-diet  for  a few  weeks  is  rational, 
and  is  followed  by  less  distention  (Minkowski). 

In  very  severe  and  extreme  cases  of  dilatation  one  may  be  com- 
pelled to  feed  exclusively  by  rectal  enemata,  for  the  preparation  of 
which  we  refer  to  the  paragraph  on  that  subject.  Soups  and  drinks 
during  meals  must  be  avoided.  Great  thirst  can  be  quenched  by 
taking  small  pieces  of  ice  into  the  mouth.  Patients  that  are  being 
treated  with  lavage  may  be  permitted  to  quench  their  thirst  before 
the  evacuation.  Moritz  has  shown  that  solid  food  is  retained 
longer  than  semisolid ; the  latter  form  is,  therefore,  preferable. 
Meats  are  given  best  in  scraped  or  finely  chopped  state,  and  must 
be  of  the  red  varieties  and  free  from  fat.  Meat  dumplings  or  balls, 


DIET  IN  CARCINOMA. 


203 


hash  of  fresh  beef  or  lamb,  Mosquera  beef-powder,  Valentine’s  or 
Wyeth’s  juice,  or  Wiel’s  beef-jelly,  are  adapted  to  dilatations  in 
which  secretion  is  preserved.  When  gastric  digestion  is  much 
lowered  the  cereal  and  leguminous  products  are  useful.  We  recom- 
mend gruels  made  from  arrowroot,  tapioca,  rice,  sago,  cerealin, 
strained  oatmeal,  after  which  we  are  accustomed  to  advise  some 
form  of  diastase,  either  the  taka  diastase  or  malt  extract.  Aleu- 
ronat  flour,  containing  much  digestible  albumin  (prepared  by  Dr. 
Hundhausen,  Hamm,  Westphalia,  Germany),  and  the  soup  meals 
of  C.  H.  Knorr  (Heilbronn,  Germany)  are  of  use  when  prepared 
according  to  our  dietetic  directions.  To  be  digestible,  even  for 
healthy  stomachs,  all  leguminous  foods  must  be  cooked  a long 
time.  For  gastric  sufferers  they  must  be  used  only  in  a condition 
of  very  fine  subdivision,  and  partial  dextrinization  of  their  starch, 
rendering  it  more  soluble.  Besides  the  products  of  this  character 
just  mentioned,  we  have  used  the  Liebig  malto-leguminose  (pre- 
pared by  William  Roth,  Jr.,  in  Stuttgart),  and  the  biscuit-legumi- 
nose  (Theodor  Fimpe,  in  Magdeburg).  The  firm  of  Hartenstein  & 
Company  (Chemnitz,  Germany)  prepare  several  good  leguminous 
flours.  The  Farbenfabriken  of  Elberfeld,  Germany,  produce  the 
valuable  mixture  of  albumoses  known  as  somatose , which  can  be 
obtained  in  the  form  of  chocolate,  cocoa,  and  biscuit.  Further 
references  in  Penzoldt  and  Stintzing’s  “ Handbuch  d.  Therapie,” 
vol.  iv,  pp.  256-258. 

The  collection  of  dietaries  will  contain  menus  for  gastric  atony 
and  dilatation  (1)  with  loss  of  secretions  or  anacidity;  (2)  with 
normal  or  augmented  secretions;  (3)  with  serious  stenotic  symp- 
toms. In  severe  cases  of  the  latter  type  even  the  most  sparing 
diet  by  the  mouth  will  be  impossible,  and  as  a last  resource  we 
must  fall  back  on  nutritive  rectal  enemata.  Sometimes  after  a 
week  to  ten  days  of  rectal  alimentation,  the  diseased  condition 
becomes  so  improved  that  partial  mouth-feeding  may  be  resumed. 

The  diet  in  the  various  types  of  carcinoma  coincides  with  that 
of  motor  insufficiency  and  dilatation  whenever  the  neoplasm  is 
causing  the  stenosis.  In  carcinoma  of  those  portions  which  do 
not  form  an  obstacle  to  the  exit  of  the  chyme,  and  where  the 
motility  is  good,  the  patient’s  appetite  must  be  stimulated  as 
much  as  possible  by  strychnin,  HC1,  bitter  tonics,  condurango, 
etc.,  and  nothing  forbidden,  as  the  physician  must  be  satisfied  if 
the  patients  eat  anything.  As  chronic  gastritis  is  always  present 


204 


DIETETIC  TREATMENT  OF  GASTRIC  DISEASES. 


even  in  these  cases,  the  diet  list  as  given  for  this  disease  is  ad- 
visable. 

In  cancer  arising  on  the  basis  of  old  gastric  ulcers,  the  ulcus 
carcinomatosum , there  is  often  a pronounced  hyperacidity  which, 
naturally,  is  best  met  by  the  diet  recommended  for  augmented 
gastric  secretion,  provided  the  stenosis  permits  it. 

Where  the  stenosis  is  at  the  cardia  the  matter  of  proper  alimen- 
tation becomes  difficult. 

So  long  as  the  stenosis, — no  matter  from  what  cause, — can  be  kept 
open  by  bougies  and  sounds,  a highly  nourishing  liquid  diet  of 
milk,  eggs,  beef-jelly,  beef-meal,  peptone,  nourishing  soups  con- 
taining somatose,  and  wines  are  indicated.  In  rare  cases  we  have 
seen  life  prolonged  by  allowing  the  esophageal  tube  to  remain  in 
situ  and  feeding  through  it  every  two  to  three  hours.  Leyden 
(Leyden-Renvers,  “ Deutsche  med.  Wochenschr.,”  1887,  No.  50) 
and  Gersunny  (“Wien.  med.  Wochenschr.,”  1887,  No.  43)  have 
strongly  indorsed  this  procedure  for  esophageal  strictures  of  car- 
cinomatous origin.  After  the  stenosis  is  no  longer  passable,  and 
gastrostomy  becomes  necessary,  in  order  that  nutrition  may  be 
carried  on  through  the  gastric  fistula.  According  to  Friedenwald’s 
studies  on  salivary  digestion  it  would  be  logical  to  advise  these 
unfortunates  to  chew  their  food  first,  and  removing  it  from  the 
mouth  insert  it  through  the  fistula.  But  where  this  is  objected  to, 
it  is  expedient  to  add  fifteen  grains  of  ptyalin  to  the  food,  which 
must  always  be  liquid  or  in  the  form  of  paste,  soup,  or  gruel. 
Finally,  when  gastrostomy  can  not  be  done,  or  permission  to  per- 
form it  is  refused,  the  only  way  to  nourish  the  patient  is  by  rectal 
enemata.  So  it  is  evident  that  the  symptoms  and  dietetic  manage- 
ment of  carcinoma  vary  greatly  according  to  its  location.  In  Sep- 
tember, 1897,  we  had  under  observation  a patient  who  had  a gastric 
tumor,  which  as  far  as  could  be  palpated  was  about  four  inches 
long  and  two  inches  wide.  There  has  been  no  evidence  of  HC1 
secretion  for  over  a year,  but,  as  the  motility  is  very  good,  there 
is  no  lactic  acid  formation.  The  Oppler-Boas  bacillus  has  been 
repeatedly  found  in  the  gastric  contents  when  there  was  temporary 
food  retention.  Permission  for  operation  was  refused.  Still,  this 
patient,  with  an  undoubted  carcinoma,  gained  twelve  pounds  in 
six  weeks,  and  had  no  subjective  complaints  while  in  our  sani- 
tarium for  digestive  diseases. 

With  anacidity  and  a fair  peristalsis  a carbohydrate  diet  is  applic- 
able to  carcinoma,  but  when  HC1  is  well  tolerated  the  various 


DIET  IN  GASTRIC  ULCER. 


205 


meats  must  not  be  forbidden.  Of  these,  Boas  prefers  the  meat  from 
various  fishes.  Where  HC1  is  not  well  tolerated,  pancreatin  is  in 
place.  Lavage  can  not  be  avoided  when  much  fermentation  and 
signs  of  dilatation  are  marked;  in  case  these  signs  are  very  annoy- 
ing, a few  days  of  exclusive  meat  diet  or  of  rectal  feeding  may  be 
necessary  to  restore  somewhat  of  the  lost  gastric  tonicity.  Long 
before  pyloric  stenosis  is  complete,  the  case  should  be  transferred 
to  the  surgeon,  as  the  resorption  from  the  stomach  itself,  even  if 
it  were  normal,  is  insufficient  to  maintain  life.  Those  materials 
that  are  readily  absorbed  from  a healthy  stomach,  such  as  albu- 
moses,  peptone,  glucose,  and  maltose,  etc.,  are  given  in  these  cases. 
There  is  little  evidence,  however,  of  their  being  absorbed.  The 
good  effects  of  gastro-enterostomy  consist  not  only  in  the  entrance 
made  for  the  food  into  the  intestine,  whereby  better  digestion 
becomes  possible,  but  also  in  an  improvement  in  the  inflammatory 
process  around  the  neoplasm,  which  is  no  longer  kept  in  continual 
irritation  by  stagnating,  fermenting  masses  of  food  in  constant 
contact  with  it.  The  main  reason  why  operations  do  not  bring  as 
much  relief  and  improvement  as  is  expected  is  to  be  sought  in  the 
delay  in  performing  them. 

The  Dietetics  of  Gastric  Ulcer  and  Erosions. — There  are 
three  types  of  gastric  ulcer  which  demand  a varying  or  separate 
dietetic  treatment.  These  are  : (1)  Light  attacks  with  pain,  hyper- 
acidity, and  pyrosis,  but  no  vomiting  of  blood.  (2)  Serious  cases 
that  have  had  hematemesis,  and  still  have  signs  of  it  at  the  time  of 
presentation.  (3)  Old,  chronic,  frequently  relapsing  gastric  ulcers. 
There  are  forms  that  run  a latent  course,  void  of  symptoms  until 
a sudden  severe  hemorrhage  surprises  the  patient  and  physician, 
and  possibly  terminates  the  case.  Erosions  which  have  no  great 
extension  laterally  nor  toward  the  depth,  and  can  be  recognized 
by  fragments  of  mucosa  found  in  the  wash-water,  yield  very 
readily  to  an  exclusive  diet  of  milk  combined  with  rest.  During 
the  gastric  hemorrhage  we  advise  that  nothing  at  all  be  given  by 
the  mouth,  not  even  water,  nor  ice  pills, — absolutely  nothing;  but 
absolute  rest,  a hypodermic  injection  of  30^  of  ergotol,  and,  if 
pain  and  restlessness  are  marked,  of  a gr.  of  morphin  sul- 
phate hypodermically,  and  a small  ice-bag  placed  over  the  epi- 
gastrium. Wiel  claims  to  have  arrested  gastric  hemorrhage  by 
lavage  with  cold  (io°  C.)  or  hot  (420  C.)  water.  Such  treatment 
in  profuse  bleeding  at  first  impresses  one  as  hazardous.  But  the 
author  has  had  very  good  results  from  lavage  with  ice-water  in 


20  6 


DIETETIC  TREATMENT  OF  GASTRIC  DISEASES. 


arresting  severe  gastric  hemorrhage.  (See  Ewald,  “ Philadelphia 
Med.  Jour.,”  vol.  n,  p.  334.)  This  course  has,  in  a very  large 
number  of  cases,  been,  as  a rule,  very  satisfactory. 

If  there  is  much  weakness  we  use  the  Boas  or  Ewald  nutritive 
enemata  on  the  day  of  and  following  the  hematemesis  ; but  if  the 
pulse  is  good  we  dispense  with  them.  On  the  day  following  the 
hemorrhage,  milk  in  teaspoonful  doses  is  given  every  half  hour; 
egg-albumen,  if  it  is  taken  willingly,  is  more  fitting,  as  it  combines 
with  a larger  amount  of  HC1,  and  when  diluted  it  does  not  stimu- 
late secretion. 

Brandy  and  wine  are  to  some  extent  irritating  to  ulcers  and 
excite  more  secretion  ; they  are  accordingly  not  given  except  there 
be  great  prostration.  On  the  third  day  it  will  be  safe  to  proceed 
to  carrying  out  a Leube  rest  cure,  with  the  consecutive  order  of 
diet  suggested  by  him  or  the  diet  lists  proposed  by  Penzoldt,  both 
of  which  present  four  different  groups  of  food-materials.  Be- 
ginning with  the  simplest  and  most  digestible,  they  gradually  lead 
up  to  a more  consistent  ordinary  household  menu. 

Each  of  these  four  diet  orders  must  be  persisted  in  from  one 
week  to  ten  days.  Penzoldt’s  and  Leube’s  diet  orders,  together 
with  our  explicit  diet  lists  for  various  stages  of  gastric  ulcer,  will 
be  appended.  The  principle  underlying  all  treatment  by  food  in 
these  cases  is  to  secure  the  greatest  amount  of  rest  and  such  sub- 
stances as  will  combine  with  the  largest  amount  of  HC1  and  relieve 
the  hyperacidity.  In  a number  of  cases  of  ulcer  we  have  found 
that  an  amylaceous  diet  was  retained  better  and  caused  less  pain 
than  scraped  beef  or  soft  eggs.  It  is  advised  on  the  same  princi- 
ples as  stated  on  pages  195—19/. 

In  chronic  and  frequently  recurring  cases  of  ulcer,  McCall, 
Anderson  (“Brit.  Med.  Jour.,”  May  10,  1890),  and  H.  B.  Donkin 
(“The  Lancet,”  September  27,  1890),  have  had  excellent  results 
from  total  exclusion  of  the  stomach  from  digestion,  by  feeding  with 
rectal  enemata  altogether ; some  of  their  cases  were  nourished  in 
this  way  for  twenty-three  days.  Riegel  (“  Zeitschr.  f.  prakt.  Aerzte,” 
1890,  No.  2)  speaks  enthusiastically  of  this  treatment  in  stubborn 
cases  of  ulcer,  and  Boas  reports  ten  cases,  all  of  which  but  one 
were  cured  by  this  method,  by  giving  three  to  four  of  his  nutritive 
enemata  daily  for  fourteen  days.  We  have  a personal  experience 
of  twenty-five  persistent  cases  of  ulcer  treated  in  this  manner, 
together  with  nitrate  of  silver,  bismuth  subnitrate  internally,  and 
rest  cure,  and  are  disposed  to  look  upon  the  treatment  with  great 


DIET  IN  SENSORY  NEUROSES. 


207 


favor.  (See  Gros,  “ Traitement  de  Malad.  de  l’estomac  par  la  cure 
de  Repos  absolu,”  etc.).  An  ulcer  must  not  be  considered  cured 
until  there  is  no  more  epigastric  pain  on  pressure  and  the  patient 
gains  weight  (Gerhardt). 

The  treatment  of  the  sensory  gastric  neuroses,  to  be  effective, 
must  combine  a number  of  remedial  agents  with  diet. 

Hyperesthesia , gastrodynia , or  gastralgia , and  neurasthenia  gastric  a 
are  morbid  states,  the  treatment  of  which  must  be  largely  directed 
to  the  central  nervous  organs.  The  same  must  be  said  of  the  motor 
neuroses  : Cardiospasm  and  pylorospasm,  nervous  vomiting , rumina- 
tion, KussmauV s peristaltic  unrest , incontinence  of  the  cardia  and  of 
the  pylorus.  These  diseases  demand  electric,  hydropathic,  climatic, 
and  medicinal  measures,  with  special  massage. 

A very  careful  investigation  into  possible  causative  constitutional 
morbid  states  (anemia,  gout,  rheumatism,  tuberculosis,  chlorosis, 
uric  acid  diathesis)  will  often  reveal  a removable  underlying  etio- 
logical foundation.  Fliess  has  reported  cases  of  gastralgia  and 
vomiting,  emanating  reflexly  from  the  nasal  mucosa,  and  has  cured 
them  by  local  treatment  (“  Neue  Beitr.  z.  Klinik  u.  Therapie  d. 
Nasal-Reflexneurose  ”).  A case  of  intense  gastralgia  that  came 
on  particularly  at  night  was  cured  by  mercurial  inunctions;  the 
author  having  suspected  syphilis,  although  this  was  denied  by 
the  patient.  In  a similar  way  attention  to  gynecological  disorders 
in  the  female  and  genito-urinary  diseases  in  the  male  have  led 
to  the  cure  of  distressing  nervous  dyspepsias.  In  the  gastric 
neuroses  of  motor  or  sensory  type  the  diet  must  be  based,  as  in  all 
previous  diseases,  as  far  as  is  expedient,  upon  the  state  of  the  secre- 
tion and  motility.  When  the  general  nutrition  is  disturbed,  the 
plan  of  treatment  most  generally  adopted  is  a fattening  rest  cure 
according  to  the  principles  laid  down  by  Weir  Mitchell  and  Play- 
fair. This  treatment,  though  not  universally  applicable,  is  the  one 
most  to  be  employed  in  nervous  vomiting  of  hysterical,  anemic, 
and  chlorotic  origin,  and  in  stubborn  cases  of  anorexia  and  gas- 
tralgia. It  is  somatic  and  psychical  at  the  same  time.  We  have 
had  ample  opportunity  to  test  the  dietetic  part  of  this  treatment  as 
it  has  been  developed  by  Burkart  in  Germany  (“  Volkmann’s  klin. 
Vortrage,”  No.  245).  And  cases  of  the  types  described  have,  in  our 
local  sanitarium  and  in  the  various  hospitals  with  which  the  author 
is  connected,  been  completely  cured.  Of  course,  organic  changes 
in  the  digestive  organs  render  the  proper  nutrition  impossible. 

Contraindications  to  fattening  cures  are : Cerebral  excitation  or 


208 


DIETETIC  TREATMENT  OF  GASTRIC  DISEASES. 


depression;  hysteria,  with  uncontrollable  vomiting;  and  visceral 
neuralgias,  which  are  expressions  of  sympathetic  nerve  diseases. 

The  best  results  with  Weir  Mitchell’s  restand  fattening  cures  are 
obtained  in  neurasthenic  or  hysterical  anorexia  with  much  emacia- 
tion, but  where  there  is  no  organic  digestive  disease.  Wherever  the 
nervous  dyspepsia  is  accompanied  by  gastritis,  atony,  or  dilatation, 
fattening  cures  may  easily  cause  pain,  pressure,  vomiting,  and  diar- 
rhea; so  that  if  such  cures  are  attempted  because  everything  else 
has  been  tried,  one  must  be  cautious  not  to  persist  in  systematic 
introduction  of  large  amounts  of  food,  even  in  divided  portions,  as 
the  frequently  repeated  small  portions  may  accumulate  when  gastric 
atony  exists,  etc.,  and  aggravate  the  symptoms. 

Burkart  begins  with  ioo  gm.  of  milk  with  Zwieback  every  two 
hours,  and  increases  it  so  that  two  to  three  liters  of  milk  per  day 
are  taken  after  fourteen  days  of  treatment.  The  milk  may  be 
flavored  with  sugar,  cocoa,  tea,  lime-water,  or  salt,  according  to 
taste ; and  after  a few  days  other  articles  of  diet  are  cautiously 
added.  We  give  Burkart’s  complete  menu  among  our  diet  tables. 

Neurasthenia  gastrica  (Ewald),  or  the  nervous  dyspepsia  of  Leube, 
when  it  occurs  in  males,  is,  in  our  experience,  not  benefited  by  the 
methods  of  Weir  Mitchell  or  Burkart.  Here  more  than  ever  the 
physician  must  endeavor  to  remove  the  cause  if  possible  (excess  in 
tobacco,  overwork,  uric  acid  diathesis,  sexual  overindulgence).  A 
definite  diet  can  not  be  given,  because  there  are  rarely  two  cases 
alike ; the  dietetic  treatment  of  nervous  dyspepsia  is  difficult,  the 
strictest  individualization  is  requisite. 

The  prognosis  as  regards  perfect  recovery  is  doubtful.  An 
attempt  with  the  Leube  or  Penzoldt  order  of  dieting  is  not  only 
rational,  but  sometimes  productive  of  lasting  improvement. 

The  Indications  for  Predigested  Foods:  Peptones,  Albu- 
moses,  Dextrose,  etc. — The  idea  of  supplying  foods  that  would 
replace  the  lost  digestive  function  of  the  stomach  or  by  presenting 
them  in  an  absorbable  form  that  would  spare  the  work  which  it  had 
become  incapable  of  performing,  was  suggested  by  the  recognition 
of  diseases  that  tended  to  destroy  the  glandular  apparatus,  or  caused 
emesis  of  the  ingested  food. 

In  such  instances  in  which  the  amount  of  albuminous  foods  that 
can  be  taken  is  very  small,  the  question  has  been  raised  whether 
peptones  are  able  to  equalize  the  deficit  of  albumin  requirement. 
As  a certain  amount  of  albuminous  food  is  indispensable  to  life, 
whenever  the  quantity  ingested  sinks  below  the  so-called  thresh- 


USE  OF  PREDIGESTED  FOODS. 


209 


old  value  of  albumin  (“  Schwellenwerth  ”),  health  begins  rapidly  to 
decline.  Deiters  has  shown  (von  Noorden,  “ Beitr.  z.  Lehre  v. 
Stoffverlust  d.gesund.  u.  krank.  Menschen,”  Heft  1,  1892)  that  even 
when  the  amount  of  albumin  ingested  sinks  below  the  threshold 
value,  peptones  and  albumoses  (Denayer’s  mixture)  are  capable  of 
maintaining  the  body  in  nitrogenous  equilibrium.  Kuhn  confirmed 
this  observation  in  Riegel’s  laboratory  with  regard  to  an  albumose 
mixture  selling  under  the  name  of  somatose ; so  that  we  may  con- 
clude that  these  products  can  replace  food-albumin  for  a time  at 
least ; still,  we  doubt  very  much  whether  it  is  expedient  or  neces- 
sary to  give  peptones  and  albumoses  in  larger  quantities.  Their 
expensiveness  would  be  no  serious  objection  if  the  advantages  of 
their  use  were  very  obvious. 

In  secretory  insufficiency  of  the  stomach  it  is  well  known  that 
the  proteolytic  power  of  the  intestine  will  utilize  most  of  the  unal- 
tered proteid. 

Even  where  the  stomach  is  excluded  from  digestion  entirely, 
albumin  is  used  up  to  a sufficient  degree  (Ogata,  “ Arch.  f.  Anat. 
u.  Physiol.,”  1883,  S.  89).  Loss  of  peptic  function,  therefore,  does 
not  prevent  sufficient  utilization  of  albumin.  There  is  an  apparent 
advantage  in  the  bland  and  unirritating  quality  of  albumoses,  but 
certainly  this  is  possessed  also  by  certain  undigested  foods  (milk, 
egg-white).  Peptones  and  albumoses  are  not  absorbed  more 
readily  when  ingested  ready-formed,  than  when  they  are  first  devel- 
oped from  albumin  in  the  stomach  (Cahn,  “ Die  Verwendung  d. 
Pepton  als  Nahrungsmittel,”  “ Berlin,  klin.  Wochenschr.,”  1893, 
No.  24). 

They  are  said  to  produce  diarrhea;  but  to  establish  this  fact,  the 
quantity  of  artificial  peptone  and  the  amount  of  nitrogen  in  the 
remaining  ingesta  must  be  considered  together,  for  the  diarrhea 
may  be  due  to  excess  of  nitrogenous  food,  which  may  be  given 
unknowingly,  since  it  is  impossible  to  determine  the  total  nitrogen 
ingested,  except  by  quantitative  analysis. 

As  an  indication  for  the  use  of  predigested  foods,  we  may  state 
the  conditions  where  the  albumin-dissolving  power  of  the  stomach 
is  permanently  reduced  or  lost,  where  the  amount  of  meat-  and 
egg-ingestion  becomes  insufficient  because  of  efforts  necessary  to 
avoid  mechanical  irritation.  If  duodenal  digestion  is  also  deranged, 
the  indication  becomes  more  urgent.  When  the  secretory  func- 
tion is  lost,  but  the  motility  preserved,  the  vicarious  intestinal  pro- 
teolysis will  digest  sufficient  proteid.  When  peristalsis  is,  how- 


210 


DIETETIC  TREATMENT  OF  GASTRIC  DISEASES. 


ever,  also  lost,  then  the  administration  of  peptones  is  of  no  benefit, 
for  we  agree  with  Cahn  (loc.  cit.)  that  in  gastrectasia  dependent 
upon  pyloric  stenosis,  peptones  are  not  absorbed,  but  remain  in 
the  stomach  just  as  water  does.  Riegel  (loc.  cit.,  p.  241),  considers 
this  deduction  of  Cahn’s  as  erroneous,  because  von  Mehring  has 
shown  that  the  stomach  does  absorb  peptone.  To  this  we  would 
reply,  that  von  Mehring  did  not  experiment  upon  dilatations  de- 
pendent upon  stenosis,  but  upon  normal  stomachs. 

In  his  experiments  Cahn  found  that  peptone  causes  an  increased 
flow  of  the  gastric  juice,  and  suggested  that  therefore  it  should 
not  be  given  in  hyperacidity  and  hypersecretion,  in  which  evi- 
dently it  is  quite  unnecessary,  as  in  these  secretory  abnormalities 
meat  and  egg  are  digested  excellently.  In  ulcer,  albumoses  may 
find  temporary  usefulness  because  of  their  unirritating  qualities, 
which,  of  course,  would  be  counterbalanced  by  their  effect  in 
increasing  the  HC1,  should  Cahn’s  conclusion  prove  true.  Pure 
peptone  represents  a proteid  not  coagulable  by  boiling  nitric 
acid,  acetic  acid,  ferrocyanide  of  potash,  nor  ammonium  sulphate. 
Such  a peptone  has,  in  our  experience,  no  field  of  usefulness  in 
practical  dietetics.  It  is  an  irritant  to  the  mucosa  of  the  digestive 
canal  and  has  an  intolerably  bitter  taste. 

In  conclusion,  we  may  state  our  personal  custom  in  the  use  of 
these  substances.  Whenever  the  ingestion  of  albumin  in  the  food 
becomes  insufficient,  or  even  where  it  is  ingested  in  sufficient 
amounts  for  a healthy  individual,  but  owing  to  some  consuming 
disease,  such  as  carcinoma  (not  hindering  peristalsis),  tuberculosis, 
etc.,  it  can  not  cover  the  nitrogen  equilibrium,  in  the  amounts 
possible  to  eat  in  ordinary  diet,  then  we  employ  albumoses  liber- 
ally, and  generally  so  mixed  with  the  food  (soups,  scraped  broiled 
meats,  in  puree)  that  the  patient  can  not  detect  them ; for  this  pur- 
pose the  tasteless  and  odorless  products — somatose,  Mosquera 
beef-meal,  etc. — are  preferable. 

Rectal  Alimentation. — In  diseases  in  which  the  approach  to 
the  stomach  is  stenosed  (carcinoma  or  stenosis  of  the  esophagus 
or  cardia),  or  in  which  the  organ  requires  a temporary  but  absolute 
exemption  from  work  (ulcer  and  some  forms  of  gastritis),  or  in 
cases  in  which  the  mildest  and  most  digestible  diet  is  not  tolerated, 
it  becomes  necessary  to  support  the  strength  by  nutritive  rectal 
enemata. 

The  history  of  the  evolution  of  the  nutritive  enema  is,  from  a 
physiological  standpoint,  very  interesting ; and  as  the  author  has 


RECTAL  ALIMENTATION. 


2 I I 


at  various  times  done  considerable  experimental  work  in  this  line, 
a brief  review  of  the  same  is  believed  essential  to  a proper  under- 
standing of  the  subject. 

The  first  to  discover  that  the  human  colon  and  rectum  absorbed 
an  emulsion  of  eggs  and  water  only  when  sodium  chlorid  was 
added  were  Voit  and  Bauer  (“  Zeitschr.  f.  Biol.,”  1869,  Bd.  v).  They 
found  that  these  foods  were  not  absorbed  in  the  absence  of  salt, 
and  in  1871  Eichhorst  (“  Phliiger’s  Archiv,”  Jahrgang  iv,  71)  con- 
firmed their  results.  Injections  of  bouillon,  milk,  and  eggs  had 
been  used  long  before  this  time,  but  no  one  ever  attempted  to 
ascertain  to  what  degree  the  mucosa  of  the  large  intestine  would 
absorb  it.  In  1872  Leube  proposed  a meat-pancreas  injection 
(“  Deutsch.  Archiv  f.  klin.  Med.,”  Bd.  x,  Reihe  in),  the  plan  emanat- 
ing from  the  idea  to  transpose  something  of  the  character  of  pancre- 
atic digestion  into  the  large  intestine.  The  preparation  of  this  useful 
enema  is  as  follows:  Take  150  to  300  gm.  of  very  finely  scraped 
beef  and  50  to  100  gm.  of  finely  chopped  pancreas  of  the  calf  or 
pig,  and  mix  with  the  addition  of  150  c.c.  luke-warm  water  in  a 
bowl ; if  desired,  25  to  50  gm.  of  fat  may  be  added  in  the  form  of 
oil  or  butter;  the  injection  must  be  made  at  the  body-temperature. 

We  have  convinced  ourselves  that  this  mixture  digests  thor- 
oughly in  the  large  intestine ; its  preparation  is  complicated,  how- 
ever, requiring  very  intimate  mixing,  and  it  rapidly  decomposes. 
Leube  reported  a case  which  he  kept  alive  six  months  by  this 
enema  exclusively,  and  in  a similar  way  Riegel  nourished  a case 
of  esophageal  stricture  for  ten  months.  Ewald  demonstrated 
that  egg-emulsion  is  absorbed  without  being  peptonized  or  salted 
(“  Zeitschr.  f.  klin.  Med.,”  Bd.  11),  and  Huber,  while  confirming 
Ewald’s  observation,  added  that  the  addition  of  salt,  or  pre- 
vious peptonizing,  really  doubled  the  amount  of  emulsified  eggs 
that  was  absorbed  in  the  colon.  Eggs,  it  must  not  be  over- 
looked, contain  a considerable  amount  of  normal  salt,  and  this 
may  explain  Huber’s  results  (“  Zeitschr.  f.  klin.  Med.,”  Bd.  xlvii) 
as  to  their  absorption  in  part,  even  without  the  addition  of  salt. 
But  it  is  an  established  fact  that  the  addition  of  sodium  chlorid 
very  much  increases  the  amount  of  eggs  that  is  absorbed. 

In  a very  interesting  series  of  experiments  Grutzner  offered  a 
physiological  explanation  of  this  phenomenon  (“  Deutsche  med. 
Wochenschr.,”  1894,  No.  48),  having  demonstrated  that  under  cer- 
tain conditions  particles  of  charcoal,  finely  cut  horse-hair,  or  saw- 
dust, impregnated  with  normal  (0.6  per  cent.)  salt  solution  and 


212 


DIETETIC  TREATMENT  OF  GASTRIC  DISEASES. 


injected  into  the  rectum  of  rabbits,  guinea-pigs,  and  rats,  are  found 
six  hours  later  all  along  the  small  intestine,  even  in  the  stomach, 
while  the  rectum  is  empty.  During  a period  of  twenty-four 
hours  before  these  injections  the  animals  were  starved.  When  the 
suspensions  of  these  particles  were  made  in  distilled  water,  HC1 
solution,  or  potassium  chlorid  solution,  instead  of  physiological 
salt  solution,  the  particles  did  not  ascend  in  the  digestive  tract. 
Griitzner  injected  starch-suspensions  in  normal  NaCl  solution  into 
the  rectum  of  human  beings,  and  after  a number  of  hours  demon- 
strated starch-grains  in  the  gastric  contents,  microscopically. 
Nothnagel  first  showed  that  sodium  chlorid  placed  on  the  serous 
surface  of  the  intestine  is  capable  of  starting  antiperistaltic  move- 
ments (“  Beitrag  z.  Physiol,  u.  Pathol,  d.  Darms,”  1884),  and 
Griitzner  interprets  this  observation  as  an  explanation  of  the 
digestion  of  egg-enemata  containing  salt.  He  assumes  that  the 
injected  mass  is  moved  upward  through  the  entire  small  intestine, 
and  so  becomes  digested  and  absorbed.  Even  Riegel  ( loc . cit., 
p.  245)  is  satisfied  with  this  interpretation,  and  adds  that  it  ex- 
plains the  negative  results  of  Voit  and  Bauer  without  salt,  and  the 
positive  ones  with  salt,  and  also  those  of  Huber. 

In  our  opinion,  the  evidences  that  food-substances  move  anti- 
peristaltically  upward  in  the  intestine  are  not  satisfactorily  given  in 
Grutzner’s  work.  It  is  undeniable  that  minute  particles  of  starch, 
charcoal,  etc.,  are  moved  from  the  rectum  toward  the  stomach  in 
man ; and  we  have  been  able  to  confirm  this  part  of  his  results,  as 
well  as  the  fact  that  salt  favors  the  ascent  and  HC1  and  KC1  im- 
pede it.  But  this  antiperistaltic  motion  we  conceive  to  be  only  a 
very  feeble  marginal  ascending  movement,  effected  by  surface  con- 
tact of  the  particles  with  the  epithelium,  which  in  turn  is  moved  by 
the  muscularis  mucosae.  This  very  slight  marginal  antiperistalsis 
is  never  visible  to  the  eye,  and  can  only  be  demonstrated  by  the 
progress  of  particles  ; it  is  not  capable  of  propelling  food  masses  ; on 
the  contrary,  we  have  convinced  ourselves  that  at  the  same  time  that 
the  marginal  peristalsis  drags  visible  particles  of  charcoal  toward  the 
stomach  with  infinitesimal  slowness,  there  may  be  an  uninterrupted 
current  of  central  food  masses  toward  the  anus.  The  marginal 
antiperistalsis  may  be  a physiological  thing,  present  at  all  times, 
and  its  object  may  be  the  raising  or  drawing  up  of  portions  of 
mucosa  from  one  place  to  another  in  order  to  bring  new  surfaces 
in  contact  with  the  ingesta,  or  to  replace  a portion  of  surface  to  its 
normal  topography  after  it  has  been  dragged  away  from  it  by  the 


PATHOLOGICAL  ANTI  PERISTALSIS. 


213 


downward  current.  The  cohesion  of  these  small  particles  with 
the  mucosa  can  be  seen  when  a piece  of  fresh  animal  intestine  is 
sprinkled  with  lycopodium  or  finely  cut  horse-hair  particles  and 
held  under  a gentle  stream  of  water;  the  gut  may  be  moved 
upward  on  the  surface  of  the  hand  while  the  water  moves  down- 
ward, and  still  many  of  the  particles  will  adhere. 

The  antiperistalsis  that  Nothnagel  produced  by  placing  crystals 
of  salt  upon  the  serosa  is  quite  a different  thing,  for  it  is  plainly 
visible  to  the  eye,  and  never  occurs  under  physiological  conditions 
(Nothnagel,  “ Erkrank.  d.  Darms,”  portion  on  “ Die  Darmbewe- 
gung,”  p.  6,  1896).  Among  the  abnormal  conditions  that  may 
cause  this  visible  antiperistalsis,  Nothnagel  states  stronger  solu- 
tions of  sodium  chloridand  the  introduction  of  food  at  an  unphysio- 
logical  entry,  as  which  in  man  we  must  consider  the  rectum.  He 
adds  ( loc . cit.)  that  from  a physiological  entry,/.  ^.,from  the  stomach, 
the  strongest  chemical  irritants  produce  only  peristaltic  movements 
toward  the  anus.  There  are,  then,  two  kinds  of  antiperistaltic  move- 
ments: (1)  Those  of  Griitzner,  being  marginal,  invisible,  possibly 
physiological,  and  not  capable  of  moving  food  masses ; (2)  those 
of  Nothnagel,  being  visible,  strong,  and  occurring  only  under 
abnormal  conditions.  Christomanos,  a pupil  of  Nothnagel,  has 
urged  an  objection  against  Grutzner’s  results  that  seems  to  invali- 
date the  conclusions  of  the  latter  ; namely,  he  found  (Christomanos, 
“ Z.  Frage  d.  Antiperistaltik,”  “ Wien.  klin.  Rundschau,”  1895,  Nos. 
12  and  13)  that  when  his  animals  were  prevented  from  licking  up 
the  expelled  rectal  contents  his  results  as  to  finding  the  particles  in 
the  stomach  were  negative.  Dauber  came  to  the  same  conclusion 
as  Christomanos,  namely,  that  the  occurrence  of  particles  of  rectal 
injections  in  the  stomachs  of  animals  did  not  take  place  when  they 
were  prevented  from  eating  their  excrement.  These  objections  are, 
however,  set  aside  by  Grutzner’s  and  our  own  observations  on  the 
human  subject.  The  experiments  of  Swiezynski  (“  Deutsche  med. 
Wochenschr.,”  1895,  No.  32)  also  confirmed  Grutzner’s  statements, 
in  that  lycopodium  injected  into  the  rectum  was  found  in  the 
stomach. 

We  must,  however,  again  emphasize  that  this  antiperistalsis  is 
not  capable  of  moving  ingesta,  and  that  it  can  not  logically  be 
taken  as  an  explanation  of  the  digestion  of  enemata. 

The  fact  that  normal  salt  solution  favors  the  invisible  marginal 
ascent  of  particles,  and  that  other  chemicals  impede  it,  is  perfectly 
natural.  For  if  this  antiperistalsis  be  physiological,  and  be  assumed 


214 


DIETETIC  TREATMENT  OF  GASTRIC  DISEASES. 


to  be  going  on  at  all  times,  normal  salt  solutions  can  not  disturb  it, 
for  they  are  the  physiological  environment  in  which  all  intestinal 
movements  occur.  But  HC1  and  KC1  are  chemical  irritants,  to 
which  the  muscularis  mucosae  reacts  by  efforts  at  expulsion. 

The  Occurrence  of  Proteolytic  Ferments  in  the  Colon  and 
Rectal  Contents. — The  author’s  explanation  of  the  digestion  of 
egg  and  milk  emulsions  in  the  rectum  and  colon  is  quite  different 
from  Griitzner’s  and  from  that  accepted  by  Riegel  and  others,  and 
is  based  on  a very  carefully  conducted  series  of  experiments  on 
animals  and  human  beings.  We  desire  to  speak  only  of  actual 
digestion,  for  there  is  good  reason  for  believing  that  albumin,  fats, 
etc.,  may  be  absorbed  from  the  large  intestine  as  such — without 
digestion. 

Without  going  into  the  details  and  technic  of  these  experiments, 
we  will  briefly  state  the  conclusions.  After  the  rectal  contents  of 
dogs  or  cats  are  sterilized  with  saturated  solutions  of  thymol  (so 
strong  that  the  crystals  float  on  top)  and  passed  through  a Pasteur 
filter,  control  cultures  are  made  to  ascertain  that  the  watery  extract 
of  the  excrement  is  sterile.  For  this  purpose  the  meat  pepton- 
gelatin  and  agar  plates  recommended  by  Nothnagel  ( loc . cit .,  p.  22) 
are  most  convenient.  The  reaction  of  human  excrement  is  gener- 
ally weakly  alkaline  or  neutral;  very  rarely  weakly  acid  under 
normal  conditions.  This  watery  extract  of  normal  rectal  contents 
contains  a substance  which  in  a digestorium  (thermostat  at  40°  C.), 
and  in  an  alkaline  medium  (equal  to  from  0.8  to  1 per  cent.  Na2C03), 
dissolves  from  36.3  to  30  - per  cent,  of  Merck  s'  dried  serum-albumin  in 
three  hours  under  aseptic  conditions.  It  will  also  digest  fibrin, 
and  has,  in  addition,  a faint  amylolytic  power,  converting  from  10 
to  14.5  per  cent,  of  starch  into  maltose  in  an  alkaline  medium  of 
0.3  per  cent.  Na2C03.  We  have  not  been  able  to  find  any  fat- 
splitting action  in  this  extract. 

As  there  are  many  bacteria  that  produce  peptone  in  the  break- 
ing down  of  proteid,  and  others  that  ferment  carbohydrates, 
the  previous  sterilization  is  necessary  in  order  to  exclude  their 
action.  Bacteria  do  not  make  peptone  for  any  philanthropic  pur- 
poses ; the  peptone  they  give  rise  to  is  an  intermediate  stage  in  a 
long  series  of  decomposition  products.  It  does  not  remain  peptone, 
but  is  rapidly  decomposed  into  amido-acids,  ammonia,  tyrosin,  etc., 
and  does  not  occur  in  the  intestine  as  peptone  pure  and  simple, 
but  mixed  with  a number  of  other  derivatives  of  albumen,  some  of 
which  are  proven  to  be  toxic.  We  state  this  because  even  among 


RECTAL  CONTENTS  AFTER  STERILIZATION.  21  5 

medical  men  the  opinion  has  been  encountered  that  the  bacterial 
peptone  might  be  of  utility  to  the  organism  in  which  it  is  formed. 
The  feces  for  our  purposes  can  not  be  sterilized  by  heat,  because 
that  Would  destroy  any  possible  enzymes  present. 

It  is  certain,  therefore,  that  rectal  contents  contain  a proteolytic 
ferment  ; also  one  having  a slight  amylolytic  power,  acting  only  in 
a faintly  alkaline  medium,  the  action  being  destroyed  in  an  acid 
medium.  Whether  these  two  digestive  actions  are  carried  out 
by  one  and  the  same  ferment  or  by  two  different  ferments  we  are 
unable  to  say.  That  it  can  not  be  pepsin  is  proven  by  the  fact  that 
it  does  not  act  in  an  acid,  but  only  in  an  alkaline,  medium. 

It  would  be  interesting  to  learn  whether  the  walls  of  the  large 
intestine  secrete  any  proteolytic  ferment.  The  colon  of  a dog  that 
is  kept  clear  of  fecal  masses  by  making  an  abdominal  fistula  and 
sewing  it  to  the  abdominal  wall  at  the  ileocecal  valve,  secretes 
an  alkaline  fluid,  which  has  no  proteolytic  powers  whatever, 
but  there  is  an  evident  amylolytic  ferment  contained  in  it.  The 
human  colon  can  be  plugged  up  in  the  transverse  portion  by 
introducing  a balloon  and  blowing  it  up  ; thereafter  the  part  be- 
tween the  rubber  balloon  and  the  anus  is  washed  out  with  sterile 
normal  salt  solution.  A secretion  is  formed  in  two  to  three  hours, 
and  can  be  collected  on  absorbent  cotton  placed  in  the  rectum, 
and  later  squeezed  out  into  a small  beaker.  The  secretion  is  alka- 
line, but  has,  after  filtration  through  a Pasteur  filter,  no  proteolytic 
power.  Therefore,  it  is  reasonable  to  assume  that  the  ferment  we 
have  demonstrated  is  derived  from  the  pancreas.  In  two  patients 
with  total  atrophy  of  the  gastric  mucosa  (atrophic  gastritis),  as 
evidenced  by  fragments  of  the  mucosa  found  in  the  wash-water,  the 
same  proteolytic  ferment  was  demonstrable  in  the  colon  contents. 
It  was  hitherto  assumed  that  the  ferments  of  the  pancreas  were 
destroyed  in  the  intestine  (see  Rosenheim,  “ Die  Erkrank.  d. 
Darms,”  p.  46).  A large  number  of  similar  experiments  as  above 
described  justifies  the  belief,  however,  that  trypsin  and  perhaps 
amylopsin  may  survive  the  passage  through  the  bowel.  Busch 
has  shown  that  digestion  may  go  on  in  the  human  intestine  with- 
out gastric  or  pancreatic  juice,  without  bile  and  secretion  of 
Brunner’s  glands  (Brficke’s  “ Vorlesungen  fiber  Physiologie,” 
Wien,  1885,  p.  352).  The  patient  on  whom  Busch  experimented 
had  received  an  abdominal  injury  by  an  accident,  in  such  a manner 
that  the  gastric  juice,  together  with  the  chyme,  pancreatic  juice, 
duodenal  secretions,  and  bile,  ran  outward  through  a fistula. 


2 l6 


DIETETIC  TREATMENT  OF  GASTRIC  DISEASES. 


Thereafter,  Busch  fed  him  through  the  fistulous  opening  communi- 
cating with  the  lower  bowel,  and  succeeded  in  maintaining  the 
nitrogenous  equilibrium.  He  lowered  coagulated  albumin  inclosed 
in  small  cotton  bags  into  the  bowel,  and  drew  them  out  by 
a string  five  hours  later,  finding  that  from  five  to  thirty-five  per 
cent,  of  the  albumin  was  dissolved.  In  Busch’s  experiments  the 
action  of  the  bacteria  can  not  be  excluded.  The  action  of  the 
succus  entericus  may  explain  the  carbohydrate  digestion,  but,  as 
no  proteolytic  ferment  could  enter  the  small  intestine,  the  digestion 
of  albumin  was  probably  due  to  bacteria. 

In  conclusion  we  may  say  that  rectal  enemata  are  digested 
probably  by  pancreatic  ferments  passing  through  the  bowel,  by 
bacteria,  and  by  the  succus  entericus,  which,  even  in  the  colon,  has 
an  amylolytic  action  ; that  certain  foods — egg-albumen,  fats,  milk — 
can  be  absorbed  as  such  without  being  digested.  Griitzner’s 
marginal  ascending  motion  of  particles  can  not  move  ingesta 
upward.  F.  Mall  (“Johns  Hopkins  Hospital  Reports,”  vol.  i, 
p.  70)  holds  that  the  propelling  force  of  the  intestines  normally 
acts  in  one  direction  only  ; the  antiperistalsis  is  found  only  as  a 
pathological  phenomenon,  and  all  of  his  efforts  to  force  the  intestine 
to  work  in  the  wrong  direction  by  reversal  (loc.  cit .,  p.  93)  were 
negative.  Under  conditions  of  great  irritation  rectal  contents  may 
be  vomited. 

Preparation  of  Rectal  Enemata : 

Indications  and  Methods  of  Administration. — The  preparation  of 
Ewald’s,  Leube’s,  and  Boas’  nutritive  enemata  is  given  under  the 
dietetic  tables.  Jaccoud  recommends  250  gm.  of  bouillon,  120  gm. 
of  wine,  yolks  of  two  eggs,  5 to  20  gm.  of  peptone.  Rosenheim  uses 
peptone  (one  to  two  drams),  two  eggs,  15  gm.  of  glucose,  and  some- 
times, if  desired,  emulsions  of  cod-liver  oil.  Singer’s  enema  (“  Cen- 
tralblatt  d.  ges.  Therap.,”  Marz,  1895)  is  very  much  like  that  ot 
Boas,  with  the  addition  of  peptone.  These  examples  will  amply 
suffice  for  all  purposes. 

Method  and  technics  of  rectal  feeding : 

(1)  Every  nutritive  injection  must  be  preceded  by  a cleansing  in- 
jection one  hour  previously. 

(2)  The  amount  of  injected  nutriment  must  not  exceed  of  a 
liter  (Sviij)  at  a time. 

(3)  After  the  injection  the  patient  must  remain  in  the  recumbent 
position  for  one  hour,  and  a hot  towel  should  be  held  firmly  against 
the  anus  for  fifteen  or  twenty  minutes. 


PREPARATION  OF  NUTRITIVE  ENEMATA.  2 1 / 

(4)  The  patient  should  lie  on  his  left  side  with  his  hips  raised 
upon  a pillow,  and  the  injection  must  be  given  very  gradually. 

(5)  If  the  rectum  is  very  irritable,  the  addition  of  a few  drops 
(10  to  20)  of  tincture  of  opium  is  serviceable. 

(6)  The  injection  should  be  made  with  a funnel  or  an  irrigating 
bottle,  never  with  a syringe.  The  best  tube  to  use  is  that  named 
after  Langdon,  as  it  is  sufficiently  soft  and  flexible  and  can  not 
kink  upon  itself. 

(7)  The  tube  should,  in  adults,  be  passed  high  up  into  the  colon  ; 
if  possible,  14  to  18  inches  should  be  introduced,  but  12  inches  will, 
as  a rule,  suffice.  The  higher  up  the  enema  is  placed,  the  less  will 
be  the  liability  of  its  rejection.  An  anatomical  and  physiological 
reason  for  placing  injections  high  is  found  in  the  nature  of  the 
anastomoses  of  the  vascular  supply  of  the  rectum,  sigmoid,  and 
colon.  The  superior  rectal  and  sigmoid  veins  communicate  with 
the  inferior  mesenteric  vein,  therefore  these  veins  conduct  whatever 
they  have  absorbed  directly  to  the  liver  through  branches  of  the 
vena  porta.  In  the  liver  the  very  important  secondary  digestion 
takes  place.  The  veins  from  the  lower  third  of  the  rectum  com- 
municate with  the  inferior  vena  cava,  and  their  contents  are  not 
conducted  to  the  liver. 

(8)  The  temperature  of  the  injection  should  be  that  of  the  body 
—98.6°  F. 

Indications  Necessitating  Rectal  Feeding. — There  are  two 
classes  of  conditions  in  which  nutritive  enemata  are  indicated : 

I.  The  first  class  comprises  patients  that  are  still  able  to  swallow 
food  and  willing  to  do  so,  but  on  account  of  the  existence  of  some 
gastric,  esophageal,  or  duodenal  disease  it  is  necessary  or  expedient 
to  rest  the  stomach  and  exe'mpt  it  from  work.  These  are : 

(1)  Gastric  Ulcer. — For  the  purpose  of  keeping  the  ulcer  free 
from  irritation  and  permitting  it  to  heal  or  to  prevent  the  starting 
up  of  hematemesis. 

(2)  Dilatations. — Either  in  the  atonic  or  benign  forms,  to  attempt 
a cure  by  relieving  the  stomach  of  the  weight  of  ingesta  and  the 
constant  fermentation;  or  in  the  malignant,  pyloric,  and  stenotic 
forms,  because  food  positively  can  not  pass  the  pylorus  and  gastro- 
enterostomy is  refused  or  impossible. 

(3)  Severe  gastric  irritations,  as  in  toxic  gastritis. 

(4)  Exhausting  diseases,  especially  the  infectious  types,  where 
secretion  and  absorption  are  'inhibited  and  food  not  retained, 
though  swallowed. 

15 


2 I 8 


DIETETIC  TREATMENT  OF  GASTRIC  DISEASES. 


(5)  Ulcer  of  the  esophagus  or  duodenum,  stricture,  ileus,  invag- 
ination, volvulus,  stenosis  of  any  part  of  the  alimentary  tract  be- 
tween stomach  and  rectum. 

II.  The  conditions  in  which  the  patients  are  unable  to  swallow 
food  are  : 

(1)  Temporary  obstruction  to  the  entrance  of  food  into  the  ali- 
mentary canal ; presence  of  new  growths  ; foreign  bodies  ; acute 
inflammations  about  mouth,  pharynx,  and  esophagus. 

(2)  Extreme  sensitiveness  of  the  mouth  and  esophagus  excited 
by  corrosive  poisons. 

(3)  Carcinoma,  cicatricial  contraction,  diverticulum,  neoplasms, 
of  esophagus  ; carcinoma  of  cardia. 

(4)  Reflex  vomiting,  as  in  pregnancy  and  sea-sickness. 

There  are  other  states  in  which  the  patients  are  either  unable  or 
unwilling  to  swallow  food,  but  in  these  feeding  by  the  tube  is  prefer- 
able to  rectal  feeding.  These  are : ( a ) Inability  to  swallow  from 
coma,  delirium,  or  paralysis  of  the  muscles  of  deglutition ; post- 
diphtheritic  paralysis.  ( b ) Insanity,  refusal  of  food.  ( c ) Total 
anorexia  (hysterical,  etc.). 

Intravascular  and  Hypodermic  Feeding . — In  1850  Hodder  first 
practised  intravenous  injection  of  milk  in  cases  of  collapse  from  chol- 
era Asiatica.  T.  G.  Thomas  about  this  time  published  a case  in 
which  y2  of  a pint  of  milk  warmed  to  body-temperature  was  injected 
into  one  of  the  brachial  veins,  with  the  result  of  saving  life. 
According  to  Gilman  Thompson  {loc.  cit.,  ,p.  383),  Fowler  has 
practised  intravenous  injection  of  peptone  and  has  also  given  six 
ounces  of  digested  beef  solution  in  this  manner.  There  seems  to 
us  no  physiological  reason  why  intravenous  or  even  intra-arterial 
feeding  should  not  be  practised  in  emergencies.  As  a safeguard, 
however,  we  would  suggest  that  every  precaution  be  taken  to  have 
the  injection  absolutely  sterile,  and  composed  of  such  substances 
as  are  normal  to  the  blood,  such  as  serum-albumin,  sterile  plasma, 
defibrinated  fresh  sterile  blood.  Much  careful  experimenting  is 
required,  however,  before  we  can  be  justified  in  using  such 
methods  on  the  sick  human  being.  Intravenous  and  intra-arterial 
injections  of  warm,  sterile,  normal  salt  solutions  have  been  ex- 
tensively used  in  Asiatic  cholera  and  in  exhausting  hemorrhages. 
We  have  had  occasion  to  use  them  in  hematemesis  after  gastric 
ulcer,  with  the  conviction  that  life  was  saved  thereby.  Transfu- 
sion of  sterile,  normal  salt  solution  into  the  areolar  connective 
tissue  of  the  breast  is  to  be  preferred  to  these  methods,  because  it 


SUBCUTANEOUS  FEEDING.  2\CJ 

requires  only  a pressure-bottle  and  sterile,  sharp-pointed  cannula 
— no  other  instruments. 

Subcutaneous  Feeding . — In  1869  Menzel  and  Perco  injected  fats, 
albumin,  and  sugar  into  dogs  and  human  beings,  and  showed  that 
liquid  oils  were  resorbed  without  causing  local  or  general  reaction. 
They  injected  nine  gm.  of  oil  into  one  patient,  at  Billroth’s  clinic, 
who  had  spinal  caries;  a swelling  as  large  as  a silver  dollar  ensued, 
but  disappeared  entirely  in  thirty  hours  (“  Wiener  med.  Woch- 
enschr.,”  1869,  No.  31). 

Attempts  have  been  made  in  the  human  being  with  injection  of 
defibrinated  calf’s-blood  by  Landenberger  (“  Wurtemberg.  med. 
Correspondenzbl.,”  Bd.  xliv,  No.  20),  with  olive  oil  by  Krueg  (Re- 
ferat  in  “ Wien.  med.  Wochenschr.,”  1875,  No.  34),  with  olive  oil 
and  milk  by  Whittaker  (“  Schmidt’s  Jahrb.,”  Bd.  clxxvii,  Heft  1), 
who  in  eight  sittings  injected  124  gm.  in  one  day — in  all  he  made 
68  injections.  Karst  recommended  defibrinated  blood  (“  Berlin, 
klin.  Wochenschr.,”  1873,  No.  49).  Eichhorn  was  so  enthusiastic 
with  his  injections  of  milk-peptone  and  cod-liver  oil  that  he  be- 
lieved the  normal  nutrition  of  an  animal  could  be  supplanted  by 
this  method  (“Wien.  med.  Wochenschr.,”  1881,  Nos.  32,  33,  and 
34).  Leube  proved  that  oils  injected  subcutaneously  were  actu- 
ally used  up  in  the  metabolism  of  the  body  (Leube,  “ Verhand- 
lung.  d.  XIV.  Congresses  f.  innere  Medicin,”  1895).  In  a case  of 
benign  hyperplastic  pyloric  stenosis  complicated  by  colitis,  the 
author  and  his  associate,  Dr.  Harry  Adler,  injected  24  gm.  of 
sterilized  olive  oil  under  the  skin  daily  for  three  weeks.  Nutritive 
enemata  were  not  tolerated  on  account  of  the  colitis.  The  oil 
injections  which  did  not  cause  the  slightest  irritation,  were  absorbed 
in  from  four  to  twelve  hours,  and,  though  no  analyses  on  meta- 
bolism could  be  executed,  it  became  evident  that  the  patient  was 
benefited  by  the  hypodermic  use  of  oil.  In  spite  of  these  experi- 
ments, it  is  very  doubtful  whether  subcutaneous  injections  of  nutri- 
tive materials  can  ever  be  utilized  to  supplant  normal  feeding. 
The  caloric  value  of  the  amounts  that  are  available  for  injection 
is  comparatively  insignificant,  the  method  quite  irritating,  and  in 
progressed  sufferers  hardly  justifiable. 


220 


APPROXIMATE  ANALYSES  OF  A MAN. 


TABLES  OF  DIETETICS. 


APPROXIMATE  ANALYSES  OF  A MAN. — (Moss.) 

(Height,  5 feet  8 inches  ; weight,  148  pounds.) 


Pounds. 

Oxygen 92.4 

Hydrogen, ....  14.6 

Carbon,  . 31.6 

Nitrogen, 4.6 

Phosphorus, 1.4 

Calcium, 2.8 

Sulphur, 0.24 

Chlorin, 0.12 


Sodium,  . . 
Iron,  . . . . 
Potassium,  . 
Magnesium,  . 
Silica,  . . . 
Fluorin,  . . 

Total, 


Pounds. 


0.12 

0.02 

0-34 

0.04 

? 

0.02 


148.30 


Landois  and  Stirling  give  the  following  table,  which  differs  some- 
what from  the  other  tables  in  the  relative  proportion  of  fats  and 
starches.  An  adult  doing  a moderate  amount  of  work  takes  in  as 
food  per  diem  : 


C. 

H. 

N. 

O. 

120  gm.  of  albumin,  containing,  .... 

90  gm.  of  fats,  containing, 

330  gm.  of  starches,  containing,  .... 

64.18 
70. 20 
146.82 

8.60 
IO.  26 
20.33 

o° 

bo 

. . 00 

28.34 

9-54 

162.85 

281.20 

39-19 

18.88 

200.73 

Add  744.11  gm.  of  O from  the  air  by  respiration. 

“ 2,818.00  “ of  H20. 

“ 32.00  “ of  inorganic  compounds  (salts). 

The  whole  is  equal  to  three  kilogm.  and  a half  (seven  pounds), 
i.  e.,  about  one-twentieth  of  the  body-weight ; so  that  about  six  per 
cent,  of  the  water,  about  six  per  cent,  of  the  fat,  about  one  per  cent, 
of  the  albumin,  and  about  0.4  per  cent,  of  the  salts  of  the  body  are 
daily  transformed  within  the  organism. 

An  adult  doing  a moderate  amount  of  work  gives  off  in  gm. : 


Water. 

C. 

H. 

N. 

O. 

By  respiration, 

330 

248.8 

? 

651-15 

By  perspiration, 

660 

2.6 

7.2 

By  urine, . . . 

1,700 

9.8 

3-3 

15-8 

11. 1 

By  feces,  

128 

20.0 

3-o 

3-o 

12.0 

2,818 

281.2 

6-3 

18.8 

681.45 

STANDARDS  FOR  DAILY  DIETARIES. 


22  I 


STANDARDS  FOR  DAILY  DIETARIES. — [Compiled  by  Atwater.) 
Weights  of  nutrients  and  calories  of  energy  (heat-units)  in  nutri- 
ents required  in  food  per  day : 


Nutrients. 

Potential 

Protein. 

Fats. 

Carbo- 

hydrates. 

Total. 

Energy. 

Gm. 

Gm. 

Gm. 

Gm. 

Calories. 

Children  to  a year  and  a half,  . 

28 

(20-36) 

37 

(30-45) 

75 

(60-90) 

140 

767 

Children  of  two  to  six  years,  . 

55 

(36-70) 

40 

(35-48) 

40 

(100-250) 

295 

1,418 

Children  of  six  to  fifteen  years, 

75 

(70-80) 

43 

(37-50) 

325 

(250-400) 

443 

2,041 

Aged  women, 

80 

50 

260 

390 

1,859 

Aged  men, 

100 

68 

35o 

518 

2,477 

Woman  at  moderate  work,  Voit , 

92 

44 

400 

536 

2,426 

Man  at  moderate  work,  Voitf  . 

118 

56 

500 

674 

3 >°5  5 

Man  at  hard  work,  Voit , . . . 
Man  at  moderate  exercise, Play- 

H5 

100 

45° 

695 

3,370 

fair,  

Active  labor,  Playfair , . . . 

119 

5i 

53i 

701 

3,  *39 

156 

7i 

568 

795 

3,629 

Hard  labor,  Playfair , .... 
Woman  with  light  exercise,  At- 

185 

7i 

568 

824 

3,748 

water,  

Man  with  light  exercise,  At- 

80 

80 

300 

460 

2,300 

water , 

100 

1 00 

360 

460 

2,820 

Man  at  moderate  work,  Atwater, 

125 

125 

45° 

700 

3,520 

Man  at  hard  work,  Atwater , . 

Man  at  moderate  work,  Mole- 

150 

150 

500 

800 

4,060 

schott,  

130 

40 

55o 

720 

3,160 

Man  at  moderate  work,  Wolff, 

120 

35 

540 

695 

3,032 

Table  of  analyses  made  by  Dujardin-Beaumetz,  showing  the  pro- 
portion of  nitrogen  present  and  also  the  combustibles  calculated 
as  carbon : 


Nitrogen. 

C + H 
Combustibles 
Calculated  as 
Carbon. 

Beef,  uncooked, 

3.00 

II.  OO 

Roast  beef,  . . 

3-53 

17.76 

Calf’s-liver, 

3-09 

15.68 

Foie  gras,  

2. 12 

65-58 

Sheeps’  kidneys,  

2.66 

12.13 

Skate,  

3.83 

12.25 

Cod,  salted, 

5.02 

16.00 

Herring,  salted, 

3-ii 

23.00 

Herring,  fresh, 

183 

21.00 

Whiting,  

2.41 

9.00 

Mackerel, 

3-74 

I9.26 

222 


STANDARDS  FOR  DAILY  DIETARIES. 


Table  of  analyses  showing  the  proportion  of  nitrogen  and  combustibles  calculated 
as  carbon  ( Continued ). 


Nitrogen. 

C + H 
Combustibles 
Calculated  as 
Carbon. 

Sole, 

1.91 

12.25 

Salmon, 

2.09 

16.00 

Carp, 

3-49 

I2.IO 

Oysters, 

2.13 

7.18 

Lobster,  uncooked, 

2-93 

10.96 

Eggs, 

1.90 

13-50 

Milk,  cow’s, 

0.66 

8.00 

Cheese  (Brie),  

2-93 

35-oo 

Cheese  (Gruyere), 

5.00 

38.00 

Cheese  (Roquefort), 

4.21 

44-44 

Chocolate, 

1-52 

58.00 

Wheat  (hard  southern,  variable  average), 

3.0° 

41.00 

Wheat  (soft  southern,  variable  average), 

1. 81 

39.00 

Flour,  white  (Paris),  . . . 

1.64 

38.50 

Rye  flour, 

i-75 

41.00 

Winter  barley, 

1.90 

40.00 

Maize, 

1.70 

44.00 

Buckwheat, - 

2.20 

42.50 

Rice, 

1.80 

41.00 

Oatmeal, 

i-95 

44.00 

Bread,  white  (Paris,  30  per  cent,  water), 

1.08 

29.50 

Bread,  brown  (soldiers’  rations  formerly), 

1.07 

28.00 

Bread,  browm  (soldiers’  rations  at  present), 

1.20 

30.00 

Bread  from  flour  of  hard  wheat, 

2.20 

3I-oo 

Potatoes, 

°-33 

11. 00 

Beans, ... 

4-5° 

42.00 

Haricots,  dry, 

3-92 

43.00 

Lentils,  dry, 

3-87 

43-oo 

Peas,  dry, 

3- 66 

44.00 

Carrots, 

0.31 

5-50 

Mushrooms, 

0.60 

4-52 

Figs,  fresh, 

0.41 

15.50 

Figs,  dry,  

0.92 

34-co 

Plums, 

0-75 

28.00 

Coffee  (infusion  of  100  gm.), 

1. 10 

9.00 

Tea  (infusion  of  100  gm  ), 

1. 00 

10.50 

Bacon, 

1.29 

71.14 

Butter,  fresh, 

0.64 

83.00 

Olive  oil, 

98.00 

Beer,  strong, 

0.05 

4-50 

Wine, 

0.15 

4.00 

THE  RELATIVE  VALUE  OF  FOODS. 


223 


TIIE  RELATIVE  VALUE  OF  FOODS.  — ( Scam  null. ) 

(The  figures  represent  percentages.) 


Articles. 

As  Mate- 
rial for 

THE 

Muscles. 

As  Heat 
Givers. 

As  Food 

FOR  THE 

Brain  and 
Nervous 
System. 

Water. 

Waste. 

Wheat, 

14.6 

66.4 

1.6 

14.0 

3-4 

Barley, 

12.8 

52.1 

4.2 

14.0 

16.9 

Oats, 

17.0 

50.8 

3-0 

13.6 

16.9 

Northern  corn, 

12.3 

67-5 

1. 1 

14.0 

51 

Southern  corn 

34-6 

39-2 

4.1 

14.0 

8.1 

Buckwheat,  

8.6 

53-o 

1.8 

14.2 

22.4 

Rye, 

6.5 

75-2 

o-5 

13-5 

4-3 

Beans, 

24.0 

40.0 

3-5 

14.8 

17.7 

Peas, 

23-4 

41.0 

25 

14. 1 

19.0 

Lentils, 

26.0 

39-o 

i-5 

14.0 

19.5 

Rice,  

5-1 

82.0 

o-5 

9.0 

3-4 

Potatoes, 

1.4 

15.8 

0.9 

74.8 

7-1 

Sweet  Potatoes, 

i-5 

21.8 

2.9 

67.5 

6.3 

Parsnips,  

2.1 

14-5 

1.0 

79-4 

3-o 

Turnips, 

1.2 

4.0 

o-5 

9°.  4 

3-9 

Carrots, 

1. 1 

12.2 

1.0 

82.5 

3-2 

Cabbage,  

1.2 

6.2 

0.8 

9i-3 

o-5 

Cauliflower, 

3-6 

4.6 

1.0 

90.0 

0.8 

Cucumbers,  

0. 1 

i-7 

0.5 

97.1 

0.6 

Milk  of  cow, 

5-° 

8.0 

1.0 

86.0 

Milk,  human,  

3-o 

7.0 

o-5 

89-5 

Veal, 

17.7 

14.3 

2-3 

65-7 

Beef, 

19.0 

14.0 

2.0 

65.0 

Lamb, 

19.6 

14-3 

2.2 

63-9 

Mutton, 

21.0 

14.0 

2.0 

63.0 

Pork, 

17-5 

16.0 

2.2 

64.3 

Chicken, 

21.6 

1.9 

2.8 

73-7 

Codfish, 

16.5 

1.0 

2-5 

80.0 

Trout, 

16.9 

0.8 

4.3 

78.0 

Smelt, 

17.0 

very  little 

5 or  6 

75-o 

Salmon, 

20.0 

some  fat 

6 or  7 

74.0 

Eels, 

17.0 

“ 

3 or  4 

75-o 

Herring, 

18.0 

“ 

4 or  5 

75-o 

Halibut, 

18.0 

“ 

3 or  4 

74.0 

Oysters, 

12.6 

0.2 

87.2 

Clam, 

12.0 

very  little 

2 or  3 

Lobster, 

14.0 

“ 

5 or  6 

79-9 

Eggs,  white  of, 

13.0 

2.8 

84.2 

Eggs,  yolk  of, 

29.8 

2.0 

51-3 

Butter, 

100. 0 

Artichoke, 

i-9 

19.0 

’ 1.8 

76.6 

0.7 

Asparagus, 

0.6 

5-4 

0.4 

93-6 

Bacon,  

8.4 

62.5 

o-5 

28.6 

Carp, 

18.0 

0.8 

2.9 

78.3 

Cheese, 

30.8 

28.0 

4-7 

36-5 

Cherries,  

0.6 

21.0 

1.0 

76.3 

1. 1 

Chocolate, 

8.8 

88.0 

1.8 

1 4 

Cream, 

3.5 

4-5 

92.0 

Currants,  

0.9 

6.8 

°-3 

81.3 

10.7 

Dates,  fresh, 

73-7 

24.0 

2.3 

Figs, 

5-o 

57-9 

3-4 

18.7 

i5-o 

Ham, 

35-o 

32.0 

4.4 

28.6 

Horse-radish 

0. 1 

4-8 

1.0 

78.2 

16.0 

224 


PERCENTAGES  OF  NUTRITION,  ETC, 


THE  RELATIVE  VALUE  OF  FOODS  ( Continued ). 


Articles. 

As  Mate- 
rial for 

THE 

Muscles. 

As  Heat 
Givers. 

As  Food 
for  the  ' 
Brain  and 
Nervous 
System. 

Water. 

Waste. 

Kidney, 

21.2 

0.9 

1.4 

76.5 

Lard, 

loo. 0 

Liver,  

26.3 

3-9 

1.2 

68.6' 

Onions, 

0-5 

5-2 

o-5 

93-8 

Pearl  barley, 

4-7 

78.0 

0.2 

9-5 

7.6 

Pears, 

0. 1 

9.6 

864 

3-9 

Pigeon,  

23.0 

1.9 

2.7 

72.4 

Prunes, 

3-9 

78.6 

4-5 

13.0 

Radishes, 

1.2 

7-4 

1.0 

89.1 

i-3 

Suet, 

100.0 

Venison,  

20.4 

8.0 

' 2.8 

68.8’ 

Vermicelli, 

47-5 

38.0 

i-7 

12.8 

Whey,  

4.6 

0.7 

94-7 

ATKINSON’S  TABLE  OF  DIGESTIBILITY  OF  NUTRIENTS  OF  FOOD 
MATERIALS. 


In  the  Food  Materials  Below. 


Of  the  Total  Amounts  of  Protein,  Fats,  and  Carbo- 
hydrates, the  Following  Percentages 
were  Digested  : 


Protein. 

Fats. 

Carbohydrates. 

Meat  and  fish, 

Practically  all 

79  to  92 

Eggs, 

“ 

96 

Milk, 

88  to  100 

93  to  98 

? 

Butter, 

98 

. . . 

Oleomargarine, 

96 

Wheat  bread, 

81  to  100 

? 

99 

Corn  (maize)  meal, 

89 

? 

97 

Rice, 

84 

? 

99 

Peas, 

86 

? 

96 

Potatoes, 

74 

? 

92 

Beets, 

72 

? 

82 

PERCENTAGES  OF  NUTRITION  IN  VARIOUS  ARTICLES  OF  FOOD.— 


Raw  cucumbers, 

Raw  melons, 

Boiled  turnips, 

Milk, 

Cabbage, 

Currants, 

Whipped  eggs, 

Beets, 

Apples, 

Peaches, 

Boiled  codfish, 

Broiled  venison, 

Potatoes,  . . . 

Fried  veal,  24 

Roast  poultry, 26 


Raw  beef, 26 

Raw  grapes, 27 

Raw  prunes, 29 

Boiled  mutton, 30 

Oatmeal  porridge, . 75 

Rye  bread, 79 

Boiled  beans, 87 

Boiled  rice, S8 

Barley  bread, 88 

Wheat  bread, 90 

Baked  corn  bread, 91 

Boiled  barley, 92 

Butter, 93 

Boiled  peas, 93 

Raw  oil, 96 


( Moss. ) 


■ 3 

\x/z 

■ 7 

• V/z 

10 

13 
, 14 
, 16 


REQUISITE  FOOD  PERCENTAGES  IN  HEALTH. 


225 


The  average  percentage  of  the  different  food  classes  needed  to 
sustain  a man  in  perfect  health  is  given  in  Kensington  Museum 
“ Handbook  on  Food  ” : 


Per  Cent. 


Water, 81.5 

Albuminoids  or  flesh-formers, 3.9 

Starches  and  sugars, 10.6 

Fat 3.0 

Salt  (NaCl), 0.7 

Phosphates,  potash  salts,  etc., 0.3 


AN  IDEAL  RATION  WITH  SOLID  FOOD. — (Mrs.  E.  H.  Richards.) 


Material. 

Amount. 

Proteid. 

Fat. 

Carbo- 

hydrates. 

Calories. 

Gm. 

Ozs. 

Gm. 

Ozs. 

Gm. 

Ozs. 

Gm. 

Ozs. 

Bread, .... 

453-6 

16 

31-75 

1. 12 

2.26 

O.08 

257.28 

9.04 

1,206.82 

Meat,  .... 

226.8 

8 

34.02 

1.20 

11-34 

0.04 

243.72 

Oysters,  . . . 

226.8 

8 

12.52 

O.44 

2.04 

O.07 

70.01 

Breakfast  cocoa, 

28.3 

1 

6.60 

O.  23 

7-5o 

0. 26 

9.60 

°-34 

135-42 

Milk 

113  4 

4 

363 

O.I3 

4.42 

O.16 

4.88 

1 o-i7 

75-55 

Broth,  . . . . j 

453-6 

16 

18.14 

O.64 

18.14 

0.64 

90.72 

3.20 

613.21 

Sugar,  . . . . 1 

28.3 

1 

27-36 

0.96 

112.17 

Butter,  . . . j 

14.17 

0.14 

12.27 

118.62 

Total,  . . 

57-97  • 

389.84 

2,575-52 

The  following  table  is  a fair  average  work  ration  in  round  num- 
bers, based  on  such  data  as  those  in  the  other  tables : 


ESTIMATED  WORK  RATION,  MAXIMUM  AND  MINIMUM.— 


(Mrs.  E.  H.  Richards.) 


Proteid,  gm.,  . . . 
Fat,  gm. , . . . 
Carbohydrates,  gm., 
Calories,  .... 


For  One  Day. 

} 125 

' \ no 
f 125 

• \ 90 

J 450 
' \ 450 

/ 3>5°°  • 

• \ 3,000 


About  30  gm.  of  salts  should  be  added  to  this  (Landois).  The 
bare  subsistence  ration  is  much  less,  as  follows  : 


ESTIMATED  LIFE  RATION. — (Mrs.  E.  H.  Richards.) 


For  One  Day.  For  One  Day. 

Proteid,  gm., 75  Carbohydrates,  gm. , ...  325 

Fat,  gm., 40  Calories, 2,000 


226 


ENERGY  PRODUCED  BY  FOODS. 


It  will  be  observed  that  the  totals  are  somewhat  less  in  this  diet 
than  those  of  the  preceding  table,  which  is  designed  for  a working 
man  who  is  developing  more  calories. 

TABLE  OF  ENERGY. 

Estimated  in  Foot-tons  instead  of  Calories. — ( Yeo.) 

Energy  developed  by  one  ounce  of  the  following  foods  when 
oxidized  in  the  body: 


Food  Stuff. 

With  Usual 
Percentages  of 
Water. 

One  Ounce 
Water  Free. 

Beef  (best  quality),  uncooked, 

Foot  -tons. 
48.5 

Foot-tons. 

199 

Meat  (served  to  soldiers),  uncooked, 

57.8 

243 

Beef  (fattened),  uncooked, 

96.0 

280 

Meat,  cooked, 

102.6 

240 

Corned  beef  (Chicago), 

124.0 

217 

Salt  beef, 

52.0 

138 

Salt  pork, 

71.6 

166 

Fat  pork, 

202.0 

336 

Dried  bacon, 

292.3 

346 

Smoked  ham, 

179.6 

267 

Whitefish, 

44-3 

209 

Poultry, 

50.7 

204 

Bread, 

87.5 

147 

Wheat-flour, 

123.6 

146 

Biscuit, 

173-3 

189 

Rice,  

126.5 

141 

Oatmeal, 

130.0 

154 

Maize, 

132.0 

160 

Macaroni,  

122.7 

146 

Millet, 

125.9 

I49 

Arrowroot, 

1 16.4 

138 

Peas  (dried), 

118.9 

151 

Potatoes, 

33-° 

I4I 

Carrots, 

14-3 

137 

Cabbage, 

13.0 

158 

Butter, 

344-5 

367 

Eggs 

67.3 

265 

Cheese, 

149.9 

245 

Milk  (cows’), new, 

26.9 

225 

Cream, 

109.2 

365 

Skimmed  milk, 

20.4 

181 

Sugar, 

126.4 

128 

Pemmican, 

Ale  (Bass’s  bottled), 

270. 1 

293 

30.0 

260 

Stout  (Guinness), 

41-5 

360 

Professor  Egleston’s  standard  of  nutrition  is  high.  He  places 
the  daily  allowance  of  nutritive  material  at  700  gm.,  divided  as  fol- 
lows: Carbohydrates,  400  gm. ; fats,  150  gm.;  proteid,  150  gm., — 
yielding  in  all  3650  calories. 


FOOD  VALUES  OF  EDIBLE  PORTIONS  OF  DIET.  227 

PERCENTAGE  COMPOSITION  OF  EDIBLE  PORTIONS  OF  GARRISON 
RATION. — ( Captain  C.  E.  Woodruff \ M.  D. , Assistant  Surgeon,  U.  S.A.) 


Water. 

Protein. 

Fats. 

Carbo- 

hydrates. 

Salts. 

Energy 

Calories, 

PER  LB. 

Bacon,  fat, 

20.0 

8.00 

69- 5 

2-5 

3,080 

Beans, 

12.6 

23.10 

2.0 

59-2 

3-1 

1,615 

Pork,  salt  and  fat,  . . . 

12. 1 

0.90 

82.8 

4.2 

3,510 

Sugar,  ground,  .... 

2.0 

97-8 

0.2 

1,820 

.Sugar,  brown  issue,  . . 

3-0 

96.5 

0-5 

L795 

Flour,  

12.5 

1 1. 00 

1.0 

74-9 

o-5 

1,644 

Beef, 

55-o 

17.10 

27.0 

0.9 

1,460 

Potatoes, 

78.9 

2.10 

0.1 

17.9 

1.0 

375 

Onions 

87.9 

1-4 

o-3 

10. 1 

0.6 

225 

Oatmeal, 

7.6 

15. 10 

7-i 

68.2 

2.0 

1,850 

Cornmeal, 

150 

9.20 

3-8 

70.6 

1.4 

1,645 

Canned  apples,  .... 

83.2 

0. 20 

0.4 

. 15-9 

0.3 

3i5 

Dried  apples,  .... 

25.0 

0.90 

1.8 

7i-5 

1.4 

1 ,418 

Tapioca  or  corn -starch, 

2.0 

97.8 

0.2 

1,820 

Butter, 

10.5 

1. 00 

85.0 

o-5 

3-0 

3,6i5 

Syrup, 

43-7 

55-o 

2-3 

1,023 

Lard, 

12.0 

0.60 

83-4 

4.0 

3,57o 

Rice, 

12.4 

7-4 

0.4 

79-4 

0.4 

1,630 

Canned  corn, 

81.3 

2.80 

1. 1 

13.2 

0.6 

345 

Canned  tomatoes,  . . . 

96.0 

0.80 

0.4 

2-5 

o-3 

80 

Macaroni  and  vermicelli, 

131 

9.00 

o-3 

76.8 

0.8 

1,406 

Milk,  fresh, 

14. 1 

0.843 

0.802 

1.069 

0.164 

418 

Milk,  condensed,  . . . 

25.0 

17.00 

11. 0 

44.00 

3-o 

L595 

Peas, 

12.3 

26.70 

1-7 

56.40 

2.9 

1,565 

Raisins, 

40.0 

0.40 

24.00 

0.6 

440 

Cheese, 

35-o 

33  00 

22.0 

5.00 

5-o 

1,600 

Prunes, 

3°° 

2.50 

12.0 

0.6 

140 

Cabbage, 

92.0 

2.10 

0.6 

5-5 

1. 1 

i55 

Ham, 

41.5 

16.7 

39- 1 

2.7 

1,960 

Apricots,  canned,  . . 

50.0 

2.00 

30.0 

0.6 

460 

Barley, 

13.00 

2.7 

76.0 

3-° 

1,800 

Chocolate, 

12.0 

20.00 

50.0 

10. 0 

4.0 

2,650 

Sausage,  

41.2 

13.80 

42.8 

2.2 

2,065 

Oysters, 

87.1 

6.00 

1.2 

3-7 

2.0 

230 

Salmon,  canned,  . . . 

63.6 

21.60 

13-4 

1.4 

965 

Crabs, 

15.0 

1.0 

526 

Crackers, 

10.3 

9-4 

70.5 

1,900 

Church  furnishes  the  following  table  showing  the  number  of  tons 
which  it  is  calculated  could  be  raised  one  foot  by  the  complete 
combustion  of  a single  pound  of  each  kind  of  food.  In  the  body 
only  about  a fifth  of  this  energy  would  develop  work,  the  rest  going 
into  heat  production  : 


I pound  beef-fat 

raises  5,649  tons  ] 

[ foot  high. 

I pound  oatmeal 

“ 2,439  “ 

“ “ 

I pound  gelatin 

“ 2,270  “ 

“ “ 

1 pound  lean  beef 

“ 885  “ 

“ “ 

I pound  potatoes 

“ 618  “ 

“ “ 

impound  milk 

“ 390  “ 

“ “ 

1 pound  ground  rice 

“ 2,330  “ 

“ “ 

228 


DIETETIC  KITCHEN. 


CHAPTER  II. 

DIETETIC  KITCHEN.— DIET  LISTS. 

In  the  following  pages  we  give  the  diet  orders  of  Penzoldt,  which 
agree  essentially  with  those  mentioned  by  Leube,  but  have  this 
advantage  over  the  latter,  that  they  contain  at  the  same  time  the 
permissible  quantities  of  each  article  of  food,  and  are  also  ex- 
panded in  other  directions. 

The  following  diet  list,  consisting  of  four  different  kinds  of  diet, 
is,  like  that  of  Leube,  especially  intended  to  be  a basis  for  a mild 
dietetic  treatment  in  cases  of  diseases  of  the  stomach  in  general 
(the  so-called  ulcer  cure  of  Leube).  By  means  of  a gradual  transi- 
tion from  a very  light  to  a stronger  and  richer  diet,  it  endeavors 
not  to  tax  the  diseased  organ  in  the  beginning,  and  gradually  to 
accustom  it  to  increased  service. 

It  is  self-evident  that  this  diet  list  may  not  with  impunity  be 
extended  in  the  same  manner  to  all  diseases  of  the  stomach. 
According  to  the  state  of  the  secretion,  the  peristalsis,  and  of  sen- 
sation, other  problems  concerning  the  diet  may  arise.  We  shall 
revert  to  the  special  details  of  the  several  forms  of  disease  when 
we  come  to  them.  It  is  necessary  only  to  give  the  principal  rules 
for  the  chief  types  of  diseases  of  the  stomach  in  this  chapter. 


PENZOLDT’ S DIET  ORDERS  FOR  GRADUAL  TRAINING  OF  THE 
DIGESTIVE  CAPACITY. 

FIRST  DIET  (ABOUT  TEN  DAYS). 


Foods  or  Drinks. 

Largest 
Quantity  at 
One  Time. 

Preparation. 

Character. 

How  to  be  Taken. 

Bouillon. 

250  gm.,  % 
liter. 

To  be  made  from 
beef. 

Lean,  very  little 
salt,  or  none  at 
all. 

Slowly. 

Cow’s-milk. 

250  gm-,  X 

liter. 

Well  boiled,  or 
sterilized 
(Soxhlet’s  ap- 
paratus) . 

Pure  milk,  or 
eventually  y 

lime-water  and 
milk. 

Eventually  with 
a little  tea. 

Eggs. 

One  or  two. 

Very  soft,  merely 
warmed  or  raw. 

Fresh. 

If  raw,  stir  into 
the  warm,  not 
boiliug,  bouil- 
lon. 

penzoldt’s  diet  orders.  229 


Penzoldt’s  Diet  Orders  for  Gradual  Training  of  the  Digestive  Capacity. — 
First  Diet  (About  Ten  Days)  ( Continued ). 


Foods  or  Drinks. 

Largest 
Quantity  at 
One  Time. 

Preparation. 

Character. 

How  to  be  Taken. 

Meat  solution 
(Leube  - Rosen- 
thal’s). 

30-40  gm. 

See  Dietetic  Kit- 
chen. 

It  may  have  only 
a faint  odor  of 
bouillon. 

By  teaspoonfuls 
or  stirred  up  in- 
to bouillon. 

Cakes  (Albert 
biscuits). 

Six. 

Without  sugar. 

Not  soaked  or 
softened,  but  to 
be  well  masti- 
cated and  in- 
salivated. 

Water. 

Y%  liter. 

Ordinary  or  nat- 
ural carbonated, 
containing  a 
little  carbonic 

acid  (Selters), 
Saratoga  Vichy, 
Londonderry 
Lithia,  Poland. 

Not  too  cold. 

SECOND  DIET  (ABOUT 

TEN  DAYS). 

Foods  or  Drinks. 

Largest 
Quantity  at 
One  Time. 

Preparation. 

Character. 

How  to  be  Taken. 

Calf’s-brain. 

100  gm. 

Boiled. 

To  be  freed  from 
all  membranes 
and  fiber. 

Preferably  in  the 
bouillon. 

Sweetbread 
(thymus  gland). 

100  gm. 

Boiled. 

Similar  to  above, 
especially  to  be 
peeled  carefully. 

Similarly  to 
above. 

Pigeons. 

One. 

Boiled. 

Only  young  ones, 
without  skin, 
tendons,  and  the 
like. 

Similarly  to 
above. 

Chickens. 

One,  the  size 
of  a pigeon. 

Boiled. 

Like  above  (no 
fattened  chick- 
ens). 

Similarly  to 
above. 

Raw  beef. 

100  gm. 

Finely  chopped 
or  scraped, 
with  a little 
salt. 

To  be  taken  from 
the  fillet  (tender- 
loin). 

To  be  eaten  with 
crackers. 

Raw  beef  sau- 
sage. 

100  gm. 

Without  addi- 
tions. 

A little  smoked. 

Similarly  to  pre- 
ceding. 

Tapioca. 

3°  gm- 

Cooked  to  a 
homogeneous 
gruel  with 
milk. 

23O  DIETETIC  KITCHEN. 


Penzoldt’s  Diet  Orders  for  Gradual  Training  of  the  Digestive  Capacity 
( Continued). 

THIRD  DIET  (ABOUT  EIGHT  DAYS). 


Foods  or  Drinks. 

Largest 
Quantity  at 
One  Time. 

Preparation. 

Character. 

How  to  be  Taken. 

Pigeon. 

One. 

To  be  fried  with 
fresh  butter, 
not  too  much. 

Only  young  ones, 
without  skin, 
etc. 

Without  sauce. 

Chicken. 

One. 

Like  above. 

Like  above. 

Like  above. 

Beefsteak. 

100  gm. 

With  fresh  but- 
ter, half  raw 
(English). 

The  meat  from 
the  fillet,  or  ten- 
derloin, well 
pounded. 

Like  above. 

Ham. 

100  gm. 

Raw,  scraped 
fine. 

Smoked,  not 
strong,  without 
bones,  the  so- 
called  “ Lachs- 
schinken.” 

With  wheat 
bread. 

French  roll,  toast, 
or  Freiberg 
pretzel. 

5°  gm. 

Baked  crisp. 

Stale  (rolls  and 
the  like). 

To  be  chewed 
very  carefully 
and  to  be  well 
salivated. 

Potatoes. 

5°  gm- 

a.  As  puree,  be- 
ing forced 
through  a 
strainer. 

b.  As  salt  pota- 
toes, mashed. 

The  potatoes  must 
be  mealy, 

crumbling  when 
mashed. 

Cauliflower. 

50  gm. 

To  be  cooked  in 
salt  water  as 
vegetables. 

Only  the  “ flow- 
ers ” to  be  used. 

FOURTH 

DIET  (ABOUT  EIGHT  TO  FOURTEEN  DAYS). 

Foods  or  Drinks. 

Larcest 
Quantity  at 
One  Time. 

Preparation. 

Character. 

How  to  be  Taken. 

Venison. 

IOO  gm. 

Roast. 

Saddle,  hung,  not 
gamy,  without 
high  flavor. 

Partridge. 

One. 

Roast,  without 
lard. 

Young  birds,  with 
skin,  tendons, 
feet,  etc.,  re- 
moved, after 
having  hung  in 
pure  cold  air 
for  twenty-four 
hours. 

DIET  LISTS.  23I 


Penzoldt’s  Diet  Orders  for  Gradual  Training  of  tiie  Digestive  Capacity. — 
Fourth  Diet  (Ahout  Eight  to  Fourteen  Days)  ( Continued ). 


Foods  or  Drinks. 

Largest 
Quantity  at 
One  Time. 

Preparation. 

Character. 

How  to  be  Taken. 

Roast  beef. 

IOO  gm. 

Fried  until  red. 

From  well-fed 
cattle,  pounded. 

Warm  or  cold. 

Fillet. 

IOO  gm. 

In  same  manner 
as  the  above. 

In  same  manner 
as  the  above. 

In  same  manner 
as  the  above. 

Veal. 

IOO  gm. 

Roast. 

Saddle  or  leg. 

Finely  cut. 

Pike.  1 

Perch-pike.  | 
Carp. 

Trout.  J 

100  gm. 

Boiled  in  salt 
water  without 
any  additions. 

Carefully  remove 
the  bones. 

In  fish  sauce. 

Caviar. 

5°  gm. 

Raw. 

Russian  caviar 

with  but  a little 
salt  in  it. 

Asparagus. 

50  gm. 

Boiled. 

Soft,  without  the 
hard  portions. 

With  a little 
melted  butter. 

Rice. 

50  gm. 

As  gruel,  forced 
through  a 

strainer. 

Soft,  boiling  rice. 

Likewise. 

Poached  eggs. 

Two  eggs. 

With  a little 
fresh  butter. 

With  salt. 

Omelette  souffle 
(Auflauf). 

Two  eggs. 

With  about  20 
gm.  sugar. 

Must  rise  well. 

To  be  eaten  at 
once. 

Stewed  fruits. 

5°  gm. 

Fresh  boiled, 
forced  through 
a strainer. 

Freed  of  all  skins 
and  seeds. 

Red  wine. 

100  gm. 

Light,  pure  Bor- 
deaux, or  reli- 
able California. 

Or  any  similar 
kind  of  pure  red 
wine. 

Slightly  wanned. 

All  of  these  foods  should  be  prepared  according  to  directions 
given  in  the  “ Dietetic  Cooking.” 


DIET  LIST  OF  EWALD  FOR  CHRONIC  GASTRITIS. 

8 a.  m. — 150  to  200  gm.  of  tea,  with  100  gm.  of  stale  wheat  bread,  toast,  or 
zwieback. 

10  a.  m. — 50  gm.  of  wheat  bread,  10  gm.  of  butter,  50  gm.  of  cold  meat  or  ham, 
and  either  one  glass  of  light  wine  or  Y of  a liter  of  milk. 

2 p.  m. — 150  to  200  gm.  of  water,  milk,  or  bouillon  of  white  meats;  100  to  125 
gm.  of  meat  or  fish,  30  to  100  gm.  of  vegetables,  80  gm.  compote. 

4.30  p.  m. — of  a liter  of  warm  milk,  chocolate,  or  one-half  milk  and  one- 
half  coffee. 

7 to  8 P.  m. — 300  gm.  of  soup,  50  gm.  of  wheat  bread,  10  gm.  of  butter. 

10  p.  m. — Occasionally  50  gm.  of  wheat  bread,  biscuit,  oT  zwieback  ; one  cup 
of  coffee. 


232 


DIETETIC  KITCHEN. 


Boas  gives  two  lists  ; the  following  contains  the  better  and  richer 
diet : 

Calories. 


8 A.  M. — 200  gm.  of  milk,  with  40  gm.  of  cocoa  and  30  gm.  of  sugar,  . . 462 

50  gm.  of  cakes,  or  50  gm.  of  zwieback,  either  one,  187 

10  a.  m. — 50  gm.  of  wheat  bread  with  30  gm.  of  butter,  343 

100  gm.  of  calf  ’s-brain  (or  100  gm.  of  sweetbread,  90  calories),  . . 140 
Or  100  gm.  of  broiled  pike,  71.75  calories. 

12  m. — Soup  of  30  gm.  of  tapioca,  10  gm.  of  butter,  1 egg, 282 

100  gm.  of  noodles, 352 


Or  100  gm.  of  spinach,  165  calories;  100  gm.  of  bean  puree, 
193  calories  ; 100  gm.  of  carrots,  40  calories ; 50  gm.  of 


potato  puree,  63.7  calories. 

100  gm.  of  breast  meat  of  young  chicken, 106.4 

100  gm.  of  veal  cutlets  (250  calories),  or,  in  its  place,  100  gm.  of 
broiled  veal,  pigeon,  venison,  or  fish. 

100  gm.  of  farina  or  omelette,  or  egg-pancake, 288 

3 p.  m. — 100  gm.  of  milk,  with  20  gm.  of  sugar,  flavored  with  tea,  . . . 147 

25  gm.  of  cakes,  93.5 

7 p.  m. — 50  gm.  of  wheat  bread,  130  gm.  of  butter, 343 

50  gm.  of  scraped  raw  beef, 459-5 


3203.4 

HEMMETER’S  DIET  LIST  FOR  CHRONIC  GASTRITIS  WITH  UNIM- 
PAIRED MOTILITY  AND  INTESTINAL  DIGESTION. 

Also  Available  for  Lowered  Nutrition  where  Intestinal  Functions  are 
Normal. 

7.30  A.  M. — If  the  bowels  are  regular,  ]/2  of  a pint  of  hot  normal  saline  solution. 
If  the  bowels  are  constipated,  a pint  of  cold  Saratoga  Vichy,  Bedford 
Magnesia  Spring,  or  plain  cold  water. 

Calories. 

Breakfast,  8 a.  m. — 3 ounces  or  100  gm.  of  farina,  boiled  with  milk,  . 127 
Or  100  gm.  of  cerealin,  boiled  with  milk; 

Or  100  gm.  of  breakfast  wheat  (strained),  boiled  with  milk. 

Calories. 


One  soft-boiled  egg 80 

Two  ounces  of  wheat  bread,  toasted, 156 

One  ounce  of  best  fresh  butter, 212 

One  cup  of  wheat  coffee  (made  of  100  gm.  of  roasted  choice  wheat, 

250  c.c.  of  boiling  water,  and  1 50  gm.  of  milk).  Instead  of  this 
the  same  portions  of  tea  and  milk  or  cocoa  can  be  used,  . . . 100 

Sugar,  10  gm.  (2^  drams), 40 


The  farina  or  cerealin  will  taste  better  if  eaten  with  a roasted 
apple. 

As  the  digestive  power  improves,  the  egg  is  served  in  form  of 
omelette,  or  poached,  on  toast. 


DIET  LISTS. 


233 

Calories. 


10.30  A.  m. — 100  gm.  of  scraped  ham  (3^  ounces) 120 

30  gm.  of  crackers  or  toast  (one  ounce), 107 

226  gm.  or  eight  ounces  of  broth.  Instead  of  broth,  milk,  kefyr, 

and  matzoon  may  be  permitted  in  the  same  quantity,  ....  306 

Dinner,  i p.  m. — Soup  made  of  250  gm.  or  eight  ounces  of  bouillon,  30 
gm.  or  one  ounce  of  rice  or  tapioca,  10  gm.  or  2 ]/z  ounces  of 
butter,  and  one  egg, 282 


In  case  of  much  weakness  and  emaciation,  y2  of  a tablespoonful 
of  somatose  should  be  added. 

The  patient  must  not  be  aware  of  the  addition  of  artificial  foods. 

Calories. 

120  gm.  of  breast  meat  of  broiled  fowl, 228 

Or  scraped  tenderloin  formed  into  patties  and  broiled  ; 

Or  steamed  or  broiled  bluefish,  trout,  white  or  yellow  perch ; 


Or  broiled  rockfish  or  sweetbreads. 

50  gm.  or  two  ounces  of  potato  puree,  637 

100  gm.  or  3 )/$  ounces  of  carrots,  steamed, 40 


Or  100  gm.  of  puree  of  beans  or  peas ; 

Or  100  gm.  of  strained  tomato  puree. 

100  gm.  of  finely  divided  spinach. 

One  cup  custard  made  of  two  eggs, 160 

Or,  instead  of  this,  100  grs.  of  sherry  gelatin,  or  stewed  apples, 
or  plums,  or  rice  in  form  of  very  light  pudding  made  with 
slices  of  apple,  no  raisins. 

One  glass  (100  gm.  or  3 ounces)  of  Hungarian  Tokay  ( J.  Palug- 

yay  & Sons,  Pressburg), 50 

This  list  is  made  intentionally  abundant  in  order  to  permit  of 
latitude  in  making  a selection. 

Instead  of  the  meats  given,  the  patient  may,  for  a change,  be 
allowed  broiled  pigeon  or  venison,  which  must  not  be  gamy  ; also 
meat  dumplings  of  scraped  beef,  scraped  pork  made  into  balls  with 
bread  crumbs,  zwieback  crumbs,  egg,  and  butter,  cooked  in  bouil- 
lon, and  a separate  sauce  is  made  and  flavored  with  scraped  sar- 
delles. 

Calories. 

3 p.  m. — One  cup  of  chocolate  made  with  30  gm.  or  1 ounce  of  breakfast 

cocoa,  or  v.  Mehring’s  Kraft-chocolate,  and  yi  of  a pint  of  milk,  135.5 

30  gm.  of  crackers,  coffee-cake  without  grated  nuts,  cinnamon 

shortcake  with  but  the  faintest  trace  of  cinnamon, 107 

If  the  sweet  chocolate  is  not  agreeable,  plain  milk,  or  a glass  of 
light  Rhine  wine  with  crackers,  is  allowable.  Coffee  in  small 
quantities  may''  be  added  to  the  milk  at  this  hour. 

16 


234 


DIETETIC  KITCHEN. 


Calories. 

Supper,  6.30  p.  m. — Broiled,  panned,  or  raw  oysters,  240  gm.  or  eight 

ounces, 70 

If  there  is  sub-  or  anacidity,  the  addition  of  a little  grated  horse- 
radish, lemon-juice,  or  catsup  to  the  raw  oysters  should  not  be 


forbidden. 

Crackers,  two  ounces  or  60  gm., 107 

Butter,  one  ounce  or  30  gm 212 

]/2  of  a pint  of  reliable  Rhine  wine, 50 


Or  y2  of  a pint  of  imported  beer,  or  yz  of  a pint  of  tea  and 
milk.  Instead  of  the  oysters,  little  neck  clams,  fresh 
scraped  beef,  finely  cut  roast  lamb  or  beef,  cold,  smoked 
chipped  beef,  or  smoked  tongue  will  answer. 

Note. — If  the  gastritis  is  evidently  due  to  abuse  of  alcohol,  the  wines  and 
beer  must  be  excluded. 


BILL  OF  FARE  FOR  CHRONIC  CATARRH  OF  THE  STOMACH,  WITH 
THE  DIGESTION  OF  THE  STOMACH  ONLY,  REDUCED. — ( Wegele.) 


Albumin. 

Fat. 

Carbo- 

hydrate. 

Alcohol. 

Morning  : 

150  gm.  of  pepton  cocoa, 

8.00 

6.0 

7-50 

25  gm.  of  butter  (on  toasted  roll),  . 

0.18 

20.8 

0.15 

Forenoon : 

1 soft  egg, 

6.00 

5-0 

Noon  : 

200  gm.  of  oatmeal  soup, 

12.50 

0-3 

18.00 

150  gm.  of  fowl, 

28.00 

I3-5 

I.80 

200  gm.  of  carrot, 

2.14 

0.4 

16.30 

Afternoon  .- 

150  gm.  of  pepton  cocoa, 

8.00 

6.0 

7-So 

25  gm.  of  butter  and  Albert  biscuit 

or  banquet  crackers, 

O.18 

20.8 

0.15 

Evening  : 

1 egg>  

6.00 

5-o 

100  gm.  of  scraped  ham,  .... 

25.00 

8.0 

100  gm.  of  macaroni,  with  toasted 

bread  crumbs, 

9.00 

0.3 

76.70 

During  the  Day  : 

200  gm.  of  wine, 

6.  co 

16.0 

75  gm.  of  toast, 

9.00 

* i-5 

63.90 

Total, 

117.20 

94.6 

236.01 

16.0 

Calories,  about 

480 

890 

| 970 

IOO 

Entire  combustion  value  about  2440  calories. 


DIET  LISTS. 


235 


BILL  OF  FARE  FOR  ATROPHIC  CATARRH.— ( Wegele-Penzoldt.) 


Albumin. 

Fat. 

Carbo- 
hydrate | 

Alcohol. 

Morning  : 

150  gm.  of  maltoleguminose  cocoa,  . 

6.00 

4.00 

'3-50 

Forenoon : 

150  gm.  of  wine, 

20  gm.  of  butter  (on  toasted  bread), 

4.00 

12.0 

0.15 

16.60 

0. 12 

Noon  : 

100  gm.  of  maltoleguminose  soup,  . 

2.60 

O.IO 

6.20 

loo  gm.  of  scraped  beefsteak,  . . . 

20.00 

6.00 

100  gm.  of  mashed  potatoes,  . . . 

3. 10 

0.50 

21.30 

10  gm.  of  malt  extract, 

0.50 

5-5° 

Afternoon : 

1 cup  of  tea  (with  toast), 

20  gm.  of  butter, 

0.15 

16.60 

0. 12 

30  gm.  of  honey, 

0.40 

22.00 

Evening : 

250  gm.  of  rice  mush, 

22.00 

8.25 

71.00 

During  the  Day  : 

75  gm.  of  toast  (or  toasted  bread),  . 

9.00 

I.50 

63.90 

10  o’clock  at  Night  : 

250  gm.  of  milk, 

8.70 

9-30 

12.00 

10  gm.  of  cognac  brandy,  .... 

... 

7.0 

Total, 

72.70 

62.85 

219.64 

19.0 

Calories,  about 

3°° 

580 

920 

13° 

Entire  combustion  value  about  1930  calories. 


BILL  OF  FARE  FOR  ATONY  OF  THE  STOMACH,  WITH  GASTRIC 
DIGESTION  REDUCED. — ( Wegele  ) 


Albumin. 

Fat. 

Carbo- 

hydrate. 

Alcohol. 

Morning  : 

150  gm.  of  leguminose  cocoa,  . . . 

6.0 

4.0 

13-5 

50  gm.  of  cream, 

1.8 

13-3 

1.8 

Forenoon : 

1 soft  egg, 

6.0 

5-o 

20  gm.  of  toast,  

2-5 

0.4 

15.0 

Noon  : 

100  gm.  of  scraped  beefsteak,  . . . 

17. 1 

6.0 

200  gm.  of  mashed  potatoes,  . . . 

4.2 

2.7 

42.6 

20  gm.  of  malt  extract, 

1.0 

11. 0 

Afternoon : 

150  gm.  of  leguminose  cocoa,  . . . 

6.0 

4.0 

13-5 

50  gm.  of  cream, 

1.8 

13-3 

1.8 

Evening: 

250  gm.  of  tapioca  pulp, 

12.0 

8.0 

11. 0 

15  gm.  of  diastase  malt  extract,  . . 

0.8 

9.0 

236 


DIETETIC  KITCHEN. 


Bill  of  Fare  for  Atony  of  the  Stomach,  with  Gastric  Digestion 
Reduced. — ( Wegele')  ( Continued ). 


Albumin. 

Fat. 

Carbo- 

hydrate. 

1 Alcohol. 

During  the  Day  : 

50  gm.  of  toast, 

6.0 

1.0 

35-o 

10  o’clock  at  Night: 

200  gm.  of  milk, 

IO  gm.  of  cognac, 

6.4 

7.2 

9.6 

6.9 

Total, 

71.6 

64.9 

163.8  | 

6.9 

Calories,  about 

290 

600 

670 

50 

Total  combustion  value  about  1610  calories. 


At  noon,  of  course,  other  kinds  of  meat  could  be  chosen,  such 
as  fowl  or  game;  likewise  at  night  rice  or  thick  gruel. 

With  fermentation  of  the  stomach,  however,  the  following  bill  of 
fare  had  best  be  used  after  a few  days : 

Morning  : 

100  gm.  of  scraped  ham  (can)  or  smoked  meat,  and  20  gm.  of  bread  crust. 
Forenoon : 

One  soft  egg  and  20  gm.  of  bread  crust  or  toast. 

Noon  : 

100  gm.  of  scraped  beefsteak  and  scrambled  eggs  (two). 

Afternoon : 

Same  as  forenoon. 

Evening  : 

Same  as  noon. 

Two  clysters  of  y2  to  1^  per  cent,  common  salt  solution. 

HEMMETER’S  DIETARY  FOR  ANACID  DILATATION. 

Calories . 

7.30  A.  m. — Lavage  with  NaCl  solution,  or  a decinormal  solution  of  HC1. 


8 A.  M. — Cerealin  with  cream,  150  gm., 395 

Mosquera  beef  chocolate,  200  gm., 140 

Malt  extract,  10  gm., 24.5 

10  A.  m. — Toast  or  aleuronat  bread  (see  dietetic  directions),  60  gm.,  . . 135 

Butter,  20  gm., 163 

12  m. — Boiled  round  of  beef,  150  gm., 440 

Mashed  potatoes,  50  gm., 63 

Spinach  or  carrots,  100  gm 165.5 

In  place  of  these,  purees  of  peas,  beans,  lentils,  or  turnips  are 
allowed. 

Omelette  souffle,  100  gm 244 

3 P.  M. — 100  gm.  of  tea,  50  gm.  of  Albert  biscuits,  10  gm.  of  milk,  . . . 254 


DIET  LISTS. 


237 

Calories. 


7 p.  M. — 100  gm.  of  scraped  ham  in  omelette, 244 

Or  60  gm.  of  scraped  ham  (262  calories). 

200  gm.  of  farina  with  milk, 432 

60  gm.  of  toast,  20  gm.  of  butter 298 

9.30  P.  M. — Milk,  300  c.c., 202 

Two  ounces  of  banquet  crackers  or  Albert  biscuits 200 


Or  in  place  of  the  milk  a glass  (two  ounces)  of  approved  Tokay 
or  Malaga. 


BILL  OF  FARE  FOR  ATONY  OF  THE  STOMACH,  WITH  THE  PRODUCTION 
OF  HYDROCHLORIC  ACID  SUSTAINED  OR  INCREASED. — ( Wegele.) 


Albumin. 

Fat. 

Carbo- 

hydrate. 

Alcohol. 

Morning: 

150  gm.  of  pepton  cocoa,  

8.0 

6.0 

7-5  j 

50  gm.  of  cream, 

1.8 

13-3 

1.8 

Forenoon : 

30  gm.  of  French  roll, 

3-o 

. 0.2 

20.0 

50  gm.  of  ham, 

12.5 

4.0 

1 egg,  

6.0 

5-0 

Noon  : 

120  gm.  of  roast  meat, 

21.0 

8.0 

200  gm.  of  mashed  potatoes,  .... 

4.2 

2.7 

42.6 

Afternoon : 

150  gm.  of  pepton  cocoa, 

8.0 

6.0 

7-5 

50  gm.  of  cream, 

1.8 

13-3 

1.8 

Evening  : 

120  gm.  of  cold  roast  meat,  .... 

21.0 

8.0 

200  gm.  of  rice, 

9.0 

6.6 

'28.6 

IO  O’CLOCK  : 

100  gm.  of  wine,  . 

3-3 

7.8 

During  the  Day: 

50  gm.  of  toast 

6.5 

1.6 

41.0 

Total, 

102.8 

74-7 

I59-1 

7.8 

Calories,  about 

420 

700 

640 

55 

Total  combustion  value  about  1815  calories. 


Instead  of  ham,  caviar  and  butter  with  slices  of  toasted  roll,  or 
scrambled  eggs  with  smoked  meat,  may  be  given  in  the  forenoon. 
At  noon,  beefsteak,  fillet,  game,  or  fowl  are  allowed,  and  for  side 
dishes  some  mashed  carrots  or  spinach.  At  night,  calf’s-foot  jelly 
and  omelette  souffle. 

In  convalescence,  10  to  15  gm.  of  condensed  milk  or  malt  extract 
three  times  daily  after  meals  can  be  prescribed,  through  which  the 
nutritive  value  of  this  diet  is  considerably  increased. 


238 


DIETETIC  KITCHEN. 


BILL  OF  FARE  FOR  ENLARGEMENT  OF  THE  STOMACH  WITH 
STENOTIC  APPEARANCES. — ( Wegele.) 


Albumin. 

Fat. 

Carbo- 

hydrate. 

Alcohol. 

Morning  : 

100  gm.  of  scraped  ham, 

25.0 

8.0 

Tea  with  50  gm.  of  cream, 

1.8 

13-3 

‘ 1.8 

Forenoon : 

2 eggs, 

20  gm.  of  sugar, 

12.0 

10.0 

16.0 

*13-8 

10  gm.  of  cognac, 

Noon  : 

100  gm.  of  scraped  beefsteak,  . . . 

20.7 

i-5 

100  gm.  of  mashed  potatoes,  .... 

3-1 

o-5 

21.3 

Afternoon  : 

Tea  with  50  gm.  of  cream, 

1.8 

13-3 

1.8 

Evening  : 

100  gm.  of  roast  chicken  (hashed) , . 

20.7 

i-5 

100  gm.  of  flour  puff-paste, 

4.2 

4-3 

22.0 

During  the  Day  : 

80  gm.  of  toast,  

8.5 

1.2 

55-o 

Night : 

200  gm.  of  milk, 

6.4 

7.2 

9.6 

Total, 

104.2 

60.8 

127.5 

13.8 

Calories,  about 

427 

565 

722 

100 

Total  combustion  value  about  1814  calories. 


With  this  bill  of  fare  it  is  most  difficult  to  have  a variety.  Beef- 
steak scraped  fine  from  lean  meat,  chicken,  pigeon,  lean  ham, 
smoked  meat,  cold  roast  beef,  and  fillet  are  recommended. 

In  the  evening  one  may  often  serve  also  calf’s-foot  jelly,  tapioca, 
or  milk  jelly.  With  occasional  improvement  condensed  milk, 
cream,  malt  extract,  and  milk  jellies  may  be  tried  by  spoonfuls 
between  meals.  Besides  these  a nutritive  clyster  (following  a 
cleansing  enema)  is  to  be  given  twice  a day  in  these  severe  cases. 
With  pronounced  stenosis,  prompt  operation  is  necessary ; where 
this  is  impossible  or  refused,  rectal  feeding  is  preferable  to  feeding 
by  the  stomach. 

One  may  waive  the  somewhat  tedious  meat-pancreas  clysters, 
when  a considerable  quantity  of  meat  is  taken  in  per  os,  and  employ 
either  Ewald’s  or  Boas’  method  of  rectal  alimentation,  since  accord- 
ing to  the  investigations  of  Eichhorst  (“  Pfluger’s  Archiv,”  Bd.  iv, 
1871),  Ewald  (“  Zeitschrift  f.  klin.  Med.,”  Bd.  xii,  1887),  and  Huber 
(“  Deutsch.  Archiv  f.  klin.  Med.,”  Bd.  xlvii),  the  digestion  of  the 
albumen  of  eggs  and  milk  proceeds  very  well  without  previous 


DIET  LISTS. 


239 


peptonization  in  the  rectum,  while  it  is  considerably  increased  by 
the  addition  of  common  salt  (one  gm.  to  one  egg)  (see  chapter  on 
Rectal  Alimentation).  Boas  (“  Diagnostik  und  Therapie  der  Magen- 
krankheiten,”  zweite  Aufl.,  1891,  S.  244)  has  followed  out  rectal 
nutrition  for  ten  to  fourteen  days,  in  cases  of  severe  gastrectasia 
with  symptoms  of  fermentation,  and  attained  not  only  the  disap- 
pearance of  the  symptoms  of  fermentation  and  a considerably 
better  general  state  of  health,  but  also  temporary  increase  in 
weight, — a success  which  lasted  from  three  to  four  months. 

If  to  the  preceding  bill  of  fare  two  more  nutritive  clysters  are 
added,  the  patient  receives  : 


Albumin. 

Fat. 

Carbo- 

hydrate. 

Alcohol. 

4 eggs,  

100  gm.  of  red  wine, 

20.0 

24.O 
. . . 

3-3 

‘7.V 

Total,  

20.0 

24.O 

3-3 

7.8 

Calories,  

82 

224 

3i 

54 

Total  combustion  value  about  391  calories. 


If  we  assume  that  of  this  only  ten  gm.  of  albumen,  two  gm.  of 
carbohydrate,  ten  gm.  of  fat,  and  four  gm.  of  alcohol  should  attain 
resorption,  we  would  obtain  a total  combustion  value  of  about  175 
calories. 

With  two  nutritive  clysters,  according  to  Boas,  the  following 
increase  would  be  attained  : 


Albumin. 

Fat. 

Carbo- 

hydrate. 

Alcohol. 

500  gm.  of  milk, 

17.0 

18.2 

24.2 

4 eggs, 

30  gm.  of  red  wine, 

40  gm.  of  leguminose  flour, 

24.0 

20.0 

2.0 

8.8 

3-6 

25.0 

Total, 

49.8 

41.8 

49.2 

2.0 

If  half  be  assumed  as  resorbed,  then  there  would  be  an  addition 
of  about  25  gm.  of  albumin,  about  20  gm.  of  fat,  about  25  gm.  of 
carbohydrate,  about  one  gm.  of  alcohol.  This  would  give  a total 
combustion  value  of  about  1850  calories  (Wegele). 


240 


DIETETIC  KITCHEN. 


BILL  OF  FARE  FOR  GASTRIC  CARCINOMA  WITHOUT  PERCEPTIBLE 
STENOTIC  APPEARANCES. — ( Wegele.) 


Albumin. 

Fat. 

Carbo- 

hydrate. 

• 

Alcohol. 

Morning  : 

150  gm.  of  maltoleguminose  cocoa,  . 

6.0 

4.0 

13-5 

Forenoon : 

200  gm.  of  kefyr, 

6.6 

4-5 

3-8 

Noon  : 

150  gm.  of  maltoleguminose  soup,  . . 

4.0 

0.15 

9-3 

100  gm.  of  scraped  beefsteak,  . . . 

20.0 

6.0 

Afternoon  : 

150  gm.  of  maltoleguminose  cocoa,  . 

6.0 

4.0 

13-5 

Evening  : 

100  gm.  of  scraped  ham, 

25.0 

8.0 

8.0 

150  gm.  of  tapioca, 

7.0 

5-o 

10  O’CLOCK  : 

200  gm.  of  kefyr, 

6.6 

4-5 

3-8 

With  the  cocoa,  30  gm.  of  honey,  . . 
With  the  kefyr,  20  gm.  of  cognac,  . . 

0.4 

22.0 

14.0 

During  the  Day  : 

50  gm.  of  toast, 

6.6 

1.0 

35-o 

Total,  

87.6 

37-i 

108.9 

15.0 

Calories,  about 

360 

35o 

45o 

100 

Total  combustion  value  about  1260  calories. 


For  a change,  tea  may  be  often  given  instead  of  cocoa ; where 
lcefyr  does  not  agree  with  the  patient,  or  is  refused  by  him,  one 
may  try  condensed  milk  with  cognac  instead ; further,  one  may  let 
him  eat  butter  upon  toast,  or  toasted  bread  with  the  tea,  and  also 
have  variety  in  the  meats,  so  long  as  the  appetite  for  them  remains. 

Naturally,  in  the  last  stages  a considerable  narrowing  of  the  list, 
both  in  quantity  and  quality,  takes  place,  and  one  must  make  the 
greatest  concessions  to  the  individual  tastes  of  the  patient.  In  the 
morning  either  cocoa  or  tea,  with  slices  of  toasted  roll  spread  with 
meat  extract  or  caviar ; then  allow  a little  wine  with  one  soft  egg,  or 
egg  with  cognac  and  sugar,  or  a glass  of  champagne ; at  noon 
sweetbread  in  soup,  smoked  ham,  pickled  meat,  smoked  meat 
(which  foods  are  more  difficult  of  decomposition),  gruel,  rice, 
mondamin  cooked  in  milk,  according  to  taste.  In  the  afternoon, 
tea  with  cognac  or  cocoa,  and  in  the  evening  calf ’s-foot  jelly,  or 
meat-extract  jelly,  or  meal  soup  will  be  suitable.  In  addition,  the 
nutritive  clysters  mentioned  above.  (A  more  detailed  calculation 
of  the  diet  at  this  stage  has  little  value,  and  is  therefore  omitted.) 


DIET  LISTS. 


24I 


(I)  BILL  OF  FARE  FOR  CURE  OF  ULCER  (TO  BE  KEPT  UP  AT  LEAST 
TEN  DAYS). — [Leube- Penzoldt-  Wegele.) 


Albumin. 

Fat. 

CARBO- 

HYDRATE. 

Morning  : 

250  gm.  of  milk, 

8.50 

9.00 

12.0 

Two  cakes  (5  gm.  each), 

I.IO 

0.50 

7-3 

IO  O’CLOCK  : 

250  gm.  of  milk  or  bouillon, 

8.50 

9.00 

12.0 

One  cake, 

0.60 

0.25 

3-7 

12  O’CLOCK  : 

150  gm.  of  bouillon, 

0-75 

0-45 

0.9 

50  gm.  of  meat  solution  (or  one  egg), 

8.50 

3.00 

3-5 

4 o’clock  : 

250  gm.  of  milk, 

8.50 

9.00 

12.0 

Two  cakes, 

1. 10 

0.50 

7-3 

150  gm.  of  bouillon, 

o-75 

0-45 

0.9 

50  gm.  of  meat  solution  (or  one  egg),  . . . . 

8.50 

3.00 

3-5 

Two  cakes, 

1. 10 

0.50 

7-3 

Total, 

47-9 

35-65 

70.4 

Calories,  about 

200 

330 

330 

Total  combustion  value  about  860  calories. 


(2)  BILL  OF  FARE  FOR  CURE  OF  ULCER  (TO  BE  KEPT  UP  AT  LEAST 
SEVEN  DAYS) . — {Leube-  Wegele.) 


Albumin. 

Fat. 

Carbo- 

hydrate. 

Morning  : 

250  gm.  of  milk, 

8.5 

9.00 

12.0 

Three  cakes, 

1.8 

o-75 

II. I 

10  O’CLOCK  : 

200  gm.  of  bouillon, 

3-2 

4.40 

3-2 

One  egg, 

6.0 

5.00 

Noon  : 

One  boiled  pigeon, 

22.0 

1. 00 

0.7 

About  200  gm.  of  rice  in  bouillon, 

5-o 

2.00 

40.0 

4 O’CLOCK  : 

250  gm.  of  milk, 

8-5 

9.00 

12.0 

Two  cakes, 

1. 1 

0.50 

7-3 

8 O’CLOCK  : 

150  gm.  of  bouillon, 

6.4 

6.70 

9.0 

100  gm.  of  sweetbread, 

28.0 

0.40 

Total, 

90.5 

38-75 

95-3 

Calories,  about  

370 

35o 

390 

Total  combustion  value  about  mo  calories. 


242 


DIETETIC  KITCHEN. 


(3)  BILL  OF  FARE  FOR  CURE  OF  ULCER  (FOR  AT  LEAST  FIVE 
DAYS).— ( Wegele.) 


Albumin. 

Fat. 

Carbo- 

hydrate. 

Morning  : 

Two  cups  of  tea  or  coffee,  with  100  gm.  of  milk, 

3-4 

3.60 

4.8 

20  gm.  of  sugar, 

0-5 

18.2 

Three  cakes, 

1.8 

0-75 

II. I 

IO  O’CLOCK  : 

200  gm.  of  bouillon, 

3-2 

4.40 

3-2 

One  egg, 

6.0 

5.00 

Noon  : 

200  gm.  of  soup, 

150  gm.  of  beefsteak, 

3-2 

6.00 

17.0 

31.0 

2.20 

100  gm.  of  mashed  potatoes, 

31 

0.85 

21.3 

4 O’CLOCK  : 

Two  cups  of  tea  with  100  gm.  of  milk,  .... 

3-4 

3.60 

4.8 

20  gm.  of  sugar, 

o-5 

18.2 

Three  cakes,  . 

1.8 

0-75 

II. I 

Evening  : 

100  gm.  of  scraped  ham, 

25.0 

8.10 

200  gm.  of  soup, 

3-2 

6.00 

17.0 

Total,  . 

86.1 

41.25 

126.7 

Calories,  about 

350 

380 

5 20 

Total  combustion  value  about  1250  calories. 


(4)  BILL  OF  FARE  FOR  CURE  OF  ULCER  (TO  BE  KEPT  UP  AT  LEAST 
ONE  WEEK). 


' 

Albumin. 

Fat. 

Carbo- 

hydrate. 

Morning  : 

Two  cups  of  tea  or  coffee,  with  100  gm.  of  milk, 

3-4 

3-6 

4.8 

20  gm.  of  sugar, 

0-5 

18.2 

One  sweetbread  (50  gm.), 

4-5 

o-5 

29.0 

10  O’CLOCK  : 

200  gm.  of  bouillon 

‘ 3-2 

4.4 

3-2 

One  egg, 

6.0 

5*° 

Noon: 

200  gm.  of  soup, 

3-2 

6.0 

17.0 

150  gm.  of  roast  fowl, 

27.6 

14.0 

i-7 

100  gm.  of  carrots  or  spinach,  . 

1.0 

0.2 

8.1 

200  gm.  of  light  flour  food, 

9.0 

8.4 

45-o 

4 O’CLOCK  : 

Two  cups  of  tea  or  coffee,  with  100  gm.  of  milk, 

3-4 

3-6 

4-8 

20  gm.  of  sugar, 

One  sweetbread, 

0-5 

18.2 

4-5 

0.5 

29.0 

Evening  : 

100  gm.  of  cold  roast  meat, 

38.2 

2.8 

250  gm.  of  tapioca, 

7.0 

5-o 

8.0 

DIET  IN  CHRONIC  DIARRHEA.  243 


(4)  Bill  of  Fare  for  Cure  of  Ulcer  (to  be  kept  up  at  least  one  week) 
( Continued). 


Albumin. 

Fat. 

Carbo- 

hydrate. 

10  o’clock  at  Night: 

250  gm.  of  milk, 

8.5 

9.0 

12.0 

Total, 

120.5 

63.0 

199.0 

Calories,  about 

495 

585 

815 

Total  combustion  value  about  1900  calories. 


Instead  of  tea  or  coffee,  milk  may  also  be  served,  by  which 
the  nutritive  value  of  this  diet  is  not  inconsiderably  increased. 
Concerning  the  first  list  it  is  to  be  remarked  that  instead  of  meat 
solution,  eggs  may  be  given  (stirred  into  the  soup). 

Further,  in  the  second  and  third  lists  it  is  allowable  to  give 
two  or  three  soft-boiled  eggs  instead  of  meat  in  the  evening. 

The  fourth  list  may,  after  a time,  be  quantitatively  and  qualita- 
tively expanded,  since  the  following  are  allowed : Meats  (fillet, 
roast  beef,  beefsteak,  roast  veal  “ from  the  leg,”  spring  chicken, 
pigeons,  partridges,  venison). 

Fish — pike  and  perch  (boiled)  are  allowable. 

Vegetables — mashed  potatoes,  spinach,  and  golden  turnips. 

Of  the  farinaceous  foods,  the  light  puff-paste  of  rice,  fine  oat- 
meal, tapioca,  and  omelette  souffle  come  under  consideration. 

At  evening,  mushes  with  whisked  eggs  ; preserved  or  stewed 
fruits  may  be  tried  gradually. 

Salads  are  entirely  to  be  avoided.  Wines  may  now  be  permitted 
in  small  quantities  before  meals.  By  gradual  increase  in  quantity, 
one  must  attempt  to  give  the  body  the  nourishment  necessary  for 
its  proper  maintenance. 


DIET  LIST  FOR  CHRONIC  DIARRHEA  (Severe  Cases).— ( Wegele). 


Albumin. 

Fat. 

Carbo- 

hydrate. 

Alcohol. 

Morning: 

200  gm.  of  acorn  cocoa,  boiled  in  water, 

2-3 

3.60 

12.0 

One  soft  egg,  

6.0 

5.00 

Forenoon : 

250  gm.  of  decoction  of  whortleberries 
(from  80  gm.  of  dried  berries),  . . 

0.6 

I.30 

4-7 

250  gm.  of  slimy  soup, 

5-5 

4.00 

7-5 

One  egg  in  the  soup, 

6.0 

5.00 

100  gm.  of  scraped  meat  (lean),  . . . 

20.7 

I.50 

50  gm.  of  rice  in  bouillon,  .... 

4.0 

0.50 

38.0 

244 


DIETETIC  KITCHEN. 


Diet  List  for  Chronic  Diarrhea  (Severe  Cases). — ( Wegele)  ( Continued ). 


Albumin. 

Fat. 

Carbo- 

hydrate. 

Alcohol. 

Afternoon : 

250  gm.  of  whortleberry  decoction,  . 

0.6 

1.30 

4-7 

Evening  : 

250  gm.  of  maltoleguminose  soup,  . . 

6-5 

0.25 

15-5 

With  one  egg, 

6.0 

5.00 

150  gm.  of  minced  chicken,  .... 

15.0 

9.00 

12.0 

During  the  Day: 

75  gm.  of  toast, 

9.0 

I 50 

42.5 

200  gm.  of  whortleberry  wine,  . . . 

7.0 

17.0 

10  o’clock  at  Night: 

250  gm.  of  barley  mush  (20;  250),  . 

5-o 

4.00 

25.0 

Total, 

87.2 

42.00 

168.9 

17.0 

Calories,  about 

360 

390 

690 

120 

Total  combustion  value  about  1440  calories. 


At  the  beginning  of  convalescence  light  flour  foods  are  allowed 
at  noon  ; afternoon,  instead  of  the  whortleberry  decoction,  acorn 
cocoa  may  be  substituted  ; at  noon,  roast  fowl,  beefsteak,  fillet, 
roast  beef,  and  gradually  pass  over  to  the  following  list : 


DIET  LIST  FOR  CHRONIC  DIARRHEA  (Less  Severe  Cases).— ( Wegele.) 


Albumin. 

Fat. 

Carbo- 

hydrate. 

Alcohol. 

Morning  : 

200  gm.  of  acorn  cocoa, 

2.30 

3-6 

12.00 

With  one  egg, . 

6.00 

.5.0 

Forenoon : 

250  gm.  of  kefyr  (four  days  old),  . . 

8.20 

5-7 

2.00 

3-2 

Noon  : 

250  gm.  of  soup, 

5-5o 

4.0 

7-50 

With  one  egg, 

6.00 

5-o 

150  gm.  of  roast  chicken, 

28.00 

10.0 

I.80 

200  gm.  of  mashed  potatoes,  .... 

6.00 

i-7 

42.70 

4 O’CLOCK  : 

250  gm.  of  acorn  cocoa, 

2.30 

3-6 

12.00 

6 O’CLOCK  : 

250  gm.  of  kefyr, 

8.20 

5-7 

2. CO 

3-2 

8 O’CLOCK : 

200  gm.  of  soup, 

3-30 

6.0 

17.00 

With  one  egg, 

6.00 

5-o 

100  gm.  of  sweetbread, 

28.00 

0.5 

IO  O’CLOCK  : 

250  gm.  of  kefyr, 

8.20 

5-7 

2.00 

3-2 

DIET  FOR  CHRONIC  CONSTIPATION.  245 


Diet  List  for  Chronic  Diarrhea.  (Less  Severe  Cases). — ( Wegele)  ( Continued ). 


Albumin. 

Fat. 

Carbo- 

hydrate. 

Alcohol. 

During  the  Day: 

75  gm.  of  toast  or  toasted  bread,  . . 

20  gm.  of  butter, 

250  gm.  of  whortleberry  wine,  . . . 

9.00 

0.15 

1-5 

16.6 

42.50 

O.I2 

8-75 

21.5 

Total, 

127.00 

79.6 

150.25 

31-3 

Calories,  about 

.52° 

740 

615 

210 

Total  combustion  value  about  2080  calories. 


After  convalescence  has  begun,  have  the  acorn  cocoa  prepared 
with  milk;  add  at  noon  light  foods;  at  night  give  milk  musH  for 
a change  ; gradually  increase  the  amount  of  kefyr  given,  and  thus 
gradually  a diet  of  about  2500  calories’  combustion  value  is  reached, 
which  is  to  be  considered  sufficient. 


DIET  LIST  FOR  CHRONIC  CONSTIPATION. — ( Wegele.') 


Albumin. 

Fat. 

Carbo- 

hydrate. 

Alcohol. 

Morning  : 

Before  breakfast,  Bedford  Magnesia 
Spring  Water,  y2  liter. 

200  gm.  of  milk  and  coffee,  .... 

3.20 

4.40 

3.20 

30  gm.  of  butter, 

0.21 

24.50 

0.15 

30  gm.  of  honey, 

o-35 

0.03 

17.00 

loo  gm.  of  Graham  bread, 

300  gm.  of  buttermilk,  

12.15 

2.80 

11.20 

Noon  : 

200  gm.  of  bouillon, 

1. 00 

0. 60 

1.20 

200  gm.  of  mutton 

23.20 

50-50 

O.70 

300  gm.  of  crisped  cabbage,  .... 

4. 20 

14.40 

21.60 

200  gm.  of  plums, 

0.80 

II.60 

300  gm.  of  white  wine  or  apple  cider, 

9.00 

24-7 

Afternoon : 

300  gm.  of  buttermilk, 

12.15 

2.80 

11.20 

Evening  : 

150  gm.  of  meat, 

28.20 

II. 00 

0.10 

30  gm.  of  butter 

0.21 

24.50 

0.15 

300  gm.  of  stewed  apples, 

1. 00 

39.00 

For  the  several  meals,  250  gm.  of  Graham 

bread,  

22.50 

2.50 

I25.OO 

After  evening  meal,  750  gm.  of  beer,  . . 

42.60 

6.50 

4.70 

28.8 

Total, 

145-77 

194.50 

245.80 

53-5 

Calories,  about 

600 

1800 

IOOO 

375 

Total  combustion  value  about  3800  calories. 


246 


DIETETIC  KITCHEN. 


This  list  is  easil)  varied  in  accordance  with  above  statements, 
and  eventually  it  may  be  diminished  along  the  entire  scale,  or  it 
may  be  changed  with  regard  to  coexistent  stomach  troubles.  For 
the  rest  it  is  to  be  noted  that  with  the  difficult  solubility  of  many 
of  the  foods  mentioned,  and  with  an  acceleration  of  digestion 
brought  about  by  the  diet  prescribed,  a considerable  part  of  the 
nutriment  introduced  with  the  “ ingesta  ” will  be  only  partially 
turned  to  the  best  advantage.  Naturally,  if  the  chronic  constipa- 
tion is  due  to  real  catarrh,  one  must  prescribe  less  irritating  food 
and  give  the  softer  vegetables,  such  as  cauliflower,  spinach,  aspar- 
agus, carrots;  also  the  legumes  and  preserves  more  in  form  of 
purees. 


DIET  LIST  FOR  HYPERACIDITY.— {Boas-  Wegele- Fleischer.) 


Albumin. 

Fat. 

Carbo- 

hydrate. 

Alcohol. 

Morning  : 

100  gm.  of  tea  with  milk, 

3-4 

3-6 

4-8 

2 soft  eggs, 

12.0 

10.0 

100  gm.  of  raw  ham, 

25.0 

8.0 

50  gm.  of  cream, 

2.0 

13-5 

i-7 

Noon  : 

200  gm.  of  aleuronat-meal  soup  (10 

al.;  20  oatmeal ; 250  soup),  . . . 

10.2 

i-7 

8.0 

150  gm.  of  beefsteak, 

58.O 

3-o 

200  gm.  of  mashed  potatoes,  .... 

6.2 

1.7 

42.6 

100  gm.  of  white  wine,  mixed  with 

Saratoga  Vichy  or  Biliner  water, 

3-5 

8.0 

Afternoon : 

100  gm.  of  tea, 

3-4 

3-6 

4.8 

150  gm.  of  cream, 

2.0 

13-5 

i-7 

Evening  : 

50  gm.  of  cold  roast  meat, 

60.2 

4.0 

2 scrambled  eggs, 

12.0 

12.0 

100  gm.  of  wine, 

3-5 

' 8.0 

For  the  several  meals,  100  gm.  of  aleuronat 

toast, 

28.3 

i-5 

66.7 

10  o’clock  at  Night  : 

250  gm.  of  milk, 

8.5 

9.0 

12.0 

Total,  

229.2 

85.1 

149.4 

16.0 

Calories,  about 

94O 

790 

600 

112 

Total  combustion  value  about  2500  calories. 


With  the  tea  a little  sugar  is  to  be  allowed,  and  the  white  wine 
is  usually  to  be  mixed  with  an  alkaline  acidulous  water  not  con- 


DIET  LIST  FOR  HYPERSECRETION. 


247 


taining  too  much  carbonic  acid  (such  as  Biliner  water).  When 
convalescence  sets  in,  the  daily  amount  of  milk  is  to  be  increased. 


DIET  LIST  FOR  HYPERSECRETION. — ( Wegele.) 


Albumin. 

Fat. 

Carbo- 

hydrate. 

Morning  : 

Tea  with  100  gm.  of  milk, 

3-4 

3-0 

4.8 

2 soft  eggs, 

12.0 

10.0 

Forenoon  : 

150  gm.  of  calf’s-foot  jelly, 

35-o 

17.0 

1.0 

Noon  : 

150  gm.  of  sweetbread  in  bouillon, 

32.0 

250  gm.  of  tapioca  mush, 

12.0 

* 8.0* 

11. 0 

50  gm.  of  cream, 

2.0 

13-5 

i-7 

Afternoon : 

200  gm.  of  milk, 

6.8 

6.0 

9.6 

Evening  : 

200  gm.  of  ham, 

48.0 

70.0 

2 scrambled  eggs, 

12.0 

12.0 

For  the  several  meals,  100  gm.  of  aleuronat  toast,  . . 

28.3 

i-5 

66.7 

10  p.  M. : 

100  gm.  of  milk, 

6-5 

6.0 

10.0 

During  Night  : 

100  gm.  of  milk, 

6-5 

6.0 

10. 0 

Total, 

218.0 

147.0 

104.8 

Calories,  about 

900 

1360 

430 

Total  combustion  value  about  2700  calories. 


Of  course,  other  meats  than  those  mentioned  above  may  be 
chosen,  only  the  glutinous  are  particularly  to  be  selected;  event- 
ually also  scraped  meat,  ham,  etc. 

With  convalescence  go  over  to  the  preceding  list.  With  nightly 
complaints  in  consequence  of  acid  formation,  there  is  to  be  rec- 
ommended, besides  milk  or  glair-water,  especially  raw  or  hard, 
grated  eggs,  and  drinking  afterward  of  alkaline  waters.  Penzoldt 
recommends  the  addition  of  one-fourth  to  one-third  lime-water  to 
the  milk. 

As  concerns  the  power  of  the  various  foods  to  combine  with 
HC1,  the  following  table  is  based  upon  results  obtained  experiment- 
ally by  Fleischer  (“  Krankh.  d.  Speiserohre,  d.  Mag.  u.  d.  Darms,” 
Wiesbaden,  1896,  p.  932)  : 


248 


DIETETIC  KITCHEN. 


Pure  HC1. 

25  Per  Cent. 
HC1. 

Per 

Cent.  HC1. 

Meats,  ioo  gm.,  Combine  With  : 

Calf  s-brain,  boiled, 

0.65 

2.6 

55-2 

Liver  pudding, 

0.80 

3-2 

6.4 

Sweetbread,  boiled, 

0.90 

3-6 

7.2 

Mettwurst, 

1. 00 

4.0 

8.0 

Saveloy, 

1. 10 

4.4 

8.8 

Black  pudding, 

1.30 

5-2 

10.4 

Pork,  boiled, 

1 .60 

6.4 

12.8 

Ham,  boiled, 

1.80 

7.2 

14.4 

Ham,  raw, 

I.90 

7.6 

15-2 

Mutton,  boiled, 

I.90 

7.6 

H-2 

Beef,  boiled, 

2.00 

8.0 

16.0 

Veal,  boiled, 

2.20 

8.8 

17.6 

Leube-Rosenthal’s  meat  solution, 

2.20 

8.8 

17.6 

Other  Foods. 

Beer, 

0. 10 

0.40 

0.80 

Milk, 

0.36 

1.44 

2.88 

Wheat  bread, 

0.30 

1.20 

2.40 

Graham  bread, 

0.30 

1.20 

2.40 

Black  (gray)  bread,  

0.50 

2.00 

4.00 

Pumpernickel, 

0.70 

2.80 

5.60 

Hand  cheese 

1. 00 

4.00 

8.00 

Fromage  de  Brie, 

1.30 

5.20 

10.40 

Edam  cheese, 

I.40 

5.60 

1 1.20 

Brick  cheese, 

I.70 

6.80 

13.60 

Pease  sausage, 

1.70 

6.80 

13.60 

Roquefort  cheese, 

2. 10 

8.40 

16.80 

Swiss  cheese, 

2.60 

10.40 

20.80 

Cocoa, 

4. 10 

16.40 

32.80 

The  author’s  personal  views  on  the  dietetic  treatment  of  hyper- 
acidity and  hypersecretion  have  been  clearly  stated  in  pages  195  to 
197,  on  the  basis  of  a very  large  number  of  quantitative  analyses 
of  the  gastric  contents  of  forty-two  normal  healthy  adults.  He  has 
become  convinced  that  proteids,  such  as  beef,  eggs,  fish,  etc.,  cause 
a stronger  secretion  of  HC1  than  amylaceous  foods,  such  as 
rice,  sago,  farina,  cerealin.  When  the  glandular  layer  is  in  a state 
of  increased  excitation  it  is  logical  to  avoid  proteid  and  albuminous 
food  as  much  as  possible.  We  have  made  numerous  prolonged 
observations  showing  that  amylaceous  foods  and  fats  can  maintain 
the  nitrogen  equilibrium,  and  even  add  to  body-weight  when 
proteids  are  excluded.  We  do  not  wish  to  defend  the  standpoint 
of  the  vegetarian,  as  we  generally  allow  a small  quantity  of  easily 
digestible  meat  for  dinner,  and  advise  about  \ liters  of  milk  if  it 
agrees  well.  The  views  of  v.  Sohlern  on  this  question  merit  care- 
ful investigation. 


FATTENING  CUKE  FOR  NEUROSES. 


249 


SCHEDULE  FOR  INTESTINAL  ANTISEPSIS  UY  MILK  DIET. 

Also  Available  in  Neurasthenia,  Sensory  and  Secretory  Neuroses. — 
{Burkart.') 

First  Day  : 

7.30  a.  m. — One-half  of  a liter  of  milk  and  two  pieces  of  toast  (the  milk  is  to  be 
taken  a mouthful  or  a spoonful  at  a time,  ^ of  a liter  in  one-half  hour). 

10  A.  m. — One-third  of  a liter  of  milk  and  one  toast. 

12.30  p.  m. — One  plate  of  soup  with  one  egg,  50  gm.  of  roast  meat.  Potato 
puree. 

3.30  p.  m. — One-third  of  a liter  of  milk  and  one  toast. 

5.30  P.  m. — One-half  of  a liter  of  milk  and  two  toasts. 

8 P.  m. — One-half  of  a liter  of  milk,  50  gm.  of  roast  meat,  wheat  bread  and 
butter. 

On  the  ninth  day  the  following  list  is  applicable  : 

7.30  a.  m. — One-half  of  a liter  of  milk  and  two  toasts. 

8.30  a.  m. — Coffee  and  cream,  wheat  bread  and  butter. 

10  A.  m. — One-third  of  a liter  of  milk  and  two  toasts. 

12  m. — One-half  of  a liter  of  milk. 

1 p.  m. — Soup  with  one  egg,  100  gm.  of  meat,  mashed  potatoes,  75  gm.  of 
stewed  prunes. 

3.30  p.  m. — One-half  of  a liter  of  milk. 

5.30  p.  m. — One-third  of  a liter  of  milk  and  two  toasts. 

8 P.  m. — One-half  of  a liter  of  milk,  60  gm.  of  meat,  wheat  bread  and 
butter. 

9.30  p.  m. — One-third  of  a liter  of  milk  and  two  toasts. 

On  the  fifteenth  day  Burkart  (in  a severe  case  of  dyspepsia  on 
hysterical  basis)  reached  the  following  most  ample  diet  list  : 


Albumin. 

Fat. 

Carbo- 

hydrate. 

7 A.  M. 

500  gm.  of  milk, 

17.0 

18.2 

24.0 

8 A.  M. 

One  small  cup  of  coffee  or  tea,  with  20  gm.  of 

cream, 

0.7 

5-o 

0.7 

80  gm.  of  cold  meat, 

30.8 

2.0 

One  French  roll, 

4-5 

o-5 

29.O 

20  gm.  of  butter, 

o-3 

16.6 

0.1 

loo  gm.  of  roast  potatoes, 

1.8 

10.0 

25.0 

IO  A.  M. 

300  gm.  of  milk, 

10.2 

10.9 

14.4 

12  M. 

300  gm.  of  milk, 

10.2 

10.9 

14.4 

1 P.  M. 

200  gm.  of  soup, 

2.2 

30 

11. 4 

200  gm.  of  roast  meat, 

76.4 

5-4 

200  gm.  of  mashed  potatoes, ‘ 

6.2 

i-7 

42.6 

125  gm.  of  prunes, 

0.4 

8-3 

200  gm.  of  flour  food,  . . .... 

12.8 

21.2 

45>° 

17 


250 


EFFECTS  OF  COOKING  ON  FOOD. 


Albumin. 

Fat. 

Carbo- 

hydrate. 

3.30  P.  M. 

500  gm.  of  milk, 

17.0 

18.2 

24.0 

5.30  P.  M. 

300  gm.  of  milk, 

10.2 

10.9 

14.4 

80  gm.  of  cold  meat, 

3°.  8 

2.0 

One  French  roll, 

4-5 

0.5 

29.O 

20  gm.  of  butter, 

0.3 

16.6 

0. 1 

8 P.  M. 

80  gm.  of  roast  meat, 

30.8 

2.0 

40  gm.  of  toast, 

0.6 

5-2 

33-2 

500  gm.  of  milk, 

17.0 

18.2 

24.0 

9.30  P.  M. 

500  gm.  of  milk, 

17.0 

18.2 

24.0 

20  gm.  of  toast, 

o-3 

2.6 

16.6 

Total, 

295.0 

199.8 

380.2 

Calories,  about 

1200 

1850 

1550 

Total  combustion  value  about  4600  calories. 


Effects  of  Cooking  on  Food. — The  practice  of  cooking  is  not 
equally  necessary  in  regard  to  all  articles  of  food.  There  are  im- 
portant differences  in  this  respect,  and  it  is  interesting  to  note  how 
correctly  the  experience  of  mankind  has  guided  them  in  this  mat- 
ter. The  articles  of  food  which  we  still  use  in  the  uncooked  state 
are  comparatively  few  ; and  it  is  not  difficult  in  each  case  to  indi- 
cate the  reason  of  the  exemption.  Fruits  which  we  consume 
largely  in  the  raw  state  owe  their  dietetic  value  chiefly  to  the 
sugar  which  they  contain ; but  sugar  is  not  altered  by  cooking. 
Salads  may  be  regarded  more  as  a relish  for  other  food,  and  as 
having  a quasi-medicinal  purpose,  rather  than  as  a substantial 
source  of  nutriment.  Milk  is  consumed  by  us,  both  cooked  and 
uncooked,  indifferently,  and  experience  justifies  this  indifference  ; 
for  Sir  William  Roberts  found,  on  trial,  that  the  digestion  of  milk 
by  pancreatic  extract  was  not  appreciably  hastened  by  previously 
boiling  the  milk.  In  the  author’s  experiments  boiled  milk  was 
digested  slower  than  unboiled  milk  by  pancreatic  juice  of  the  dog. 

This  eminent  writer  characterizes  our  practice  in  regard  to  the 
oyster  as  being  exceptional  and  furnishing  a striking  example  of 
the  general  correctness  of  the  popular  judgment  on  dietetic  ques- 
tions. The  oyster  is  almost  the  only  animal  substance  which 
we  habitually,  and  by  preference,  eat  in  the  raw  or  uncooked  state  ; 
and  it  is  interesting  to  know  that  there  is  a sound  physiological 


CHEMICAL  CHANGES  PRODUCED  BY  COOKING.  25  I 

reason  at  the  bottom  of  this  preference.  The  fawn-colored  mass 
which  constitutes  the  dainty  of  the  oyster  is  its  liver,  and  this  is 
little  else  than  a heap  of  glycogen,  or  animal  starch.  Associated 
with  the  glycogen,  but  withheld  from  actual  contact  with  it  during 
life,  is  its  appropriate  digestive  ferment — the  hepatic  diastase.  The 
mere  crushing  of  the  dainty  between  the  teeth  brings  these  two 
bodies  together,  and  the  glycogen  is  at  once  digested,  without 
other  help,  by  its  own  diastase.  The  oyster  in  the  uncooked  state, 
or  merely  warmed,  is,  in  fact,  self-digestive.  But  the  advantage  of 
this  provision  is  wholly  lost  by  cooking,  for  the  heat  employed 
immediately  destroys  the  associated  ferment,  and  a cooked  oyster 
has  to  be  digested  like  any  other  food — by  the  consumer’s  own 
digestive  powers. 

With  regard,  however,  to  the  staple  articles  of  our  food,  the 
practice  of  cooking  them  beforehand  is  universal.  In  the  case  of 
the  farinaceous  articles  cooking  is  actually  indispensable.  When 
men  under  the  stress  of  circumstances  have  been  compelled  to  sub- 
sist on  the  uncooked  grain  of  the  cereals,  they  have  soon  fallen 
into  a state  of  inanition  and  disease.  By  the  process  of  cooking, 
the  starch  of  the  grain  is  not  only  liberated  from  its  protect- 
ing envelopes,  but  it  undergoes  a chemical  change  by  which 
it  is  transformed  into  the  gelatinous  condition,  which  facilitates 
the  action  of  the  diastatic  ferments.  A change  of  equal  impor- 
tance seems  to  be  induced  in  the  proteid  matter  of  the  grain.  Sir 
William  Roberts  found  that  the  gluten  of  wheat  was  much  more 
digestible  by  both  artificial  gastric  juice  and  by  pancreatic  extract 
in  the  cooked  than  in  the  uncooked  state.  In  regard  to  meat  the 
advantage  of  cooking  consists  chiefly  in  its  effects  on  the  connec- 
tive tissue  and  the  tendinous  and  aponeurotic  structures  associated 
with  muscular  fiber.  These  are  not  merely  softened  and  disinte- 
grated by  cooking,  but  are  chemically  converted  into  the  soluble 
and  easily  digested  form  of  gelatin.  Sir  William  Roberts  made  in- 
structive observations  on  the  effects  of  cooking  on  the  contents  of 
the  egg.  The  change  induced  on  egg-albumen  by  cooking  is  very 
striking.  For  the  purpose  of  testing  this  point  he  employed  a 
solution  of  egg-albumen  made  by  mixing  white-of-egg  with  nine 
times  its  volume  of  water.  This  solution,  when  heated  in  the  water- 
bath,  does  not  coagulate  nor  sensibly  change  its  appearance,  but  its 
behavior  with  the  digestive  ferments  is  completely  altered.  In  the 
raw  state  this  solution  is  attacked  very  slowly  by  pepsin  and  acid, 
and  pancreatic  extract  has  almost  no  effect  on  it ; but  after  being 


252 


THE  PALATE  A SKILFUL  GUIDE. 


cooked  in  the  water-bath  the  albumin  is  rapidly  and  entirely 
digested  by  artificial  gastric  juice,  and  a moiety  of  it  is  rapidly 
digested  by  pancreatic  extract.* 

Indications  of  the  Palate. — Sir  William  Roberts  (“  Digestion 
and  Diet”)  holds  that  “the  indications  of  the  palate  are  of  great 
importance  in  the  regulation  of  diet,  and  should  always  be  inquired 
into  and  carefully  considered.  The  palate  is  placed  like  a dietetic 
conscience  at  the  entrance  gate  of  food,  and  its  appointed  function 
is  to  pass  summary  judgment  on  the  wholesomeness  or  unwhole- 
someness of  the  articles  presented  to  it.  It  acts  under  the  in- 
fluence of  a natural  instinct,  which  is  rarely  at  fault.  This  instinct 
represents  an  immense  accumulation  of  experience,  partly  acquired 
and  partly  inherited.  It  is,  of  course,  not  infallible — no  instinct 
is ; but  so  close  and  true  are  the  sympathies  of  the  palate  with 
the  stomach  and  the  rest  of  the  organism  that  its  dictates  are 
entitled  to  the  utmost  deference  as  those  of  the  rightful  authority 
in  the  choice  of  food.  I am,  of  course,  aware  that  the  palate — or, 
rather,  the  civilized  palate — is  not  always  credited  with  these  solid, 
good  qualities.  Some  persons  there  are,  not  medical  authorities, 
who  distrust  its  office  and  regard  its  indications  with  suspicion,  as 
if  they  were  the  suggestions  of  some  frivolous  and  wanton  agency, 
tempting  men  to  a vain  gratification  of  the  senses,  rather  than  as 
those  of  an  honest  and  skilful  guide  in  the  choice  of  food.  This 
puritanical  view  of  the  palate  is  wholly  unscientific ; it  moreover 
implies,  to  speak  figuratively,  a gross  slander  on  a responsible  and 
rarely  endowed  organ,  which  has  performed  in  the  past,  and  still 
performs,  most  difficult  and  most  complicated  functions  with  con- 
spicuous success;  for  who  shall  venture  to  say  that,  in  the  evolu- 
tion of  the  human  animal  from  the  short-lived,  immoral,  and  stupid 
savage,  with  his  diet  of  wild  fruit,  roots,  raw  flesh,  and  unfiltered 
water,  to  the  status  of  civilized  man,  the  promptings  of  the  palate 
have  not  played  an  important  and  even  indispensable  part  ? We 
are  apt  to  forget  that  there  is  no  such  a thing  as  an  absolutely  good 
or  an  absolutely  bad  flavor  to  the  animal  palate.  Sweet  things  are 
indifferent  to  the  palate  of  the  carnivora;  and,  conversely,  the  taste 
of  flesh  has  no  attraction  to  the  herbivora.  Each  animal  has  its 
own  gustatory  standard,  which  is  accurately  adjusted  to  the  wants 
of  its  particular  economy.” 


* Raw  egg-albumin  does  not  require  digestion  and  can  be  absorbed  from  the  intestine 
as  such ; in  the  stomach  it  invariably  undergoes  digestion  by  pepsin  hydrochloric  acid. 


DIETETICAL  COOKING. 


253 


DIETETICAL  COOKING .* 

General  Remarks. — It  is  evident  that  the  subtle  art  of  cooking 
can  be  practised  with  advantage  to  those  suffering  from  indigestion 
only  by  those  who  understand  thoroughly  the  general  fundamental 
principles  of  the  art,  and  have  in  addition  some  experience  therein. 
But  if  diligence,  care,  and  cleanliness  are  very  desirable  qualities 
in  cooking  for  people  in  good  health,  they  become  an  absolute 
necessity  for  those  who  undertake  the  preparation  of  food  for  diges- 
tive organs  whose  functions  are  impaired.  By  no  means  should 
the  attention  be  taken  from  the  work  by  other  matters,  for  in  that 
case  the  care  which  is  necessary  will  suffer,  and  the  most  scrupu- 
lous cleanliness  must  be  applied  (Wegele). 

It  should  be  understood  here  that  we  have  confined  ourselves  to 
the  most  necessary  things,  and  have  not  considered  the  details  con- 
cerning the  arrangement  of  the  kitchen,  construction  of  the  fire- 
place, the  cooking  utensils  and  fuel,  food-stufifs  or  their  adulteration  ; 
and,  further,  we  have  not  undertaken  the  description  of  complicated 
dishes,  but  have  given  directions  for  the  preparation  of  only  the 
simplest  every-day  dishes  in  such  a way  as  to  serve  dietetical  pur- 
poses. In  this  respect  the  advice  of  Penzoldt  deserves  considera- 
tion, to  use  vessels  with  protecting  lids  for  the  keeping  of  foods 
which  are  to  be  eaten  later  when  cold.  Naturally  all  food-stuffs 
must  be  of  the  best  quality,  for  the  best  is  just  good  enough  for  the 
sick.  Aside  from  this,  nothing  in  the  slightest  degree  spoiled  may 
be  used  in  cooking  for  the  sick.  In  the  eulogy  of  the  palate  we 
have  already  emphasized  appetizing  preparation,  for,  as  is  well 
known,  dyspeptics  are  easily  seized  by  nausea,  while,  on  the  other 
hand,  a suitable  way  of  preparing  food  may  stimulate  the  appetite. 
For  the  same  reason,  every  after-taste  due  to  the  character  of  the 
cooking  utensils  or  their  uncleanliness  is  to  be  avoided  as  far  as 
possible,  and  the  utensils  should  be,  wherever  possible,  earthen, 
enameled,  or  nickel-plated.  Food  must  never  be  brought  to  the 
table  too  hot,  for  the  patients  are  thus  tempted  to  eat  them  in  this 
state  in  spite  of  the  directions  of  the  physician,  and  on  this  account 
it  is  best  to  put  the  food  on  a second  plate  or  cup.  The  contrary 

* We  have  availed  ourselves  of  a large  number  of  works  in  compiling  this  particular 
chapter.  The  name  of  the  originator  of  any  particular  article  of  diet  has  been  added  to 
the  directions  given  whenever  it  was  obtainable.  Of  the  larger  works  used  we  mention 
Sir  William  Roberts,  Munk  and  Uffelmann  (last  edition  by  C.  A.  Ewald),  Wegele, 
Biedert  and  Langermann,  Leyden’s  “ Handbuch  der  Ernahrungstherapie,”  Gilman 
Thompson,  Boas,  Penzoldt  and  Stintzing’s  “ Handbuch  der  Therapie,”  etc. 


254 


GENERAL  DIRECTIONS  REGARDING  COOKING. 


is  just  as  injurious,  and  it  is  therefore  well  to  prepare  foods,  which 
are  subject  to  rapid  cooling,  in  vessels  with  double  bottoms,  filled 
with  hot  water.  Concerning  the  seasoning  of  the  dishes,  only  a 
moderate  use  of  cooking  salt  is  allowed,  and  other  spices  are  not 
to  be  used  without  the  permission  of  the  physician  ; Wegele  strictly 
forbids  the  use  of  citron  or  pomegranate  skins  in  dietetical  cooking. 
Water  which  is  to  be  used  for  cool  drinks  should  be  boiled  and 
then  allowed  to  cool. 

Concerning  the  measures  used  in  the  following  chapter, — 

I teaspoon  equals  about  5 gm., 

I tablespoon  equals  about  15  gm. , 

I soup  plate  equals  about  250  gm. , 

I cup  equals  about  200  to  250  gm. , 

I wineglass  equals  about  150  gm., 

in  which  calculation  naturally  no  attention  has  been  paid  to  the 
specific  gravity  of  the  different  substances. 

I.  Drinks  and  Liquid  Foods. 

Barley  Soup  (Ringer). — To  a tablespoonful  of  pearl  barley 
washed  in  cold  water  add  two  or  three  lumps  of  sugar,  the  rind  of 
one  lemon,  and  the  juice  of  half  a lemon.  On  these  pour  a quart 
of  boiling  water,  and  let  the  mixture  stand  for  seven  or  eight  hours. 
Strain.  The  barley  water  should  never  be  used  a second  time. 
Half  an  ounce  of  isinglass  may  be  boiled  in  the  water.  If  not 
needed  at  once,  these  barley  preparations  should  be  kept  in  the 
refrigerator,  and  warmed  when  required.  They  are  unpalatable  if 
taken  cold. 

Rice-water,  or  Mucilage  of  Rice  (Pavy). — Thoroughly  wash 
one  ounce  of  rice  with  cold  water.  Then  macerate  for  three  hours 
in  a quart  of  water  kept  at  a tepid  heat,  and  afterward  boil  slowly 
for  an  hour,  and  strain.  A useful  drink  in  dysentery,  diarrhea,  and 
irritable  states  of  the  alimentary  canal.  It  may  be  sweetened  and 
flavored  in  the  same  way  as  barley  water. 

Lemonade  (Pavy). — Pare  the  rind  from  a lemon  thinly,  and  cut 
the  lemon  into  slices.  Put  the  peel  and  sliced  lemon  into  a pitcher 
with  one  ounce  of  white  sugar,  and  pour  over  them  one  pint  of 
boiling  water.  Cover  the  pitcher  closely,  and  digest  until  cold. 
Strain  or  pour  off  the  liquid. 

Beef-essence  (Yeo). — Cut  the  lean  of  beef  into  small  pieces 
and  place  them  in  a wide-mouthed  bottle  securely  corked,  and  then 
allow  it  to  stand  for  several  hours  in  a vessel  of  boiling  water. 


DRINKS  AND  LIQUID  FOODS.  255 

This  may  be  given  in  teaspoonful  doses  to  infants  who  can  not  take 
milk,  and  in  larger  quantities  to  adults. 

Beef-tea  {Germain- See). — Meat  cut  into  small  pieces,  cold 
water  added,  and  then  gradually  heated  to  140°  or  160°  F.  Press, 
strain,  and  flavor  with  salt  and  pepper.  This  is  much  inferior  to 
the  preparations  made  with  hydrochloric  acid. 

Chicken  Broth  {Bartholomew). — Skin  and  finely  mince  a small 
chicken  or  half  of  a large  fowl,  and  boil  it,  bones  and  all,  with  a 
blade  of  mace,  a sprig  of  parsley,  and  a crust  of  bread,  in  a quart 
of  water  for  an  hour,  skimming  it  from  time  to  time.  Strain 
through  a coarse  colander. 

Chicken,  Veal,  or  Mutton  Broth  {Yeo). — Chicken,  veal,  or 
mutton  broth  may  be  made  like  beef-tea,  substituting  chicken,  veal, 
or  mutton  for  beef,  boiling  in  a saucepan  for  two  hours,  and 
straining.  For  chicken  broth  the  bones  should  be  crushed  and 
added.  For  veal  broth  the  fleshy  part  of  the  knuckles  should  be 
used.  Either  may  be  thickened  and  their  nutritive  value  increased 
by  the  addition  of  pearl  barley,  rice,  vermicelli,  or  semolina. 

Mutton  and  Chicken  Broths  {Osier). — Mince  a pound  of  either 
chicken  or  mutton,  freed  from  fat,  put  into  a pint  of  cold  water,  and 
let  stand  in  a cold  jar  on  ice  two  or  three  hours.  Then  cook  for 
three  hours  over  a slow  fire,  strain,  cool,  skim  fat  off,  add  salt,  and 
serve  hot  or  cold.  Such  broth  is  much  better  than  any  manufac- 
tured meat  preparations.  Good  mutton  broth  is  difficult  to  make 
on  account  of  the  meat  containing  so  much  fat. 

Raw  Meat  Diet  {Ringer). — Use  two  ounces  of  rump  steak; 
take  away  all  fat,  cut  into  small  squares  without  entirely  separat- 
ing the  meat,  place  in  a mortar,  and  pound  for  five  or  ten  minutes  ; 
then  add  three  or  four  tablespoonfuls  of  water  and  pound  again  for 
a short  time,  afterward  removing  all  sinews  or  fiber;  add  salt  to 
taste.  Before  using,  place  the  cup  or  jar  containing  the  pounded 
meat  in  hot  water  until  just  warm. 

Or  scrape  the  beefsteak  with  a sharp  knife,  and  after  removing 
all  fat  and  tendon,  if  not  already  in  a complete  pulp,  pound  in  a 
mortar.  Flavor  with  salt  and  pepper.  This  may  be  taken  in  the 
form  of  a sandwich,  between  thin  bread  and  butter,  or  mixed  with 
water  to  the  consistency  of  a cream.  If  preferred,  the  meat  may  be 
rolled  into  balls  with  a little  white-of-egg,  and  boiled  for  two  or 
three  minutes,  or  until  the  outside  turns  gray,  just  long  enough  to 
remove  the  raw  taste. 

Chicken  Jelly  {Adams). — Clean  a fowl  that  is  about  a year  old, 


256 


DRINKS  AND  LIQUID  FOODS. 


remove  skin  and  fat ; chop  fine,  bones  and  flesh,  in  a pan  with  two 
quarts  of  water  ; heat  slowly,  skim  thoroughly,  simmer  five  to  six 
hours  ; add  salt,  mace,  or  parsley  to  taste ; strain  ; cool.  When 
cool,  skim  off  the  fat. 

The  jelly  is  usually  relished  cold,  but  maybe  heated.  Give  often 
in  small  quantities. 

Milk-punch.  — Make  by  adding  brandy  or  whiskey  or  rum  to 
milk  in  the  proportion  of  about  one  to  four  or  six  parts  of  milk  ; 
flavor  with  sugar  and  nutmeg ; shake  well. 

Sherry  or  Brandy  and  Milk  {Ringer). — To  one  tablespoonful 
of  brandy  or  one  wineglassful  of  sherry,  in  a bowl  or  cup,  add  pow- 
dered sugar  and  a very  little  nutmeg  to  taste.  Warm  a breakfast 
cupful  of  new  milk  and  pour  into  a pitcher.  Pour  the  contents 
from  a height  over  the  wine,  sugar,  etc.  The  milk  must  not  boil . 

Junket  {Anderson). — Sweeten  with  white  sugar  one  pint  of  good 
milk.  If  wine  is  allowed,  a dessertspoonful  of  sherry  is  an  improve- 
ment. Heat  to  new-milk  warmth,  pour  into  a shallow  dish,  and 
stir  in  two  teaspoonfuls  of  essence  of  rennet.  This  will  form  a 
slight  curd.  Grate  a little  nutmeg  over  it,  or  add  a pinch  of  pow- 
dered cinnamon.  Serve  when  quite  cold.  In  cold  weather  the 
milk  should  be  placed  in  a warm  room  to  set.  An  excellent  food 
and  good  substitute  for  milk  in  typhoid  fever,  etc. 

Egg-nog. — Egg-nog  is  made  by  adding  the  beaten  yolk  of  egg 
and  a little  spirits  to  a tumblerful  of  milk,  stirring  well,  adding 
sugar  and  white  of  the  egg,  separately  beaten.  The  digestibility 
of  both  of  these  highly  nourishing  and  stimulating  preparations  is 
enhanced  by  the  addition  of  y2  of  an  ounce  of  lime-water,  which 
does  not  affect  the  taste. 

Egg  and  Wine  {Ringer). — Take  one  egg,  y2  of  a glass  of  cold 
water,  one  glass  of  sherry,  sugar,  and  a very  little  nutmeg,  grated. 
Beat  the  egg  to  a froth  with  a tablespoonful  of  cold  water.  Make 
the  wine  and  water  hot,  but  not  boiling;  pour  on  the  egg,  stirring 
all  the  time.  Add  sufficient  sugar  to  sweeten,  and  a very  little 
nutmeg.  Put  all  into  a porcelain-lined  saucepan  over  a gentle 
fire,  and  stir  one  way  till  it  thickens,  but  do  not  let  it  boil.  Serve 
in  a glass,  with  crisp  biscuits  or  sippets  of  toast. 

Milk  for  Pudding  or  Stewed  Fruit  {Ringer). — Boil  a strip  of 
lemon  and  two  cloves  in  a pint  of  milk;  mix  y2  of  a teaspoonful 
of  arrowroot  in  a little  cold  milk  and  add  it  to  the  boiling  milk; 
stir  it  until  about  the  consistency  of  cream.  Have  ready  the 
yolks  of  three  eggs  beaten  up  well  in  a little  milk.  Take  the  hot 


DIETETIC  FOODS  AND  DRINKS. 


257 


milk  off  the  fire,  and  as  it  cools  add  the  eggs  and  a teaspoonful  of 
orange-flour  water,  stirring  it  constantly  till  quite  cool.  Keep  it 
in  a very  cool  place  until  required  for  use. 

Arrowroot  Blancmange  {Ringer). — Take  two  tablespoonfuls  of 
arrowroot,  ^ of  a pint  of  milk,  lemon,  and  sugar  to  taste. 

Mix  the  arrowroot  with  a little  milk  to  a smooth  batter;  put  the 
rest  of  the  milk  on  the  fire  and  let  it  boil,  sweeten  and  flavor  it, 
stirring  ail  the  time  till  it  thickens  sufficiently.  Put  into  a mold 
until  quite  cold. 

Arrowroot  ( Pavy ). — Mix  thoroughly  two  teaspoonfuls  of  arrow- 
root  with  three  tablespoonfuls  of  cold  water,  and  pour  on  them 
y2  of  a pint  of  boiling  water,  stirring  well  meanwhile.  If  the  water 
is  quite  boiling,  the  arrowroot  thickens  as  it  is  poured  on,  and 
nothing  more  is  necessary.  If  only  warm  water  is  used,  the 
arrowroot  must  be  boiled  afterward  until  it  thickens.  Sweeten 
with  loaf-sugar,  and  flavor  with  lemon-peel  or  nutmeg,  or  add 
sherry,  port-wine,  or  brandy  if  required.  Boiling  milk  may  be 
employed  instead  of  water,  and  when  this  is  done  no  wine  must 
be  added,  as  it  would  otherwise  curdle. 

Oatmeal  Gruel  (Plain). — Two  tablespoonfuls  of  oatmeal,  one 
saltspoonful  of  salt,  one  scant  teaspoonful  of  sugar,  one  cup  of 
boiling  water.  Cook  for  thirty  minutes;  then  strain  through  a 
fine  wire  strainer  to  remove  the  hulls,  place  again  on  the  stove, 
add  the  milk,  and  heat  just  to  the  boiling  point.  Serve  hot. 

Farina  Pudding  (U.  S.  Army  Hospital  Recipe  for  12  Men). 
— Farina,  y2  of  a pound;  milk,  two  pints;  water,  one  pint;  sugar, 
2 y2  ounces;  eggs,  four  ounces;  nutmeg,  y2  of  an  ounce. 

Directions. — Put  the  water  into  a stewpan  with  a little  salt. 
When  it  boils  stir  in  the  farina.  Let  it  boil  twenty  minutes.  Stir 
in  the  milk,  which  must  be  hot.  Beat  the  eggs  until  they  are 
very  light ; mix  the  sugar  with  them.  Stir  in  the  eggs  and  sugar 
with  the  farina.  Add  the  spice.  Put  it  into  a moderate  oven  and 
bake  a half  or  three-quarters  of  an  hour. 

Port- wine  Jelly  {Ringer). — Put  into  a jar  one  pint  of  port-wine, 
two  ounces  of  gum  arabic,  two  ounces  of  isinglass,  two  ounces  of 
powdered  white  sugar-candy,  y of  a nutmeg  grated  fine,  and  a 
small  piece  of  cinnamon.  Let  this  stand  closely  covered  all  night. 
The  next  day  put  the  jar  into  boiling  water  and  let  it  simmer  until 
the  contents  are  dissolved ; then  strain,  let  stand  till  cold,  and  then 
cut  into  small  pieces  for  use. 

Nutritious  Coffee  {Ringer). — Dissolve  a little  isinglass  in  water, 


258 


DIET  LISTS. 


and  then  put  Y/2  of  an  ounce  of  freshly  ground  coffee  into  a sauce- 
pan with  one  pint  of  new  milk,  which  should  be  nearly  boiling 
before  the  coffee  is  added ; boil  both  together  for  three  minutes. 
Clear  it  by  pouring  some  of  it  into  a cup  and  dashing  it  back 
again,  add  the  isinglass,  and  let  it  settle  on  the  hob  for  a few 
minutes.  Beat  up  an  egg  in  a breakfast  cup  and  pour  the  coffee 
upon  it ; if  preferred,  drink  it  without  the  egg. 

Glair-water. — Into  200  c.c.  of  cold  water  which  has  previously 
been  boiled,  put  with  constant  stirring  the  white  of  one  egg,  and 
add,  according  to  prescription,  three  teaspoonfuls  of  powdered 
sugar,  or  grape-sugar,  or  10  gm.  of  cognac.  The  white  of  an  egg 
equals  about  12  calories;  15  gm.  of  sugar  equals  about  50  calories  ; 
10  gm.  of  cognac  equals  50  calories. 

Kefyr. — It  is  best  to  procure  moist  lcefyr  mushrooms  (not  the 
dried  grains)  prepared  for  immediate  use.  They  can  be  pro- 
cured from  the  Caucasian  Kefyranstalt  in  Breslau,  or  from  Dr.  M. 
Lehmann,  Berlin  C.  (43  and  44  Heiligegeist  Strasse).  Pour  away 
the  liquid  contained  in  the  bottle,  wash  the  mushrooms  in  a luke- 
warm (about  1 50  R.  or  18.7°  C.)  soda  solution  of  5 : 1000,  rinse  with 
clean  lukewarm  water,  and  after  pouring  off  the  water  place  the 
mushrooms  in  a vessel  of  porcelain  or  Bunglan  clay  of  two  liters’ 
capacity.  Previously  two  liters  of  milk  should  have  been  boiled 
and  allowed  to  cool  again.  Now  pour  the  milk,  whose  tempera- 
ture should  be  about  150  R.  or  18. 70  C.,  upon  the  mushrooms, 
close  the  vessel  tightly,  and  let  it  stand  twenty-four  hours  in  a place 
whose  temperature  is  130  to  150  R.  or  1 8.7°  C.  (in  summer  in  the 
cellar),  during  which  time  it  is  expedient  to  often  stir  the  milk  care- 
fully. At  the  expiration  of  this  time  it  should  be  stirred  again,  and 
the  milk  is  then  poured  through  a moderately  fine  wire  sieve  into 
thoroughly  cleaned  bottles  with  patent  stoppers.  These  bottles 
are  again  to  be  kept  twenty-four,  thirty-six,  forty-eight,  or,  at  the 
highest,  fifty-four  hours  (according  as  kefyr  one,  two,  three,  or  four 
days  old  has  been  prescribed)  in  a place  whose  temperature  is  kept 
at  about  150  R.  or  18. 70  C.,  lying,  not  standing  up,  and  are  then 
ready  for  use. 

The  process  of  fermentation  may  be  hastened  by  frequent  shak- 
ing, also  with  heat,  on  which  account  the  fermentation  takes  place 
more  quickly  in  midsummer,  and  the  kefyr  consequently  will  be 
finished  sooner.  The  mushrooms  which  remained  in  the  sieves 
after  pouring  off  the  milk  into  the  patent  flasks  must  each  time  be 
rinsed  with  lukewarm  water  and  freed  from  particles  of  cheese, 


MEAT  EXTRACTS,  ETC. 


259 

and  afterward  placed  again  in  the  thoroughly  clean  porcelain  ves- 
sel, and  milk  is  then  again  poured  upon  them.  After  two  or  three 
days  the  preparation  is  so  regulated  that  each  day  two  bottles  (of 
one  liter  each)  become  ready  for  use,  for  which  reason  four  patent- 
stoppered  bottles  are  necessary.  Once  a week  the  bottles  must  be 
rinsed  with  a lukewarm  soda  solution  of  5 : 1000  instead  of  with 
lukewarm  water,  in  order  to  free  them  from  acid.  At  first  let  the 
patient  drink  one  wineglassful  two  or  three  times  a day,  then  l/^ 
of  a liter,  and  constantly  increase  the  quantity  until  the  prescribed 
dose  has  been  reached.  One  hundred  gm.  of  kefyr  equal  about 
45  calories. 

Almond  Milk. — Thirty  grs.  of  sweet  almonds  and  two  bitter 
almonds  are  blanched  after  they  have  lain  twenty-four  hours  in 
cold  water.  One  can  also  scald  the  almonds  with  boiling  water; 
then  they  can  be  easily  pressed  out  of  their  hulls  after  a few  min- 
utes. The  almonds  are  either  ground  in  a mill  or  pounded  in  a 
mortar,  then  mixed  with  of  a liter  of  warm  water  or  warm 
milk,  and  the  mixture  is  allowed  to  stand  two  hours,  after  which 
it  is  strained  through  a cloth  and  the  juice  well  pressed  out. 

Thirty  grs.  of  almonds  equal  200  calories  ; 250  gm.  of  milk 
equal  170  calories. 

Extract  of  Meat  ( according  to  Wiel),  “ Succus  carnis  recenter 
expressus.” — Meat  free  from  fat  is  chopped  fine,  arranged  in  sev- 
eral layers,  which  are  separated  by  coarse  (filter)  linen,  and  sub- 
jected to  pressure  in  a colander  ; the  juice  is  given  pure  (as  medi- 
cine) by  the  teaspoonful,  or  also  diluted  with  beef-tea,  but  must 
not  be  subjected  to  a temperature  higher  than  50°  R.  or  62.5°  C., 
for  otherwise  the  albuminous  parts  contained  in  it  would  coagu- 
late. “Valentine’s  meat-juice”  (extract)  may  serve  as  a good 
substitute  for  the  fresh  extract  of  meat  particularly  prepared.  A 
teaspoonful  of  this  preparation  is  diluted  with  one  to  two  table- 
spoonfuls of  cold,  or,  at  the  most,  lukewarm,  water;  the  yolk  of 
one  egg  may  also  be  added. 

Meat-extract  Ice  ( according  to  v.  Ziemssen). — One  k.  of  fresh 
beef  is  cut  into  pieces  the  size  of  a hand,  and  is  wrapped  in  coarse 
lattice-like  linen,  put  under  a lever-press  and  slowly  pressed  ; this 
is  best  done  by  an  apothecary.  The  juice  is  caught  in  a porcelain 
dish.  In  this  way  one  gets  about  500  gm.  This  is  mixed  with 
250  gm.  of  sugar  and  20  gm.  of  freshly  pressed  lemon-juice  (though 
this  had  better  be  omitted  for  dyspeptics),  and  20  gm.  of  cognac, 
containing  extract  of  vanilla,  which  has  been  well  stirred  with 


26o 


DIET  LISTS. 


the  yolks  of  three  eggs,  are  added,  and  the  whole  is  placed  in  a 
freezer. 

Bottled  Bouillon  ( accoi'ding  to  Uffelmanri). — Three  hundred  gm. 
of  fresh,  lean  meat  are  cut  into  small  blocks  and,  without  any  ad- 
dition, are  put  into  a clean  bottle  with  wide  mouth.  This  is  closed, 
if  there  be  no  suitable  stopper,  with  a stopper  of  pure,  sterilized 
cotton,  and  placed  in  a vessel  of  warm  water,  slowly  heated,  and 
the  water  should  be  allowed  to  boil  one-half  hour.  The  bottle, 
which  is  now  to  be  taken  out,  contains  about  ioo  gm.  of  a turbid, 
brown  broth,  which  is  poured  off  without  straining. 

Simple  Bouillon,  or  Beef-tea. — One-half  of  a k.  of  lean  beet 
is  cut  into  small  pieces,  put  into  a pot  holding  about  three  liters, 
with  a well-fitting  cover,  or  into  a steam  cooking  apparatus.  This 
is  to  be  filled  with  cold  water,  and  the  meat  to  be  boiled  three  to 
four  hours.  According  as  the  bouillon  is  desired  concentrated  or 
dilute,  the  liquid  which  evaporates  must  be  replaced  by  the  addi- 
tion of  boiling  water.  Finally,  one  obtains  about  two  liters  of 
bouillon,  and  the  meat  which  remains  is  of  no  further  use.  To 
obtain  greater  palatability  and  a prettier  color  the  meat  may  be 
first  browned  in  a little  hot,  pure  lard  before  cooking,  fresh  soup 
herbs  or  a handful  of  dried  Knorr’s  julienne  added;  then  finally 
add  the  three  liters  of  cold  water. 

Meat-jelly  ( according  to  Hepfi). — Good  beef,  free  from  fat  and 
bones,  is  cooked  on  the  water-bath  with  a little  water  for  sixteen 
hours,  until  it  congeals  into  jelly.  Often  one  is  compelled  to  use 
artificial  preparations  in  the  making  of  bouillon  or  in  strengthen- 
ing weak  bouillon.  The  most  reliable  in  this  respect  is  Liebig’s 
extract  of  meat  (about  ten  c.c.  to  250  gm.),  or  Cibil’s  bouillon  (one 
tablespoonful  to  250  gm.);  very  convenient  also  are  Quaglio’s 
bouillon  capsules.  If  at  the  same  time  one  wishes  to  give  to  the 
bouillon  an  increased  nutritive  value,  one  can  add  one  teaspoonful 
of  meat-peptone;  or  either  Mosquera  Julia  beef-meal,  Armour’s 
vigoral,  or  Valentine’s  meat-juice  may  be  used. 

A preparation  which  is  often  of  service  is  Leube-Rosenthal’s 
meat  solution.  One  k.  of  beef  is  chopped  fine,  put  into  a vessel 
with  one  liter  of  water  and  twenty  gm.  of  pure  hydrochloric  acid, 
which  vessel  is  put  in  a Papin  steam  cooking  apparatus,  in  which 
it  should  boil  ten  to  fifteen  hours  (with  frequent  stirring).  After  this 
the  mass  is  put  into  a mortar  and  ground  to  an  emulsion.  After 
a further  cooking  of  fifteen  hours  with  bicarbonate  of  soda  it 
becomes  neutral,  and  is  then  steamed  to  a consistency  of  mush, 


PREPARATION  OF  SOUPS  WITH  FILLERS. 


26l 


and  put  into  four  cans,  which  are  to  be  soldered.  As  the  making 
of  this  preparation  requires  much  time  and  particular  care,  it  is 
advisable  to  procure  it  from  one  of  the  following  firms,  who  put  it 
upon  the  market  in  cases  of  k.  (enough  for  an  adult  for  one 
day)  : Armour  & Co.,*  Parke,  Davis  & Co.,f  Dr.  Mirus’sche  Hof- 
apotheke  (R.  Stutz),J  Huffner’s  Hof-  und  Ratsapotheke  (R.  Wahr- 
burg),!  C.  Reinhardt  (formerly  Charrier).§ 

Soups  with  Fillers. 

(a)  Soups  with  Fillers  from  the  Cereal  Kingdom. — The  grains  in 
question  (such  as  barley  or  peeled  barley,  oats,  green  corn,  rice) 
should  be  softened  the  night  before  in  cold  water,  in  which  they 
are  to  remain  until  the  following  forenoon.  Then  the  water  is 
poured  off  and  the  grains  are  put  on  the  fire  with  weak,  cold 
bouillon,  where  they  should  be  kept  boiling  at  least  three  hours  ; 
one-half  hour  before  serving,  the  soup  is  strained  through  a fine  hair 
sieve,  and,  after  the  addition  of  a little  meat-extract,  is  made  to 
boil  again  ; salt  is  then  added  as  required,  and  to  one  plate  of  soup 
the  yolk  of  one  egg  may  be  added.  If  one  is  to  prepare  a single 
plate  of  such  soups,  the  soup  meals  of  Knorr  in  Heilbronn  are  very 
serviceable,  although  they  do  not  become  gelatinous  like  the  soups 
prepared  from  whole  grains,  and  are  not  so  appetizing.  These 
meals  must  be  stirred  with  cold  bouillon  to  a thin  liquid  mass, 
and  allowed  to  run  into  boiling  beef-tea,  which  after  that  must 
boil  at  least  one  to  two  hours  longer.  Twenty  gm.  of  meal  is 
calculated  for  one  plate  of  soup.  In  serving,  one  can  add  also 
the  yolk  of  an  egg.  The  nutritive  value  of  these  soups  may  be 
considerably  increased  by  the  addition  of  aleuronat  flour.  It  is 
best  to  take  eight  gm.  of  aleuronat  flour  and  sixteen  gm.  of  oat-  or 
green-corn  meal  for  one  plate  of  soup.  ||  The  aleuronat  meal  is 
mixed  with  cold  water  (or  beef-tea),  and  is  added  to  the  soup  only 
after  the  latter  has  boiled  one-half  hour.  The  meal  swells  hardly 
at  all,  and  for  that  reason  more  of  the  two  flours  is  to  be  taken  than 
is  necessary,  ordinarily,  in  making  of  soup.  Soups  prepared  with 
twenty  gm.  of  oatmeal,  or  leguminose  meal,  barley-meal,  tapioca, 
rice,  etc.,  have  a combustion  value  of  about  seventy  to  seventy-five 
calories,  which  is  increased  about  sixty  calories  by  the  addition  of 
the  yolk  of  one  egg. 


* Chicago.  f Detroit,  Mich.  J Jena.  g Berlin  W.,  27  Behren  Strasse. 

||  Can  be  procured  from  Dr.  Hundhausen’s  Starkefabrik,  Hamm  in  Westfalen;  4^  k. 
cost  seven  marks,  C.  O.  D. 


262 


DIET  LISTS. 


( b ) Tapioca  Soup. — For  this  soup  the  French  tapioca  of  N.  & J. 
Bloch  in  Paris,  and  Knorr  in  Heilbronn,  had  best  be  used,  which 
can  be  had  in  most  of  the  larger  fancy  groceries  in  packages  of 
250  gm.  For  one  plate  of  soup  a heaped  teaspoonful  of  these 
grains  is  boiled  for  half  an  hour  with  beef-tea,  which  has  been 
boiling  for  some  time  previous,  and  to  this,  after  a quarter  of  an 
hour,  a little  extract  of  meat,  sufficient  to  cover  the  point  of  a 
knife,  is  added;  if  this  be  added  later, just  before  serving,  the  taste 
of  the  extract  is  easily  distinguished,  which  is  disagreeable  to  many 
patients. 

(c)  Sweetbread  Soup. — The  sweetbread  is  soaked  for  one  hour  in 
cold  water,  which  is  during  this  time  often  to  be  renewed  ; then  it  is 
boiled  in  slightly  salted  beef-tea  or  salt  water  (to  which  one  may 
add  one  teaspoonful  of  julienne  for  improving  the  flavor)  for  one 
hour.  After  it  is  cooked  completely  soft  it  is  taken  out  of  the 
beef-tea  and  freed  from  all  skins,  blood-vessels,  etc.  Now  it  can 
be  cut  either  in  pieces  the  size  of  a walnut,  which  one  lays  on  the 
soup-plate  and  then  pours  over  the  beef-tea,  or  the  sweetbread  can 
be  forced  through  a fine  sieve ; beef-tea  is  poured  over  the  mass 
and  the  whole  is  again  put  on  the  fire  until  it  boils,  after  which  the 
soup  maybe  served.  The  latter  proceeding  is  rather  to  be  recom- 
mended in  the  case  of  dyspeptics.  One  hundred  gm.  of  sweet- 
bread (raw)  is  equivalent  to  about  90  calories. 

( d ) Brain  Soup. — A calf’s  brain  is  allowed  to  lie  in  cold  water 
for  one  hour,  in  order  to  draw  out  the  blood  contained  in  it ; then 
the  water  is  poured  off,  the  brain  is  once  more  thoroughly  washed 
and  cooked  in  weakly  salted  beef-tea  or  salt  water,  with  the  addi- 
tion of  one  teaspoonful  of  julienne,  for  one  hour.  Then  immedi- 
ately force  it  through  a fine  sieve,  dilute  the  mush  with  beef-tea,  and 
cook  it  again.  In  serving,  the  yolk  of  an  egg  may  be  added.  One 
hundred  gm.  of  calf’s-brain  equal  140  calories. 

(e)  Soup  Containing  Meat  ( according  to  Professor  M.  Rosenthal). — 
Scraped  raw  beefsteak  is  chopped  fine  and  forced  through  a sieve  ; 
the  mass,  soft  as  butter,  is  thoroughly  mixed  with  the  yolk  of  an 
egg,  and  mixed  in  minute  particles  to  a greater  or  less  degree 
with  boiling  soup. 

(/)  Meat- puree  Soup  ( according  to  Hedwig  Heyl). — Twenty  gm. 
of  grated  rolls  are  cooked  for  one-quarter  of  an  hour  with  of  a 
liter  of  bouillon.  Stewed  chicken-meat  is  pounded  fine,  passed 
through  a hair  sieve,  and  25  gm.  of  it  are  stirred  together  with 
one  tablespoonful  of  cream  or  one  teaspoonful  of  meat-peptone  ; 


PREPARATION  OF  SOUPS  WITH  FILLERS.  263 

several  spoonfuls  of  soup  are  added,  and  now  beaten  up  with  the 
entire  mass,  and  served  without  further  cooking. 

(g)  Roll  Soup  (according  to  Hedwig  Iieyl). — Thirty  gm.  of  grated 
rolls  are  roasted  with  ten  gm.  of  butter,  without  coloring  the 
latter  ; ^ of  a liter  of  bouillon  is  poured  over  and  slowly  boiled 
for  half  an  hour.  The  yolk  of  an  egg  is  beaten  up  with  a table- 
spoonful of  sweet  or  sour  cream,  and  then  put  into  the  soup,  and 
the  latter  is  passed  through  a sieve  upon  the  previously  warmed 
plate  (equal  to  about  240  calories). 

(h)  Soup  Biscuit. — Forty  gm.  of  butter  are  stirred  for  one- 
quarter  of  an  hour,  afterward  mixed  with  two  whole  eggs,  a little 
salt  is  added,  and  at  last  40  gm.  of  flour.  In  order  to  make  the 
mass  rise  more  easily,  one  can  add  three  gm.  of  baking-powder 
(consisting  of  bicarbonate  of  soda  and  tartaric  acid,  which  can  be 
had  in  most  drug-stores  in  packages  of  30  gm.).  A long,  square, 
sheet-iron  mold  is  rubbed  with  butter ; the  mass  is  put  into  it 
and  baked  in  the  oven  with  moderate  heat  for  half  an  hour. 
When  the  biscuit  has  cooled  off  it  is  taken  out,  cut  into  blocks, 
and  can  then  be  added  to  the  various  soups  (such  as  sweetbread, 
brain,  or  pea  soup).  The  whole  mass  corresponds  to  about  630 
calories. 

(i)  Noodle  Soup  ( Vermicelli  Soup). — The  noodles  (only  the  best 
quality)  must  be  boiled  half  an  hour  in  very  good  bouillon.  A 
soup  of  about  ten  gm.  of  vermicelli  equals  about  50  calories. 

(P)  Butter -dumpling  Soup. — Thirty  gm.  of  butter  is  stirred  one- 
quarter  of  an  hour,  one  whole  egg  and  a little  salt  being  added  ; 
stir  the  same  and  mix  well  with  the  butter,  and  then  add  30  gm.  of 
flour.  With  a teaspoon  rather  long  lumps  are  cut  out  of  the 
dough  and  put  into  boiling  beef-tea,  in  which  they  must  boil 
twenty  minutes  more  on  a fire  not  too  strong.  The  whole  mass 
equals  about  420  calories. 

(/)  Green-pea  Soup  (Mashed). — Fresh  green  peas  are  boiled  in 
salt  water  until  thoroughly  soft ; in  advanced  seasons,  when  they 
are  no  longer  very  young,  add  ^ of  a gm.  of  carbonate  of  soda ; 
canned  peas  are  also  very  good  at  any  time  for  making  this 
soup.  Let  the  water  run  off  through  a strainer,  force  the  peas 
through  a fine  sieve,  mix  with  a teaspoonful  of  flour  (aleuronat 
flour),  pour  beef-tea  over  the  mass  and  cook  again;  100  gm.  of 
peas  equal  75  calories  ; of  a liter  (420  gm.)  of  peas  gives  280 
gm.  of  mashed,  equal  to  300  calories. 


DIET  LISTS. 


264 

II.  Fish. 

Fish  for  the  table  of  a sick  person  should  never  be  boiled  or 
fried  in  fat,  but  boiled  only  in  water.  Of  the  fresh-water  fish  the 
trout,  the  perch-pike  ( Lucioperca  sandra),  pike,  carp,  grayling, and 
salmon  come  under  consideration  here.  Of  salt-water  fish  the 
black  or  sea-bass,  sea-trout,  the  bluefish  (. Pomatomus  saltator ), 
the  mackerel,  cod,  rockfish,  and  haddock  are  suitable.  The  fish  is 
carefully  freed  from  scales,  rubbed  inside  with  salt,  and  boiled  in 
very  strongly  salted  water,  in  which  it  is  allowed  to  remain,  accord- 
ing to  its  size,  from  one-quarter  to  one-half  hour.  All  spices 
are  to  be  omitted;  only  a handful  of  dried  julienne  may  be  put  in 
the  boiling  water,  by  which  the  flavor  is  considerably  increased. 
All  fat  and  pungent  sauces  are  to  be  avoided,  and  even  hot  butter 
will  generally  not  agree  with  the  dyspeptic  ; so  that  it  is  best  to 
put  only  a little  fresh  butter  on  the  fish  when  serving.  Of  the  sea- 
fish,  the  cod,  rose-fish,  and  haddock  are  to  be  recommended.  Their 
preparation  is  the  same,  except  that  they  are  soaked  one-quarter  of 
an  hour  previously  in  fresh  water  (not  in  boiling,  but  cold  water), 
in  which  is  put  a large  quantity  of  salt  and  also  some  julienne. 
The  vessel  must  be  large  enough  to  allow  the  fish  to  be  surrounded 
on  all  sides  by  the  water.  A two-  or  three-pound  haddock  must 
remain  on  the  fire  thirty  to  forty  minutes  to  be  thoroughly  done ; 
sea-fish  also  are  to  be  served  with  fresh  butter. 

III.  Meats. 

1.  Sirloin  (Fillet). — For  the  tenderness  of  beef  it  is  of  impor- 
tance that  it  be  allowed  to  hang  long  enough  ; for  this  two  to  four 
days  are  necessary  in  summer,  in  winter  as  many  as  eight  days ; 
only  in  the  coldest  season  must  it  be  protected  from  frost,  through 
which  it  becomes  very  dry.  The  meat  is  freed  from  all  fat,  the 
membranous  parts,  well  beaten,  washed  and  salted,  and  then  put 
into  a stewpan  with  hot  lard,  in  which  it  is  quickly  turned  over 
several  times.  The  meat  loses,  in  roasting  in  the  English  style,  ten 
per  cent,  in  weight,  and  in  slow  roasting,  thirty  per  cent,  in  weight. 
To  prepare  a fillet  in  English  style,  so  that  it  is  still  red  inside,  one 
calculates  for  each  pound  of  meat  one-quarter  of  an  hour;  so  that 
a four-pound  roast  requires  one  hour’s  roasting.  It  is  entirely 
unsuitable  to  try,  by  means  of  sticking  with  a fork,  how  far  the 
roast  is  done,  for  much  juice  is  lost  by  this,  and  the  cook  must 
learn  by  practice,  by  the  nature  of  the  pan,  the  thickness  of  the 
roast,  the  strength  of  the  fire,  to  calculate  the  period  of  time  neces- 


PREPARATION  OF  MEATS. 


265 


sary  for  the  completion  of  the  roast.  During  roasting  frequently 
add  spoonfuls  of  beef-tea,  so  that  the  butter  does  not  become  too 
dark,  but  the  bouillon  must  never  be  poured  upon  the  meat  itself. 
One-quarter  of  an  hour  before  serving,  the  roast  is  taken  out  of 
the  pan,  all  fat  is  carefully  skimmed  from  the  sauce,  a tablespoonful 
of  white  flour  and  a teaspoonful  of  aleuronat  flour  are  mixed  with 
a little  cold  bouillon,  a little  extract  of  meat  is  added,  and  this  thin 
mixture  is  then  added  to  the  sauce  of  the  roast,  which  is  again 
made  to  boil,  and  the  roast  is  again  laid  into  it  until  serving.  One 
hundred  gm.  of  beef  roasted  in  English  style  equal  about  210 
calories. 

2.  Roast  Beef. — This  roast  is  good  and  juicy  only  when  in  large, 
thick  pieces.  The  preparation  is  exactly  the  same  as  the  preceding. 
It  is  juicier  when  roasted  on  the  spit,  though  in  most  households 
the  necessary  equipments  are  wanting.  With  this  meat,  which  has 
a tolerably  coarse  grain,  a sufficient  time  for  hanging  is  absolutely 
necessary. 

3.  Raw  Beefsteak  ( according  to  Lenbe). — From  the  loin,  which 
has  hung  a sufficient  time,  as  much  meat  is  scraped  off  with  a dull 
spoon-handle  as  can  be  separated  without  violence,  until  one  has  a 
mass  of  about  150  gm.  The  mass  thus  scraped  off  is  slightly 
salted,  made  into  a very  small  cake,  and  eaten  either  entirely  raw 
or  just  roasted  on  the  surface  in  fresh  butter.  One  hundred  gm. 
equal  about  120  calories. 

4.  Beefsteak  ( according  to  Wiet). — Take  some  of  the  best  sirloin 
and  cut  across  a piece  as  thick  as  a thumb ; after  this  has  been 
well  pounded  and  slightly  salted  on  one  side,  it  is  put  into  an  iron 
or  enameled  pan,  fried  for  one  minute  on  one  side  in  fresh  butter, 
then  turned,  gravy  poured  over,  and  is  fried  on  the  other  side  only 
one-half  of  a minute,  after  which  it  is  immediately  served  on  a 
warmed  plate.  One  hundred  gm.  equal  about  130  calories. 

5.  Beefsteak  in  Oil. — From  a well-hung  fillet  a piece  as  thick  as 
a thumb  is  cut,  all  skins  and  fat  removed,  the  same  well  pounded 
and  salted.  Then  spread  on  both  sides  with  the  finest  olive  oil, 
cover  up  well,  and  allow  it  to  remain  thus  two  hours.  Thereafter 
put  into  the  pan  and  fry  without  any  further  grease  (except  the  oil 
previously  spread  over  it)  till  it  is  brown  on  both  sides.  The  time 
necessary  for  frying  varies  from  five  to  ten  minutes,  according  to 
the  degree  one  wishes  it  done  inside. 

6.  Roast  Veal. — The  leg  of  veal,  after  it  has  hung  a sufficient 
time,  is  freed  from  the  thick  outside  skin  and  laid  in  sweet  milk  for 

18 


266 


DIET  LISTS. 


one  or  two  days  in  summer,  two  or  four  days  in  winter,  by  which 
it  becomes  tender  and  soft.  Before  using,  it  is  carefully  washed, 
thoroughly  skinned,  and  well  salted ; thereupon  it  is  larded  with 
fresh  lard  and  roasted  in  tolerably  hot  butter  or  white  beef-fat,  of 
which  about  200  gm.  are  necessary.  For  the  rest  it  is  treated 
like  any  other  roast,  except  that  it  is  best  (in  the  case  of  veal)  to 
roast  until  well  done,  which  for  a small  roast  takes  two  hours,  for  a 
large  one  three  hours.  In  the  English  way  one  and  one-quarter 
to  two  hours  are  sufficient.  Roast  veal,  when  the  bone  is  not  pre- 
viously taken  out,  gives  a very  good,  thick  sauce";  so  that  in  most 
cases  it  is  necessary  to  add  only  a little  bouillon  after  the  fat  has 
been  skimmed  off.  Its  value  in  calories  is  about  the  same  as  that 
of  lean  beef. 

7.  Veal  fricandeau  is  also  laid  in  milk  a few  days  before  using, 
which  milk  it  is  best  to  let  sour,  for  the  flavor  is  thus  increased;  it 
must  be  done,  however,  in  such  a manner  that  the  milk  covers  the 
meat  completely.  For  the  rest,  the  meat  is  treated  as  any  other 
veal  roast,  except  that  one  and  a half  hours’  roasting  with  a good 
fire  will  suffice.  The  sauce  is  to  be  mixed  with  flour,  and  it  can  be 
given  a piquant  flavor  by  the  addition  of  some  cream. 

8.  Veal  Cutlets  {Chops). — The  ribs  of  the  calf  are  separated  from 
the  backbone ; the  single  cutlets  separated  from  each  other  are 
washed  and  freed  from  skins,  pounded,  salted,  and  fried  in  a pan 
with  hot  butter.  They  will  be  more  tender  if  they  have  lain  one 
day  previously  in  milk;  in  this  case  they  need  be  fried  only  eight 
or  ten  minutes,  but  otherwise  it  is  preferable  to  fry  them  from  one- 
half  to  one  hour,  not  leaving  them  long  in  one  place,  often  shoving 
them  to  and  fro,  during  which  time  a piece  of  fresh  butter  is  also 
added,  and  the  melted  butter  is  constantly  poured  over  the  cutlets. 
Before  serving,  some  good  liquor  from  a roast  is  added.  To  cover 
cutlets  with  bread-crumbs  is  not  advisable  in  dietetic  cooking. 
One  hundred  gm.  of  fried  veal  cutlets  (also  the  following  veal 
dishes)  equal  230  calories. 

9.  Scotched  Collop. — From  the  leg  of  veal,,  which  has  lain  in 
milk  two  or  three  days,  cut  slices  as  thick  as  your  thumb,  wash, 
beat  and  salt  them,  and  put  them  in  a pan  with  hot  butter,  where 
they  must  be  allowed  to  brown  slightly  on  both  sides.  Then  pour 
in  one  glass  of  white  wine  and  some  bouillon,  cover  up  tightly, 
and  let  them  steam  altogether  for  about  one  and  a quarter  hours, 
pouring  in  some  bouillon  from  time  to  time.  The  addition  of  sour 
cream  improves  the  flavor ; but  the  digestibility  is  decreased  by 


PREPARATION  OF  FOWL,  POULTRY,  ETC.  26? 

the  sour  cream.  Then  skim  off  all  fat  and  with  Hour  prepare  a 
sauce  as  directed  above. 

10.  Fillet  of  Veal. — From  the  fricandeau  piece  cut  strips  one  cm. 
thick  and  six  cm.  wide,  and  prepare  them  exactly  as  in  No.  9;  in 
the  middle  lay  a few  pieces  of  middling,  roll  them  up  and  tie  with 
cord.  For  the  rest  proceed  exactly  as  in  the  case  of  scotched 
collop. 

1 1.  Veal  Steak. — Cut  from  the  leg  pieces  as  thick  as  your  thumb, 
weighing  about  100  gm.,  pound  them  well,  wash,  salt  and  lay  them 
in  a pan  with  hot  butter,  and  fry  them,  with  frequent  turning,  for 
ten  minutes.  Either  add  some  sauce  from  a roast  or  prepare  one 
from  bouillon,  flour,  and  meat-extract,  which  is  put  into  the  pan, 
and  then  let  the  steaks  fry  in  it  for  two  minutes  longer. 

12.  Lamb's  Saddle. — The  saddle  of  a young  animal  is  laid  in 
milk  for  two  days,  or  the  milk  is  allowed  to  sour,  through  which  a 
venison-like  flavor  is  obtained.  Before  using,  the  roast  is  washed, 
freed  from  fat  and  skins,  and  larded  with  fresh,  unsmoked  bacon; 
then  it  is  put  into  a pan  with  previously  heated  beef-fat  or  good 
butter,  in  which  it  must  immediately  be  turned  several  times.  It 
is  roasted  one  and  a half  hours,  during  which  time  it  is  to  be  dili- 
gently basted  by  the  addition  of  beef-tea.  In  the  last  hour  pour 
in  one  glass  of  white  wine  and  as  much  bouillon  as  the  sauce  has 
boiled  down.  With  sour  cream  the  roast  becomes  particularly 
well  flavored,  but  not  every  patient  can  stand  it.  The  sauce  is  pre- 
pared, as  in  other  roasts,  with  flour. 

13.  Roast  Fowl. — Fowl  destined  for  roasting  must  be  picked  and 
cleaned  immediately  after  killing,  and  then  it  is  allowed  to  hang  in 
a cool  place  at  least  one  day ; in  winter,  two  to  four  days — for  which 
reason  one  should  always  inquire,  in  buying  dressed  poultry,  how 
long  it  has  been  killed. 

(a)  Young  cockerels  must  be  scalded  before  picking.  Before 
roasting,  the  hair  must  be  singed  off,  and  they  must  be  carefully 
washed  and  rubbed  with  salt  inside  and  outside ; afterward  they 
are  put  in  a pot  with  plenty  of  hot  butter,  roasted  brown  on  both 
sides,  with  frequent  basting,  for  which  three-quarters  to  one  hour 
is  necessary.  The  sauce  is  made  as  above,  with  a little  flour.  One 
hundred  gm.  of  raw  chicken  equal  100  calories. 

( b ) Capons  and  pullets  should  be  roasted  with  little  butter, 
since  they  are  generally  fat  enough.  According  to  their  size  they 
must  be  roasted,  with  frequent  basting,  from  one  and  one-half  to 
two  hours. 


268 


DIET  LISTS. 


(c)  Young  pigeons  are  treated  just  as  young  cockerels.  Time 
of  roasting,  about  three-quarters  of  an  hour. 

( d ) The  pheasant  yields  a fine  roast  after  it  has  hung  about 
eight  to  fourteen  days.  Roast  it  from  two  to  three  hours,  with 
plenty  of  butter  and  frequent  basting. 

( e ) The  Partridge. — The  same  must  be  young,  and  must  have 
been  killed  several  days  before  using,  in  order  to  furnish  a tender 
roast.  After  it  has  been  picked,  cleaned,  and  washed,  it  is  put  into 
a tolerable  quantity  of  hot  butter,  and  a piece  of  fresh  butter  is 
also  put  inside  the  partridge.  On  the  other  hand,  wrapping  with 
bacon  is  less  to  be  recommended  for  those  having  stomach  trouble, 
and  a roast  just  as  juicy  can  be  obtained  by  diligent  basting;  the 
palatability  can  also  be  increased  by  the  addition  of  white  wine 
and  sour  cream.  Time  of  roasting,  one  and  one-quarter  hours. 

(/)  Boiled  Cockerels  and  Pigeons. — They  are  prepared  just  as 
for  roasting,  then  laid  in  boiling,  slightly  salted  bouillon,  to  which 
a little  julienne  has  been  added,  and  boil  one  to  one  and  one- 
quarter  hours.  Very  young  pigeons  are  cooked  soft  in  three- 
quarters  of  an  hour;  likewise  very  young  cockerels. 

14.  Roast  Game. 

{a)  Roast  Hare. — The  hare  is  skinned  and  then  cleaned,  but  the 
liver,  heart,  head,  etc.,  are  not  to  be  used  in  cooking  for  the  sick. 
After  the  roast  has  been  thoroughly  washed  within  and  without,  it 
is  well  salted  and  larded  with  fresh  (not  smoked)  bacon,  and 
treated  exactly  as  the  roast  lamb,  so  that  it  is  done  in  about  one 
and  one-half  hours.  By  the  addition  of  sour  cream  the  roast  hare 
becomes  very  good,  but  in  this  way  it  does  not  agree  with  every 
one.  The  sauce  is  prepared  in  the  same  way  as  in  the  case  of  fillet 
roast,  with  flour  and  beef-tea. 

( b ) Roast  Venison  (Doe). — The  venison  saddle  is  the  most  bene- 
ficial game  for  those  who  have  stomach  troubles.  It  is  to  be  treated 
exactly  as  the  roast  hare,  only  it  must  be  roasted  about  two  and 
one-half  hours,  on  account  of  its  size.  The  joint  of  venison  will 
gain  considerably  in  tenderness  and  flavor  if  it  is  laid  in  light  red 
wine  a few  days  before  using;  for  the  rest  it  is  to  be  treated  exactly 
as  the  venison  saddle,  only  it  must  be  roasted  two  and  one-half, 
three,  or  four  hours,  according  to  size.  The  sauce  is  the  same  as 
with  roast  hare.  But  game  can  also  be  treated  in  the  English 
fashion,  by  roasting  it  only  a short  time,  as  in  the  case  of  fillet  and 
roast  beef.  A venison  joint  thus  requires  one  and  one-quarter 
hours,  approximately,  with  strong  heat,  and,  if  very  heavy,  one  and 


STEWED  MEATS. 


269 


one-half  hours.  A venison  saddle,  if  young  and  tender,  requires 
three-quarters  of  an  hour;  if  older,  one  and  one-quarter  hours.  In 
this  way  the  meat  remains  juicier  and  stronger. 

(< c ) Venison  saddle  (stag)  is  to  be  treated  in  the  same  way, 
except  that  it  must  be  roasted  a correspondingly  longer  time  ; but 
generally  the  meat  is  not  as  tender  and  palatable  as  that  of  the  doe. 
One  hundred  gm.  of  game  (roast)  equal  about  215  calories  (when 
thoroughly  done). 

15.  Stewed  Meats. 

(a)  Preserved  Veal. — The  meat  from  a leg  or  breast  which  has 
hung  sufficiently  is  cut  into  pieces  the  size  of  a walnut;  the  latter 
are  put  into  a small  stewpan  with  hot  butter,  and  a little  salt 
sprinkled  over  ; immediately  after  they  have  been  once  turned  in 
the  butter,  y2  of  a glass  of  white  wine,  about  75  gm.,  is  poured  in 
and  the  whole  covered  up  well  and  stewed  for  one  and  a quarter 
hours  with  moderate  heat,  some  good  bouillon  being  added  from 
time  to  time.  One-quarter  of  an  hour  before  serving,  the  sauce  is 
prepared  in  the  way  before  indicated ; and  immediately  before  serv- 
ing, the  yolk  of  an  egg  is  mixed  with  water  and  put  into  the  sauce. 

( b ) Preserved  Sweetbread. — The  sweetbread  is  cooked  till  it  is 
soft  as  in  the  case  of  soup,  is  skimmed,  cut  into  two  halves,  and  ten 
minutes  before  serving  is  laid  in  butter-sauce,  to  be  prepared  in  the 
following  way  : A little  piece  of  butter  is  melted  in  a small  dish, 
without  being  allowed  to  brown  ; then  one  tablespoonful  of  flour  is 
added,  well  mixed  with  the  butter;  then  pour  in  cold  bouillon  and 
a little  white  wine,  so  that,  after  the  sauce  has  boiled,  the  whole 
forms  a tolerably  thick  liquid.  The  amount  of  the  ingredients  must 
be  determined  by  the  amount  of  sauce  desired.  Before  serving,  the 
yolk  of  an  egg  is  added  to  the  sauce. 

(e)  Stewed  Cockerels  or  Pigeons. — A young  cockerel  or  pigeon 
is  dressed  as  for  roasting,  quartered  into  equal  parts,  slightly  salted 
and  laid  in  a stewpan  in  which  a small  piece  of  butter  has  been  pre- 
viously melted  without  being  browned.  The  stewpan  is  covered 
tightly  and  the  poultry  stewed  slowly  for  a quarter  of  an  hour. 
Then  y of  a glass  of  white  wine,  about  75  gm.,  and  some  good 
bouillon  are  added,  and  it  is  again  allowed  to  stew  for  about  three- 
quarters  of  an  hour  longer,  a little  beef-tea  being  added  from  time 
to  time.  The  sauce  is  the  same  as  in  the  case  of  stewed  veal.  One 
hundred  gm.  of  meat  equal  about  120  calories. 

1 6/ Dishes  from  Chopped  Fresh  Meat. — Be  warned  against  allow- 
ing the  butcher  to  chop  the  meat,  as  in  some  cases  less  desirable  or 


270 


DIET  LISTS. 


less  appetizing  meat  may  be  mixed  in.  Every  household  should 
possess  a machine  for  chopping  meats  ; in  cases  where  there  is  none, 
do  not  mind  the  trouble  of  chopping  or,  preferably,  scraping  it 
yourself. 

(a)  Roast  Chopped  Meat. — One-half  of  a pound  of  veal,  y2  of  a 
pound  of  beef,  and  y2  of  a pound  of  pork,  not  entirely  lean,  are  put 
through  the  chopping  machine;  the  whole  mass  is  then  mixed  in  a 
dish  with  three  whole  eggs,  y of  a liter  of  milk,  I y grated  rolls, 
and  a tolerable  amount  of  salt ; if  the  dough  then  seems  too  stiff,  a 
little  more  milk  may  be  added.  The  mass  is  made  into  a longish 
cake  and  roasted  in  hot  lard  or  good  butter  (ioo  gm.)  first  on  one 
side  and  then  on  the  other,  until  it  is  light  brown.  Time,  one  hour 
and  a quarter.  From  this  hardly  any  sauce  will  be  obtained  ; hence 
one  must  be  prepared  from  flour,  bouillon,  extract  of  meat,  and  a 
little  white  wine,  which  is  to  be  poured  over  a quarter  of  an  hour 
before  serving.  One  hundred  gm.  of  this  roast  equal  about  250 
calories. 

( b ) Cutlets  from  Chopped  Meat. — The  same  mixture  as  in  the 
preceding  is  made  into  little  cutlets,  allowed  to  fry  on  both  sides  in 
hot  butter  until  light  brown ; then  skim  off  all  fat,  prepare  a butter 
sauce,  pour  it  over,  and  let  it  fry  with  this  for  another  half-hour. 

( c ) Meat  Balls  (Veal). — One  pound  of  meat  from  the  leg  is 
chopped  up  fine  in  the  machine ; 40  gm.  of  butter  are  stirred  to 
foam,  two  whole  eggs,  and  one  roll,  grated  fine,  are  added  ; also  a 
little  salt,  and  according  to  taste  of  the  individual  a little  finely 
chopped  parsley.  Of  this  mass  flat  cakes  are  made  and  cooked 
for  one-quarter  of  an  hour  in  salt  water ; butter  sauce,  or,  when 
allowed,  anchovy  sauce,  is  added,  which  is  to  be  poured  over  the 
cakes  one-quarter  of  an  hour  before  serving.  One  hundred  gm. 
equal  250  calories. 

1 7.  Dishes  from  Chopped  Roast  Meat. 

(a)  Hash. — In  a little  butter  or  lard  put  some  finely  chopped 
roast  meat  (veal,  fowl,  or  game),  stew  for  five  minutes  with  frequent 
stirring  and  pour  over  any  sauce  remaining  from  the  roast,  or 
make  a special  sauce  as  follows  : Sprinkle  some  fine  flour  upon 

the  stewed  meat,  mix  well,  pour  in  a little  white  wine  and  enough 
bouillon  so  as  to  produce  a rather  thick  gruel.  Then  stew  for  one- 
quarter  of  an  hour  longer  with  moderate  heat,  keeping  the  vessel 
well  covered.  The  hash  is  now  done.  A little  extract  of  meat 
added  will  improve  the  flavor.  One  hundred  gm.  equal  about  225 
calories. 


PREPARATION  OF  JELLIES. 


27 


(, b ) Meat  Pudding. — Sixty  gm.  of  butter  are  stirred  until  foamy, 
four  yolks  of  eggs,  salt,  and  a little  fine-cut  parsley  added.  Two 
French  rolls  are  grated  fine,  the  inside  cut  into  small  pieces  and 
soaked  in  milk,  in  which  it  remains  one  hour;  170  gm.  of  roast 
meat  are  cut  fine  or  chopped  in  a machine  ; the  grated  rolls  are 
taken  out  of  the  milk,  pressed,  and  with  the  chopped  roast  meat 
mixed  with  the  other  mass  (butter  and  eggs).  If  allowed,  two 
tablespoonfuls  of  sour  cream  may  also  be  added.  Lastly,  the 
whipped  whites  of  four  eggs  are  mixed  in,  and  the  whole  dough  is 
put  in  a mold  rubbed  with  butter  and  stewed  with  dust  from  the 
rolls.  In  this  the  pudding  is  cooked  for  one  and  three-quarter 
hours  in  a water-bath.  Any  sauce  remaining  from  a roast  is  added 
(or  anchovy  sauce).  One  hundred  gm.  equal  about  200  calories. 

(c)  Omelette  Souffle  from  Remnants  of  Roasts. — Forty  gm.  of 
finely  cut  roast  meat  are  mixed  with  one  tablespoonful  of  sweet  or 
sour  cream  ; a little  salt  and  the  yolk  of  an  egg  are  added  ; the 
whipped  white  of  an  egg  is  mixed  in ; the  mass  is  put  into  a small 
porcelain  mold  and  baked  in  a well-heated  oven  for  twenty  min- 
utes; sauce  from  a roast  is  added.  The  whole  mass  equals  215 
calories. 

(< d ) Sweetbread  Pudding  (according  to  Hedwig  Hehl). — Twenty- 
five  gm.  of  French  rolls  are  grated  and  laid  in  milk.  The  sweet- 
bread is  cooked,  until  soft,  in  bouillon  or  salt  water,  skinned,  and 
cut  into  small  blocks.  Thirty  gm.  of  butter  are  stirred  until  foamy, 
and  two  yolks  of  eggs,  the  roll  which  has  been  pressed  out,  a little 
salt,  parsley,  and  the  blocks  of  sweetbreads  are  put  into  the  butter, 
with  which  the  whipped  white  of  an  egg  is  mixed  ; the  whole  is 
put  into  a cup'  well  rubbed  with  butter,  covered,  and  cooked  for 
three-quarters  of  an  hour  in  the  water-bath.  Anchovy  sauce  or 
meat  gravy  is  added.  One  hundred  gm.  equal  about  150  calories. 

IV.  Jellies. 

1.  WieVs  Jelly , for  Dyspeptics. — Takeoff  the  skin  and  meat  from 
a calf’s  foot,  mash  the  bones,  and  put  on  the  stove  with  some  cold 
water  until  it  is  heated  to  foaming,  when  all  refuse  will  be  sepa- 
rated. After  rinsing  off  the  scum  with  cold  water,  put  the  bones 
with  y of  a k.  of  beef,  or  y2  of  an  old  hen,  and  1^  liters  of  water, 
and  five  gm.  of  salt,  and  boil  slowly  from  four  to  five  hours.  Pour 
the  jelly  thus  formed  through  a fine  sieve,  and  place  overnight  in 
the  cellar.  Next  morning  take  off  the  layer  of  fat,  and  to  clarify  the 
cold  jelly  add  one  egg  with  the  mashed  shell,  and  mix  with  steady 


272 


DIET  LISTS. 


beating  and  stirring.  Then  subject  the  whole  with  constant  beating 
and  stirring  to  a temperature  of  not  over  6o°  R.  (or  else  the  white 
of  the  egg  will  curdle).  If  the  jelly  begins  to  show  grains,  cover 
and  let  cool  until  the  white  of  egg  becomes  flaky  and  separates. 
Hereupon  strain  a few  times  more  until  it  becomes  perfectly  clear, 
add  five  gm.  of  extract  of  meat,  and  pour  the  jelly  into  a mold 
and  let  cool  again.  An  addition  of  gravy  from  a roast  is  very  pala- 
table. It  must  be  mixed  in  while  the  mass  is  still  warm  and  liquid. 
The  dish  is  very  palatable  with  cold  fowl,  but  does  not  keep  well 
in  summer,  and  had,  therefore,  best  be  put  on  ice. 

2.  Ichthyocolla  Jelly. — Cut  fifteen  gm.  of  ichthyocolla  into  small 
pieces  and  let  soften  in  ^ of  a liter  of  cold  water  for  eight  to  ten 
hours  ; boil  for  one-quarter  of  an  hour  and  add  gravy  from  a roast 
and  extract  of  meat.  Pour  the  mass  when  hot  through  a fine  cloth, 
or,  better,  through  filter-paper.  One  can  add  to  100  gm.  of  the 
liquid  also  0.5  gm.  of  hydrochloric  acid  or  ten  gm.  of  white  wine. 

3.  Milk  Jelly. — Boil  two  liters  of  milk  for  five  to  ten  minutes  with 
250  gnl*  of  sugar.  To  the  well-cooled  mixture  add,  while  slowly 
stirring,  a solution  of  thirty  gm.  of  white  gelatin  in  250  gm.  of 
water,  and  also  add  three  wineglassfuls  (400  gm.)  of  good  Rhine 
wine,  or  thirty  gm.  of  cognac ; afterward  pour  the  mass  into  a form 
and  let  cool.  One  hundred  gm.  equal  about  250  calories. 

V.  Vegetables. 

1.  Asparagus. — The  asparagus  stems  are  washed,  peeled  from  the 
top  downward,  and  the  lower  woody  ends  cut  off ; then  they  are 
bound  in  a small  bundle,  and  cooked  until  soft  in  salt  water,  which 
requires,  according  to  the  thickness  of  the  stems,  one-half  to  one 
hour;  a large  quantity  of  water  must  be  used  in  cooking,  otherwise 
the  asparagus  easily  takes  an  ugly  color.  Make  a butter  sauce 
with  yolk  of  egg.  Dyspeptics  can  take  only  the  soft  heads  without 
sauce.  One  hundred  gm.  equal  about  20  calories. 

2.  Spinach. — The  spinach  leaves  are  carefully  picked,  washed,  and 
laid  in  boiling  salt  water,  in  which  they  are  to  be  cooked  slowly, 
without  being  covered ; otherwise  they  lose  their  color  easily. 
After  twenty  minutes  put  them  on  a sieve,  pour  cold  water  over 
them,  and  press  them.  Then  cut  the  spinach  very  fine  or  pass 
through  a hair  sieve,  lay  in  a little  melted  butter,  dust  flour  over  it 
several  times,  and  add  strong  bouillon.  Lastly,  mix  in  the  yolk 
of  an  egg  with  cold  bouillon.  One  hundred  gm.  equal  165  calories 
(prepared  from  250  gm.  of  spinach  leaves). 


PREPARATION  OF  VEGETABLES. 


273 


3.  Comfrey  or  Brnisezvort. — Wash,  clean  carefully,  cut  in  pieces 
two  inches  long,  and  also  split  the  thicker  pieces  lengthwise.  Mix 
one  tablespoonful  of  flour  with  one  liter  of  water  and  one  table- 
spoonful of  vinegar,  and  lay  each  cleaned  piece  of  root  in  the  mix- 
ture. Afterward  they  are  again  rinsed  on  a sieve  with  clean  water, 
laid  in  melted  butter,  salted,  covered  tightly  and  stewed,  adding 
strong  bouillon  from  time  to  time.  According  to  size  and  age  the 
roots  require  boiling  from  three-quarters  to  one  and  one-half  hours 
in  order  to  become  soft.  One  hundred  gm.  equal  about  1 20  calories. 

4.  Green  Peas. — The  peas  (j^)  are  hulled  and  stewed  in  15  gm. 
of  butter  and  bouillon  as  the  preceding;  time,  from  one  to  one  and 
a half  hours.  Or,  take  canned  peas  and  put  the  opened  can  in  hot 
water,  or  cook  them  with  the  same  amount  of  butter  and  some 
salt.  For  the  sick  it  is  advisable  to  pass  the  peas  through  a sieve 
and  serve  them  as  a puree.  One-half  of  a liter  of  peas  yield  280 
gm.  of  pea  puree;  of  this*  100  gm.  equal  160  calories. 

5.  Carrots. — Carrots  are  serviceable  in  the  dietetic  kitchen  only 
when  very  young  and  tender.  They  are  cleaned,  washed,  cut  into 
pieces  and  then  stewed  similarly  to  peas.  The  time  is  also  the 
same.  If  it  is  desired  to  serve  them  as  a puree,  they  are  passed 
through  a hair  sieve  after  they  are  cooked.  A little  flour  is  dusted 
over  them  and  they  are  cooked  to  a thick  mush.  One  hundred 
gm.  of  puree  equal  120  calories. 

6.  Beans  [Green). — Young  beans  are  cleaned,  washed,  cut  fine, 
and,  like  the  peas,  stewed  in  butter  and  bouillon.  In  a season 
when  there  are  no  young,  fresh  vegetables,  one  can  use  to  advan- 
tage canned  beans,  of  which  Prince  beans  (Flagiolettes)  are  the 
most  tender.  One  hundred  gm.  equal  about  40  calories. 

7.  Cauliflozver. — The  cauliflower  is  cleaned,  washed,  and  treated 
like  the  asparagus.  Time  of  cooking,  one-half  hour.  One  hun- 
dred gm.  equal  about  60  calories. 

8.  Rice  in  Bouillon. — Thirty  gm.  of  rice  are  washed  twice  on  the 
previous  evening,  and  then  water  in  which  a little  carbonate  of 
soda  has  been  dissolved  is  poured  over  it,  so  that  the  rice  may 
swell  during  the  night;  then  the  water  is  drained  off,  and  the  rice 
with  a piece  of  butter  and  some  strong  bouillon  is  put  in  a stew- 
pan  and  stewed  for  one  and  one-quarter  hours,  tightly  covered, 
except  the  last  quarter  of  an  hour;  finally  the  beaten-up  yolk  of  an 
egg  is  added.  Now  rinse  out  a small  porcelain  dish  with  cold 
water,  without  drying  it,  and  press  the  rice  into  it,  let  stand  five 
minutes  and  then  turn  the  mold.  The  amount  is  calculated  for  one 


274 


DIETETIC  KITCHEN. 


person,  and  is  best  suited  for  a side  dish  to  meats.  The  whole 
equals  about  225  calories. 

9.  Chestnut  Puree. — One-half  kilo  of  chestnuts  are  peeled  and 
boiled  in  water  so  long  as  to  get  the  second  (inside)  skin  off  easily. 
The  chestnuts  are  laid  upon  a sieve  until  all  the  water  has  drained 
off.  Then  they  are  mashed  in  a dish  and  afterward  pressed  through 
a hair  sieve.  One  hundred  gm.  of  butter  are  melted  in  a stewpan 
on  the  fire;  a little  salt  and  sugar,  enough  to  cover  the  point  of  a 
knife,  are  added  (to  the  butter),  and  then  the  chestnuts  are  put  in. 
Stew  them,  with  frequent  stirring,  for  one-half  hour,  and  pour  in 
enough  bouillon  to  get  a mush  not  too  thick. 

VI.  Side  Dishes  From  Eggs  and  Flour. 

1.  Scrambled  Eggs. — Two  eggs  are  thoroughly  beaten  with  a 
little  salt  until  the  yolk  and  white  are  completely  mixed.  Then  melt 
five  gm.  of  butter  in  a small  enameled  vessel,  add  the  egg  mixture, 
and  heat,  with  continued  stirring,  until  a rather  thick  mush  is 
formed.  Serve  in  a well-warmed  dish.  This  dish  is  suitable  with 
cold  roast,  ham,  smoked  meat,  etc.  Two  scrambled  eggs  equal 
about  200  calories. 

2.  Potato  Puree. — Peel  ^ of  a pound  of  very  mealy  potatoes, 
cut  into  quarters,  wash,  and  cook  until  soft  in  a steam-cooking 
apparatus;  then  pass  through  a coarse  hair  sieve;  add  20  gm. 
of  fresh  butter,  a little  salt,  and  60  to  70  gm.  of  warm  milk,  and 
beat  thoroughly  for  five  minutes  while  the  mixture  is  on  the  fire, 
until  it  becomes  very  foamy.  This  must  only  be  prepared  just 
before  serving,  as  it  loses  flavor  in  standing.  One  hundred  gm. 
equal  about  125  calories. 

3.  Suabian  Dumplings. — One  hundred  gm.  of  flour,  two  eggs,  two 
tablespoonfuls  of  milk,  and  a little  salt  are  thoroughly  stirred 
together;  the  dough  is  put  in  a special  sieve  (coarse),  through 
which  it  is  forced  and  allowed  to  drop  into  strongly  salted 
boiling  water.  One  must  take  a large  pot  with  plenty  of  water,  so 
that  the  dumplings  may  rise  better  ; they  are  allowed  to  boil  for  half 
an  hour.  When  done  they  are  poured  on  a large  sieve,  and  remain 
until  all  the  water  has  drained  off.  Meanwhile  melt  in  a stewpan 
ten  gm.  of  fresh  butter,  put  the  dumplings  into  it,  shake  them 
well,  and  serve.  The  sieve  necessary  is  known  only  in  South 
Germany,  but  it  can  be  made  by  any  tinner,  for  it  is  like  an 
ordinary  strainer,  the  holes  having  a diameter  of  one  cm.  (about 
J-  of  an  inch).  One  hundred  gm.  equal  175  calories.. 


EGG  AND  FLOUR  SIDE  DISHES. 


275 


4.  Roll  Dumplings. — Rolls  from  the  day  before  are  grated  (that  is, 
the  crust),  the  inside  is  cut  into  slices  and  cold  milk  poured  over  until 
the  bread  is  thoroughly  soft,  for  which  at  least  an  hour  is  necessary. 
Meanwhile  stir  60  gm.  of  butter  for  one-quarter  of  an  hour,  and 
add  slowly  four  eggs  and  a little  salt.  Then  squeeze  the  milk  out 
of  the  slices  and  stir  them  with  the  butter  and  eggs  until  finely 
divided.  In  order  to  test  whether  the  mass  be  of  the  right  con- 
sistency, make  a lump  as  large  as  a walnut  and  boil  in  salt  water. 
If  it  breaks,  a little  dust  from  grated  rolls  must  be  added.  When 
the  dough  has  acquired  the  necessary  firmness,  make  dumplings 
the  size  of  an  apple  (about  seven  from  the  given  quantity  of 
ingredients).  After  they  have  boiled  well  for  one-quarter  of  an 
hour  in  salt  water,  take  them  out  with  a sieve  spoon,  cut  in  half, 
and  serve.  One  hundred  gm.  equal  250  calories. 

5.  Vermicelli ( Water  Noodles  or  Vegetable  Noodles'). — For  the  dough 
take  180  gm.  of  flour,  and  three  eggs,  which  are  to  be  mixed  with 
the  flour  in  a dish  ; then  put  the  dough  on  a board,  and  knead  well 
with  the  hands  until  it  is  tender.  Then  form  it  in  the  shape  of  a 
long  sausage  and  cut  into  four  equal  parts.  First  take  one  part : 
knead  into  a flat,  round  cake  ; weigh  off,  in  addition,  20  gm.  of  flour ; 
dust  the  board  and  rolling-pin  with  this,  and  roll  out  thin  (20  gm. 
of  flour  will  suffice  for  all  the  four  parts  of  the  dough).  At  each 
turning  of  the  dough  dust  the  board  again  with  flour,  so  that  the 
dough  may  not  stick  and  tear.  The  necessary  thinness  is  reached 
when  one  can  distinguish  through  the  dough  the  pattern  of  a piece 
of  calico,  etc.,  laid  underneath.  When  thin,  lay  the  four  parts 
on  a clean,  white  cloth  near  the  fire;  let  them  become  half  dry, 
and  cut  into  strips  one  cm.  broad,  which  are  to  be  separated  and 
hung  up  in  the  kitchen  for  twelve  hours  to  dry.  They  can  be  kept 
for  some  time  in  a tureen.  When  using,  lay  them  for  ten  minutes 
in  boiling  salt  water;  pour  off  the  water  through  a strainer,  and 
put  the  noodles  in  a dish.  Vegetable  noodles  of  a very  good  quality 
are  now  also  made  by  factories.  One  hundred  gm.  of  boiled  noodles 
equal  about  190  calories. 

6.  Macaroni. — Buy  only  the  best  quality.  Put  in  a vessel  with 
much  boiling  water,  and  after  it  has  boiled  ten  minutes  pour 
off  the  water;  pour  over  some  more  boiling  salt  water  and  let  boil 
for  half  an  hour.  Drain,  put  in  astewpan  with  a little  butter  (which 
is  on  the  fire),  mix,  and  serve  immediately.  One  hundred  gm. 
equal  about  150  calories.  One  can  also,  instead  of  putting  hot 
butter  over  the  macaroni,  add  a butter  sauce,  described  under 


2/6 


DIETETIC  KITCHEN. 


“preserved  sweetbread.”  When  the  macaroni  has  been  drained, 
put  in  a porcelain  dish  in  which  it  is  served,  pour  the  thickish 
sauce  over  and  put  the  dish  for  ten  minutes  in  the  oven. 

VII.  Flour,  Milk,  and  Egg  Dishes. 

1.  Rice  Mush. — Thirty  gm.  of  rice  (Caroline  rice  is  the  best)  are 
twice  thoroughly  washed  the  night  before  ; then  cold  water,  in 
which  a little  carbonate  of  soda  has  been  dissolved,  is  poured  over, 
and  allowed  to  stand  until  the  next  day.  Before  using,  the  water 
is  poured  off ; of  a liter  of  milk  is  boiled  and  the  rice  then  added 
and  boiled,  well  covered  up,  for  one  and  one-quarter  hours  on  a 
moderate  fire,  with  frequent  shaking.  If  the  milk  becomes  too 
thick  from  boiling  before  the  rice  has  been  thoroughly  softened, 
add  a little  more  hot  milk.  Whip  the  whites  of  two  eggs,  and  just 
before  serving  mix  lightly  with  the  rice;  if  it  is  desired  to  make  it 
more  nourishing,  the  yolks  of  the  two  eggs  can  also  be  added 
before  the  whites  (this  quantity,  for  one  person,  equals  700  calories). 
One  hundred  gm.  equal  about  160  calories. 

2.  Tapioca. — Boil  of  a liter  of  milk  ; mix  20  gm.  of  best  im- 

ported tapioca  and  boil  for  one-quarter  of  an  hour  longer,  with 
constant  stirring.  Further  procedure  same  as  with  rice  (in  the 
same  way  oatmeal  may  also  be  treated).  Value  in  calories  of 
above  quantity,  about  250. 

3.  White  Pot. — Moisten  in  a small,  well-enameled  pan  65  gm.  ot 
fine  sugar  with  one  tablespoonful  of  water,  and  burn  to  caramel 
sugar.  This  requires  great  care,  for  the  sugar  easily  becomes  too 
dark  and  then  takes  on  a bitter  taste.  On  a hot  stove,  not  over  an 
open  fire,  one  must  constantly  stir  the  sugar  with  a tin  spoon  until 
it  gets  a fine  brown  color.  During  this  process  heat  a tin  form, 
such  as  are  usually  used  for  sweet  dishes,  jelly,  etc.,  and  pour  into 
it  the  sugar  as  soon  as  it  has  browned,  and  let  it  spread  on  all  sides 
until  the  surface  of  the  plate  is  covered.  Then  let  cool.  Now  beat 
up  three  whole  eggs  in  a dish,  add  of  a liter  of  unboiled  milk, 
the  contents  of  a package  of  vanilla,  or  of  a stick  of  vanilla 
boiled  in  milk,  powdered  sugar  to  taste,  mix  the  whole  thoroughly, 
and  pour  into  the  form  with  the  sugar,  which  is  now  cold.  Put  on 
a water-bath,  cover,  and  boil  until  the  mass  has  amalgamated,  which 
can  be  tried  by  thrusting  in  a teaspoon.  Take  out  the  form,  allow 
it  to  cool,  and  turn  over  on  a plate.  This  is  a pleasant,  cooling, 
well-tasting  dish,  nourishing  as  well  as  easily  digestible.  One 
hundred  gm.  equal  about  30  calories. 


PREPARATION  OF  PUDDINGS. 


2 77 


4*  Egg  Creme  ( according  to  Mrs.  Dr.  Pariser). — For  this  one 
reckons,  for  one  person,  one  yolk  of  egg,  two  tablespoonfuls  of 
beaten  cream  flavored  with  vanilla,  sugar  according  to  taste,  and  a 
few  drops  of  arrack  or  cognac.  The  yolk  of  egg  is  first  beaten 
with  sugar  to  foam.  Then  the  whipped  cream  is  added  and  well 
mixed  in ; lastly,  a few  drops  of  arrack  or  cognac  are  added,  and 
the  whole  served  in  wineglasses. 

5.  Vanilla  Creme  {according  to  Mrs.  Dr.  Hughes'). — Stir  four  yolks 
of  eggs  to  foam,  with  of  a pound  of  fine  sugar  ; boil  of  a 
liter  of  milk 'with  some  vanilla  and  add  immediately  to  the  eggs  ; 
mix  with  an  egg-beater  and  again  put  on  the  fire,  with  continual 
stirring.  Six  pieces  of  white  gelatin  are  dissolved  in  a little  hot 
water  and  poured  into  the  mass  while  the  latter  is  still  on  the  fire. 
As  soon  as  it  is  risen,  take  quickly  from  the  fire,  pour  through  a 
strainer  and  nearly  allow  it  to  cool,  with  constant  stirring.  Then 
the  whipped  whites  of  four  eggs  are  added  and  the  mass  poured 
into  a porcelain  dish  which  has  been  rinsed  with  cold  water  ; allow 
it  to  cool,  and  turn  over  just  before  using.  A fruit  sauce  may  be 
served  with  the  creme . 

6.  Roll  Pudding. — Stir  thirty  gm.  of  butter  until  foamy,  add  yolks 
of  two  eggs,  with  one  tablespoonful  of  fine  sugar,  fifteen  gm.  of 
grapes,  fifteen  gm.  of  raisins,  and  twenty  gm.  of  finely  grated 
almonds.  The  outsides  of  two  French  rolls  are  grated  off,  the 
insides  cut  in  pieces,  soaked  one  hour  in  milk,  and  then  squeezed 
thoroughly  and  mixed  with  the  rest  of  the  mass.  Now  the  whole 
is  thoroughly  mixed,  the  whipped  whites  of  two  eggs  stirred  in, 
and  the  dough  put  into  a form  rubbed  with  butter  and  dusted  with 
roll  dust.  Either  bake  the  pudding  for  three-quarters  of  an  hour 
in  the  water-bath  or  bake  in  a small  porcelain  dish  for  one-half  of 
an  hour  in  an  oven.  Add  vanilla  or  wine  sauce.  If  necessary,  the 
almonds,  raisins,  and  grapes  may  be  omitted.  One  hundred  gm. 
equal  about  250  calories. 

7.  Tapioca  Pudding. — Thirty-five  gm.  of  tapioca  are  cooked  for 
five  to  seven  minutes  with  of  a liter  of  milk  until  it  turns  to  a 
thick  mush.  Meanwhile  stir  to  foam  twenty-five  gm.  of  butter ; 
add  yolks  of  two  eggs  and  one  small  tablespoonful  of  fine  sugar, 
and  stir  this  mass  into  the  no  longer  hot,  but  still  warm,  mush. 
After  rubbing  a small  porcelain  form  with  butter,  whip  the  whites 
of  two  eggs,  add,  and  mix  with  the  mass.  Put  into  the  form  and 
bake  the  pudding  in  a well-heated  oven  for  three-quarters  of  an 
hour.  One  hundred  gm.  equal  175  calories. 


278 


DIETETIC  KITCHEN. 


8.  Flour-mush  Pudding . — Melt  twenty  gm.  of  butter  in  a sauce- 
pan ; mix  in  smoothly  fifty  gm.  of  flour  and  of  a liter  of  milk,  and 
cook  the  mush  until  it  separates  from  the  pan.  Then  let  cool  a little, 
and  add  afterward  one  yolk  of  egg.  Now  stir  until  foamy  twenty 
gm.  of  butter,  to  which  add  yolks  of  two  eggs,  I ]/2  tablespoonfuls  of 
sugar  and  one  teaspoonful  of  arrack,  and  with  this  mass  mix  the 
cooked  mush  ; then  whip  the  whites  of  the  three  eggs,  mix  lightly 
with  the  mass,  fill  into  a form  rubbed  with  butter  and  dusted  with 
roll  dust,  and  let  cook  for  one  hour  in  the  water-bath.  One  hun- 
dred gm.  equal  about  220  calories. 

9.  Rice  Pudding. — Thirty-five  gm.  *of  finest  rice  is  soaked  the 
night  before,  as  in  the  case  of  rice  mush.  Heat  ^ of  a liter  of  milk, 
add  the  rice ; cover  and  cook  slowly  until  entirely  soft;  stir  25  gm. 
of  butter  to  foam,  add  two  yolks  of  eggs  and  one  tablespoonful  of 
sugar.  When  the  rice  has  become  lukewarm,  mix  in  the  other 
mass ; whip  two  whites  of  eggs,  put  the  dough  in  a porcelain  form 
rubbed  with  butter,  and  bake  in  an  oven  for  half  an  hour.  One 
hundred  gm.  equal  about  150  calories. 

10.  Biscuit  Pudding. — Five  yolks  of  eggs  are  stirred  for  half  an 
hour  with  of  a pound  of  fine  sugar  ; then  add  a small  table- 
spoonful of  fine  flour  and  a little  vanilla;  also  a little  arrack  and 
five  whipped  whites  of  eggs.  Rub  a pudding  form  with  butter 
and  dust  with  fine  roll  crumbs;  fill  in  the  mass  and  cook  for  one 
hour  in  the  water-bath.  One  hundred  gm.  equal  215  calories. 

1 1.  Noodle  Pudding. — Of  the  best  egg  noodles  (fine)  take  seventy 
gm.,  crumble  to  pieces,  throw  into  of  a liter  of  boiling  milk,  and 
boil  for  half  an  hour.  Meanwhile  stir  50  gm.  of  butter  until  foamy, 
add  three  yolks  of  eggs  and  about  one  tablespoonful  of  fine  sugar, 
and  mix  this  mass  with  the  half-cooled  mush.  At  last  whip  the 
whites  of  three  eggs,  mix  with  the  rest,  put  the  whole  in  a form 
rubbed  with  butter,  and  bake  the  pudding  for  one  hour  in  the  oven. 

12.  Omelette  Souffle. — Stir  the  yolk  of  an  egg,  with  one  table- 
spoonful of  fine  sugar,  for  a quarter  of  an  hour;  add  on  the  point 
of  a knife  a little  of  the  finest  flour,  one  tablespoonful  of  arrack, 
and  the  whipped  whites  of  eggs.  In  an  omelette  pan,  melt 
five  gm.  of  butter,  and  meanwhile  put  on  the  hearth  a porcelain 
soup  plate,  which  must  fit  the  pan  exactly,  and  heat  the  plate  well. 
Then  put  the  dough  in  the  pan  and  cover  this  immediately  with 
the  hot  plate.  Now  bake  the  omelette  with  a moderate  fire  until 
the  surface  has  become  solid,  which  requires  four  or  five  minutes ; 
then  turn  over  on  another  warmed  flat  plate ; then  fold  in  the  middle, 


MISCELLANEOUS  PREPARATIONS.  279 

strew  sugar  over,  and  serve  at  once.  The  whole,  about  240  calo- 
ries. 

13.  Souffle  Baked  in  the  Oven. — Stir  the  yolks  of  two  eggs,  with 
35  gm-  of  sugar,  for  a quarter  of  an  hour;  add  on  the  point  of  a 
knife  a little  fine  flour,  and  one  tablespoonful  of  arrack  and  the 
whipped  whites  of  two  eggs;  then  at  once  fill  the  dough  into  a 
porcelain  form  rubbed  with  butter,  and  bake  for  eight  to  ten  minutes 
in  the  oven.  The  whole,  about  370  calories. 

14.  Snowballs  in  Vanilla  Creme. — One  liter  of  milk,  with  one 
tablespoonful  of  fine  sugar,  mixed,  is  used  in  the  cooking.  The 
whites  of  four  eggs,  with  one  tablespoonful  of  sugar,  are  whipped 
until  stiff.  Then  from  the  whipped  eggs  longish  lumps  are  cut  out 
with  a tin  spoon  and  these  put  into  the  boiling  milk.  The  milk 
must  be  put  on  the  fire  in  a largo,  wide  can  so  that  the  snowballs 
may  expand.  One  must  never  put  more  than  six  in  the  pan  at 
one  time.  When  they  have  lain  one  minute  in  the  milk,  turn  them  ; 
let  them  lie  another  minute  on  the  other  side,  take  them  out  care- 
fully, and  lay  on  a large  platter.  After  the  whole  has  thus  been 
treated,  take  the  four  yolks  of  eggs,  mix  with  a teaspoonful  of  fine 
flour,  y of  a liter  of  milk,  and  a package  of  vanilla,  and  make  of 
them  a creme.  When  this  begins  to  boil  take  it  from  the  fire;  let 
it  cool,  and  just  before  serving  place  the  snowballs  upon  the  creme 
in  a porcelain  dish. 

VIII.  Miscellaneous. 

1.  Stewed  Apples. — Peel  good  apples,  cut  them  and  stew  with  a 
little  water  and  sugar,  according  to  taste  ; then  pass  through  a 
coarse  hair  sieve.  One  hundred  gm.  equal  about  seventy-five 
calories. 

2.  Pears. — Peel  good  pears,  cut  in  halves,  but  do  not  take  out 
seeds,  put  on  the  fire  with  plenty  of  water  and  a little  sugar,  and 
boil  until  soft;  a little  wine  added  will  improve  the  palatability. 

3.  Wine  Sauce  or  Chandeau. — Two  yolks  of  eggs  are  beaten  up 
in  a small  pan  with  y2  of  a teaspoonful  of  the  finest  potato 
flour;  then  slowly  stir  in  y of  a liter  of  good  wine  and  add  two  to 
three  tablespoonfuls  of  fine  sugar.  Put  on  the  fire  and  stir  until 
the  sauce  has  gained  a thick  consistency ; then  immediately  take 
from  the  fire  and  cover;  now  whip  two  whites  of  eggs,  and  pour 
the  sauce  into  this  slowly,  with  vigorous  stirring,  and  serve  at 
once.  Reckoning  the  value  in  calories  of  the  alcohol,  100  gm. 
equal  about  1 10  calories. 


28o 


DIETETIC  KITCHEN. 


4.  Vanilla  Sauce. — Mix  two  yolks  of  eggs  with  one  table- 
spoonful  of  fine  sugar,  add  ^ of  a liter  of  cold  milk,  a little  vanilla 
or  ]/2  of  a package  of  vanillin.  The  sauce  is  put  on  the  fire  and 
stirred  until  it  begins  to  thicken.  Then  take  from  the  fire  imme- 
diately and  serve.  One  hundred  gm.  equal  about  125  calories. 

5.  Aleuronat  Bread  ( according  to  Dr.  Huth , “ Aerztl.  Centralbl.,” 
August,  1894,  No.  46). — Mix  500  gm.  of  aleuronat  flour  and  1500 
gm.  of  rye  flour;  mix  one-half  of  this  mass  with  one  liter  of  warm 
water,  two  good  tablespoonfuls  of  salt,  and  180  gm.  of  yeast  finely 
divided  in  a little  water ; set  this  dough,  sprinkled  with  a little 
flour,  to  rise.  After  the  usual  rise  the  dough  is  worked  up  with 
the  remaining  flour  into  two  loaves.  These  are  baked  in  square 
pans  (10,  15,  20  cm.)  rubbed  with  butter;  after  letting  them  rise 
well  once  more,  they  are  baked  for  two  hours  with  strong  heat. 

6.  Nutritive  Enematci : 

(a)  Meat  Pancreas  Clyster  (according  to  Leube).- — One  hundred 
and  fifty  gm.  of  good  beef  are  scraped  and  then  chopped  fine  ; 50 
gm.  of  fresh  pancreatic  gland,  free  from  fat  (either  of  a cow  or  of  a 
hog),  are  mixed  with  this  and  stirred  carefully,  wdth  the  addition  of 
not  more  than  150  gm.  of  lukewarm  water.  Injections  of  from 
50  to  not  more  than  100  gm.  at  a time,  in  a lukewarm  state,  by 
means  of  a simple  funnel,  ending  in  a nozzle  which  must  have  a 
wide  opening.  The  mixture  will  keep  only  a short  while.  One 
hundred  gm.  equal  about  120  calories. 

( b ) Nutritive  Enema  (according  to  Ewald). — Two  or  three  eggs 
are  beaten  smooth  with  one  tablespoonful  of  cold  water  and  a little 
salt — as  much  as  can  be  held  on  the  point  of  a knife.  Wheaten 
starch,  as  much  as  can  be  held  on  the  point  of  a knife,  is  boiled 
with  y2  of  a cup  (100  gm.)  of  a 20  per  cent,  solution  of  grape  sugar 
and  one  wineglass  (150  gm.)  of  red  wine  added.  Then  the  solu- 
tion is  cooled  to  30°  R.,  and  the  eggs  are  stirred  in  slowly.  One 
can  add  also  one  teaspoonful  of  meat  peptone,  but  this  is  not 
absolutely  necessary.  Nutritive  clysters  are  to  be  injected  while  at 
blood  heat  and  in  quantities  of  250  gm.  at  a time.  Previously  the 
rectum  must  have  been  cleansed  by  a purgative  clyster.  The 
addition  of  grape  sugar  had  better  be  omitted,  since  through  it 
decomposition  and  irritations  of  the  intestines  arise  (Wegele).  It 
contains  about  400  calories.* 

*In  calculating  the  value  in  calories  of  the  nutritive  clysters  it  is  to  be  noted  that  the 
amount  of  resorption  is  difficult  to  determine,  since  it  depends  upon  the  state  of  the 
intestines,  the  skill  of  the  patient  in  retaining  the  enema,  etc.  It  is  therefore  well  to 
assume  only  one-half  as  resorbed. 


MISCELLANEOUS  PREPARATIONS. 


281 


( c ) Nutritive  Clyster  (according  to  Boas). — Warm  250  gm.  of 
milk,  stir  with  two  yolks  of  eggs,  one  teaspoonful  of  common 
salt,  and  one  tablespoonful  of  wheaten  starch,  and  afterward  add 
one  tablespoonful  of  red  wine.  If  the  mucous  membrane  of  the 
rectum  is  easily  irritated,  one  may  add  four  to  five  drops  of  tincture 
of  opium.  Such  clysters  may  be  administered  from  one  to  four 
times  in  twenty-four  hours  (heated  to  blood  heat),  with  a long,  soft, 
rectal  tube  and  a Heger’s  funnel.  Contains  about  four  hundred 
calories. 

(d)  Meat  Bouillon-wine  Clyster  (according  to  Fleiner). — This 
consists  of  eighty  gm.  of  beef-tea  and  forty  gm.  of  mild  white 
wine ; to  be  injected  two  or  three  times  a day  at  body-heat. 
According  to  Fleiner,  these  clysters  bring  sleep  to  weakened 
patients. 

7.  Alcoholic  Pancreas  Extract  ( according  to  Dr.  Reichmart). — A 
fresh  ox  pancreas  is  freed  from  fat  and  skin  immediately  after  kill- 
ing, chopped  up,  and  y2  of  a liter  of  12  to  15  per  cent,  alcohol  is 
poured  over.  Let  stand  two  to  three  days  in  a cool  place,  and 
filter.  One  wineglass  for  each  meal. 

The  following  is  a meat  food  recommended  in  the  absence  of 
secretion  of  hydrochloric  acid  : 

Meat  Dumplings  with  Sardelle  Dressing  ( according  to  Mrs.  J.  C. 
Hemmeter). — Take  ^ of  a cup  of  finely  scraped  beef,  ^ of  a cup 
of  lean  pork  ground  through  the  meat-chopper.  Add  salt  and  a 
small  amount  of  nutmeg;  2^3  ounces  of  butter  creamed,  yolks  of 
two  eggs  creamed  ; two  ounces  of  stale  bread  soaked  in  cold  water; 
after  it  is  softened  press  it  dry  and  add  to  the  meat ; then  add  the 
beaten  white  of  two  eggs  and  mix  all  thoroughly.  Turn  into 
thirty  dumplings  and  boil  for  five  minutes. 

Dressing. — Take  one  cup  of  beef  bouillon,  add  four  sardelles 
scraped  fine,  the  juice  of  ^ of  a lemon  and  boil  this  for  ten  min- 
utes. Thereafter  add  y2  of  a glass  of  white  wine,  one  teaspoonful 
of  cornstarch,  lastly  the  yolks  of  two  eggs  stirred  in  a little  water  ; 
then  strain  and  pour  over  the  dumplings.  Serve  only  in  a covered 
tureen. 

Gelatin  Cream  [according  to  Mrs.  J.  C.  Hemmeter)  for  Anacidity 
Without  Symptoms  of  Stagnation. — Juice  of  two  oranges  and  one 
lemon  (a  little  flavor  of  vanilla  extract  may  be  added  if  made  for 
the  healthy),  y of  a pound  of  sugar  ; stir  well  and  then  add  one 
pint  of  cream  and  beat  until  thick.  Dissolve  y2  of  a box  of  gelatin 
in  y2  of  a pint  of  cold  water;  heat  very  gradually  until  all  is  thin 
19 


282 


REST  AND  EXERCISE  OF  THE  STOMACH. 


and  dissolved.  When  cool  add  the  cream,  and  beat  until  it  is  stiff. 
May  be  poured  into  a mold  and  given  any  shape.* 


THE  USE  AND  ABUSE  OF  REST  AND  EXERCISE  FOR  THE 
DIGESTIVE  ORGANS. 

In  this  connection  we  may  consider  rest  and  exercise  before  and 
after  meals  in  reference  to  the  entire  body,  and  rest  and  exercise  as 
applicable  to  the  stomach  and  intestines  only.  Bodily  exercise 
increases  metabolism  and  therefore  the  appetite,  and  gives  rise  to  a 
greater  demand  for  food,  but  when  it  is  carried  too  far,  as  in  the 
overtrained  athlete,  fatigue  may  ensue  and  the  appetite  disappear 
entirely.  Concerning  the  frequent  question  whether  one  should 
sleep  after  taking  meals  or  not,  or  take  exercise,  much  diversity 
of  opinion  exists.  The  edict  of  the  Medical  School  of  Salermo 
was  : “ Post  coenam  stabis  aut  passus  mille  meabis,”  which  the 
Germans  have  translated  as  follows  : “ Nach  dem  Essen  sollst 

du  stehn  oder  tausend  Schritte  gehn  ” (“  After  eating  thou  shalt 
stand  or  walk  1000  steps  ”).  This  question  is  not  easy  to  decide 
either  way,  for  sleep  reduces  the  peristaltic  energy  of  the  stomach, 
and  thereby  reduces  the  rate  of  digestion.  A healthy  person 
during  sleep  is  robbed  of  the  impetus  which  deep  breathing 
imparts  to  the  stomach  by  descent  of  the  diaphragm. 

For  most  digestive  sufferers,  however,  all  bodily  exercise,  even 
moderate  movements  following  immediately  on  large  meals,  con- 
stitutes more  or  less  of  a torment.  In  all  conditions  of  gastric 
atony  and  myasthenia  bodily  rest  is  indispensable,  because  the 
stomach  empties  itself  easier  in  the  reclining  position.  Excepting 
in  conditions  of  pronounced  obesity  and  arteriosclerosis,  I gener- 
ally permit  an  hour  of  sleep  after  the  larger  meals  in  all  dyspeptic 
diseases.  Blood  pressure  is  increased  during  the  digestive  act,  and 
for  that  reason  sleep  in  a horizontal  position  is  preferably  avoided 
in  the  two  conditions  which  I have  excluded.  Physical  exertion, 
bathing,  or  training  immediately  after  meals  is  not  to  be  advised, 
because  it  may  exert  undue  pressure  upon  the  stomach,  and  divert 
the  blood  which  this  organ  requires  to  the  overactive  muscles. 
Reading  or  writing  after  meals  may  be  harmful  for  three  reasons  : 


* The  author  is  greatly  indebted  to  Mrs.  J.  C.  Hemmeter  for  compiling  and  testing 
many  of  the  most  important  recipes  in  the  “ Dietetic  Kitchen.” 


THERAPY  OF  REST  AND  EXERCISE.  283 

1.  Because  it  compels  a wrong  position  of  the  body,  inclining 
it  too  much  forward. 

2.  Because  of  possible  compression  of  the  region  of  the  stomach, 
due  to  cramped  position  or  to  pressing  against  the  edge  of  the 
table. 

3.  Because  of  mental  exertion. 

All  psychic  or  emotional  excitement  immediately  before,  during, 
or  after  meals  is  harmful,  and  it  is  best  not  to  eat  at  all,  if  the  mind 
is  occupied  with  some  distressing  thought.  All  gastric  sufferers  in 
whom  neurasthenia  is  a factor  should  rest  after  meals,  and  those 
with  pronounced  neurasthenia  should  be  permitted  to  sleep,  for 
during  sleep  nervous  energy  accumulates  and  this  may  aid  in 
restoring  the  lost  digestive  power.  In  all  patients  with  motor 
insufficiency  of  the  first  degree  I prefer  to  order  sleep  after  meals. 
In  the  second  and  third  degrees  of  this  mechanical  defect  rest  in 
bed  becomes  imperative.  All  anatomical  diseases  of  the  stomach 
require  rest,  and  in  ulcer,  cancer,  and  acute  gastritis  rest  is  a “ sine 
qua  non.” 

Mental  Rest. — A large  number  of  men  of  high  intellectual  ca- 
pacity are  gastric  sufferers.  This  comes  from  the  universal  abuse 
of  the  mental  energies  contemporaneous  with  overtaxing  the  di- 
gestive organ.  The  cerebral  rest  during  and  after  meals  is  more 
imperative  than  muscular  rest.  Dyspeptics  ought  not  to  read  their 
mail  or  papers  before  meals,  lest  some  emotional  news  be  imparted, 
reducing  the  appetite  of  these  impressionable  patients.  Many 
gastric  atonies  are  fundamentally  caused  by  an  overwrought  ner- 
vous system.  This  one,  almost  universal,  modern,  bad  habit  of 
overtaxing  the  brain  and  nerves  is  a more  dangerous  and  frequent 
cause,  lying  unknown  and  unrecognized  at  the  foundation  of 
many  incipient  gastric  diseases,  than  all  others  put  together. 

Dietetic  Exercise. — Some  forms  of  gastric  disease  do  not  re- 
quire any  extraordinary  amount  of  rest.  It  is  not  very  easy  to 
define,  exactly,  in  just  which  cases  exercise  of  the  stomach  is  re- 
quired (as  by  administration  of  carefully  adapted  diet),  and  which 
cases  require  comparative  rest.  There  is  a form  of  chronic  gastritis, 
of  very  slow  progression,  in  which  there  is  a slow  atrophy  of  the 
oxyntic  and  ferment  cells  in  the  peptic  ducts.  I have  watched 
cases  of  this  type  off  and  on  for  twelve  years,  and  have  learned 
by  experience  that  a sparing  diet  and  too  much  rest  favors  the 
progress  of  the  atrophy,  whereas  a proportionate  amount  of  food 
to  keep  up  the  caloric  equilibrium  will  keep  the  peptic  cells  at 


284 


DIETETIC  GYMNASTICS. 


work;  for  work  in  this  case  means  growth  and  sustenance  to 
the  histological  elements  of  the  gastric  mucosa.  It  is  a mistake 
in  those  cases  to  level  down  the  diet  to  the  digestive  capacity  of 
the  stomach.  It  should  rather  be  leveled  up,  until  the  digestion 
can  effectually  deal  with  the  amount  of  food  required  to  maintain 
the  nitrogen  balance.  It  would  be  just  as  fatal  a mistake  to  treat 
such  a stomach  by  repose  (few  and  small  meals  requiring  little 
digestive  work)  as  it  would  be  to  treat  a mitral  regurgitation 
with  relaxed  ventricular  walls  by  absolute  repose  and  exclusion  of 
exercise.  The  modern  conception  of  heart  disease  teaches  that  the 
stronger  the  ventricular  wall  can  be  developed,  the  sooner  we  can 
bring  on  a muscular  hypertrophy,  the  more  effectively  will  com- 
pensation be  established  and  the  patient  have  comparative  free- 
dom from  the  consequences  of  his  valvular  insufficiency  (Schott- 
Nauheim  treatment  for  heart  diseases).  The  forms  of  chronic  gas- 
tritis that  I refer  to  are  always  associated  with  a good  motility,  so 
that  there  is  no  stagnation  or  retention  of  food  at  any  time.  In 
purely  nervous  anorexia  the  appetite  can  be  restored  more  effec- 
tively by  feeding;  in  fact,  if  the  disease  is  persistent  and  expresses 
itself  by  absolute  refusal  of  food,  it  had  best  be  treated  by  forced 
feeding.  (See  p.  190.)  In  hyperesthesia  and  achylia  gastrica 
dietetic  gymnastics,  when  scientifically  employed  in  the  manner 
described,  are  sometimes  more  beneficial  than  indiscriminate  rest. 
In  all  cases  where  the  tonicity  of  the  gastric  muscularis  is  re- 
duced, and  in  cases  of  gastroptosis  and  vertical  position  of  the 
stomach  the  meals  should  be  small  in  quantity  and  all  bodily 
movements  after  the  meals  must  be  avoided.  Kussmaul  (S. 
Fleiner,  “ Samml.  klin.  Vortr.,”  Neue  Folge,  No.  103)  has  called 
attention  to  the  fact  that  large  meals  and  abundant  ingestion 
of  liquids,  when  such  abnormalities  of  position  and  size  of  the 
stomach  exist,  may  cause  a transient  mechanical  obstruction  of 
the  duodenum.  This  occurs  particularly  if  exercise  is  taken  after 
the  meals  and  the  body  kept  in  an  erect  position,  which  causes  a 
stretching  and  dragging  of  the  greater  curvature.  The  heavily 
loaded  pyloric  portion  of  the  stomach  sinks  and  drags  along  the 
movable  first  portion  of  the  duodenum,  but  at  the  place  where  the 
duodenum  is  rigidly  fixed  to  the  spinal  column  the  bowel  becomes 
kinked  off.  (See  Anatomy  of  Duodenum,  p.  39.) 

Therefore,  in  all  forms  of  dilatation  and  abnormal  positions  of 
the  stomach,  physical  rest  of  the  body  after  meals,  and  as  much 


AMERICANS  EAT  TOO  MUCH.  285 

physiological  rest  of  the  stomach  as  can  be  consistently  given,  is 
imperative.* 

The  most  explicit  recent  exposition  of  the  physiological  action 
of  rest  to  the  digestive  organs  and  the  prolonged  substitution  of 
exclusive  rectal  alimentation  for  gastric  alimentation,  is  found  in 
a book,  by  Dr.  A.  P.  Gros  (“  Traitement  de  Certaines  Maladies  de 
LEstomac  par  la  Cure  de  Repos  Absolu  et  Prolonge  de  L Estomac 
Avec  Alimentation  Rectale  Exclusive ,”  Paris,  1898).  This  valuable 
book  contains  a complete  history  of  rectal  feeding  for  the  treat- 
ment of  gastric  diseases;  the  technics  and  the  indications  for 
such  treatment  and  an  exhaustive  bibliography  of  the  subject 
extending  over  nine  pages.  Dr.  Gros  has  employed  this  rest 
treatment  not  only  in  ulcer  of  the  stomach  with  and  without 
hematemesis,  but  also  in  hypersecretion,  in  hyperacidity  of  long 
standing,  in  gastric  catarrh  with  nervous  anorexia,  in  the  vomiting 
of  pregnancy,  and  in  the  stenoses  of  pylorus  of  diverse  origin. 

From  a great  many  observations  which  I have  made  on  persons 
living  at  hotels,  etc.,  I have  concluded,  by  approximate  determina- 
tion of  the  amount  of  calories  contained  in  their  daily  food,  that 
the  average  American  in  the  better  classes  of  life  eats  entirely  too 
much.  Of  course,  it  was  possible  to  get  at  the  caloric  value  of  the 
food  only  approximately,  but  allowing  the  widest  margin  for  possible 
sources  of  error,  I found  that  the  average  number  of  calories  rep- 
resented in  the  food  taken  was  four  thousand  and  forty  per  day 
for  the  average  adult  observed.  This,  of  course,  represents  only 
the  classes  of  individuals  who  can  live  at  hotels  of  the  better 
standard.  As  the  amount  of  caloric  energy  required  for  a man  of 
moderate  muscular  work  is  only  thirty-five  hundred,  the  excess  of 
food  taken  is  very  evident.  When  sickness  comes  on,  the  common 
error  is  frequently  made  to  introduce  more  food  if  possible  than  in 
health,  on  the  supposition  that  the  weakened  body  requires 
strengthening.  This  excess  of  good  food  and  wine  in  our  modern 
treatment  of  disease  is  as  pernicious  as  the  bleeding,  vomiting, 
purging,  and  sweating  of  our  medical  ancestors. 

In  an  interesting  little  book,  by  Dr.  Dewey,  of  Meadville,  Pa., 
entitled  “The  True  Science  of  Living”  (Henry  Bill  Publishing 


* The  value  of  rest  to  the  stomach  and  rest  to  the  body  in  diseases  of  the  digestive 
organs  is  forcibly  set  forth  in  a contribution  by  Dr.  C.  D.  Spivalc  (“  Rest — A Neglected 
Factor  in  the  Treatment  of  Gastro-intestinal  Disorder,”  “The  Journal  of  the  American 
Medical  Association,”  July  30,  1897). 


286 


TWO  MEALS  A DAY. 


Company,  London,  1895),  it  is  advised  that  temporary  complete 
starvation  until  there  is  once  more  a healthy  appetite  is  the  best 
cure  for  a host  of  dyspepsias,  debilities,  bodily  and  mental  depres- 
sions, headaches,  etc.,  and  that  for  similar  less  severe  disturbances 
of  nutrition  the  great  remedy  is  to  leave  out  the  breakfast,  so  as  to 
give  the  stomach  a long  rest  of  sixteen  hours  or  more,  with  the 
object  of  allowing  it  to  recuperate  and  accumulate  secretory  energy 
after  the  last  meal  of  the  previous  day.  One  can  not  fail  to  be  im- 
pressed with  the  force  of  Dr.  Dewey’s  logic  and  the  correctness  of 
his  main  contention.  I have  frequently  put  this  matter  to  a test 
in  private  practice,  but  instead  of  omitting  the  breakfast  I advise 
excluding  the  supper.  The  breakfast  is  taken  at  8 a.  m.  and  the 
dinner  at  2 p.  m.  This  was  preferred  because  a large  number  of  my 
patients  were  hard-worked  business  men  and  it  was  considered  in- 
expedient to  permit  them  to  go  the  entire  morning  on  an  empty 
stomach.  Six  hours  after  the  dinner,  between  8 and  9 p.  m.,  I order 
the  stomach  thoroughly  washed  out,  and  the  patient  retires  on 
a perfectly  empty  clean  stomach,  and  the  organ  is  given  twelve 
hours  of  absolute  rest  to  store  up  its  physiological  energy. 

Curiously  enough,  the  quantity  of  food  taken,  when  only  two 
meals  a day  are  allowed  in  this  manner,  is  often  somewhat  increased 
beyond  the  amount  which  was  hitherto  taken  in  three  meals. 
Digestion  is  more  perfect,  the  appetite  is  keener,  nutrition  is  stimu- 
lated. On  the  recommendation  of  Alexander  Haig  (“  Uric  Acid 
as  a Causation  of  Disease,  ” fourth  edition,  London,  1897,  p.  628), 
who  found  this  plan  a most  powerful  stimulant  to  digestion  and 
nutrition,  I made  a thorough  trial  of  Dr.  Dewey’s  suggestion  on 
my  own  person,  with  the  result  that  at  present  I still  carry  out 
the  two-meal-per-day  plan. 

Resting  the  stomach  will  enable  it  to  do  much  better  work  and 
leads  to  a keen  hunger  otherwise  unknown.  Haig  concludes  that 
if  anything  will  demonstrate  the  insane  folly  of  stuffing  a dyspep- 
tic stomach  with  fresh  food  every  three  or  four  hours,  an  experi- 
ence of  this  kind  ought  to  do  it,  and  I can  confirm  his  suggestion 
that  almost  the  only  danger  attendant  on  taking  two  meals  a day, 
in  place  of  three  or  four,  is  that  of  overeating.  The  two-meal-a- 
day  plan  is  one  of  the  most  effective  means  of  combatting  intes- 
tinal flatus  which  arises  from  undigested  residues.  It  is  quite 
possible  for  a man  to  be  better  nourished  on  a little  food  eaten 
slowly  and  well  mixed  with  saliva  than  on  a great  deal  of  food 
eaten  very  quickly.  I have  seen  a number  of  cases  where  persons 


DIETETICS  OF  ALCOHOL. 


287 


seemed  undernourished  on  three  to  four  meals  a day  who  gained 
weight  and  showed  a better  appetite,  and  no  undigestible  residues 
in  the  stools  when  but  two  meals  a day  were  allowed.  It  is  quite 
conceivable  that  persons  may  be  in  a state  of  starvation,  not  from 
any  want  of  food,  but  from  the  fact  that  the  digestive  capacity  is 
constantly  overpowered  by  excess  of  food.  The  so-called  uric-acid- 
free  diet,  which  Haig  urgently  recommends  in  form  of  a diet  con- 
sisting almost  exclusively  from  substances  derived  from  the  vege- 
table kingdom,  is,  in  my  experience,  not  universally  applicable  to 
digestive  diseases.  It  should,  however,  be  more  employed  than  it 
has  been  hitherto,  particularly  in  those  stomach  affections  asso- 
ciated with  hyperacidity.  In  the  beginning  no  surprising  bene- 
ficial results  may  be  evident,  but  the  success  of  the  treatment 
depends  on  the  persistency  with  which  it  is  carried  out.  Haig 
permits  the  use  of  milk,  butter,  and  cheese,  but  forbids  meats  of 
any  kind. 


CHAPTER  III. 

THE  DIETETICS  OF  ALCOHOL  AND  ALCOHOLIC 
BEVERAGES. 

The  literature  on  the  subject  of  the  physiological  action  and  the 
metabolic  and  dietetic  influences  of  alcohol  is  very  extensive.  Its 
abnormal  growth  appears  to  those  who  make  an  effort  to  keep 
abreast  of  the  progress  and  advancement  of  experimental  thera- 
peutics, out  of  all  proportion  to  any  real  increase  in  our  knowledge 
of  the  subject.  We  are  directly  concerned  only  with  the  (1)  value 
(if  any)  of  alcohol  as  a food;  (2)  as  a tonic  and  stimulant;  (3)  its 
effects  upon  the  digestive  functions.  The  use  of  alcohol  in  any 
shape  is  wholly  unnecessary  for  the  use  of  the  human  organism 
in  health.  A large  number  of  persons  prolong  their  lives  by 
total  abstinence.  This  should  be  so  stated  with  emphasis,  since 
there  are  so  many  who  imagine  it  is  indispensable,  when  in 
reality  they  are  injured  by  it.  The  effects  of  alcohol  on  other 
organs  than  the  stomach  are  very  important ; but  we  must  refer 
to  the  literature  on  the  special  experiments  : For  the  influence 


288 


DIETETICS  OF  ALCOHOLIC  BEVERAGES. 


of  C2H60  on  the  heart,  see  J.  C.  Hemmeter,  “ The  Comparative 
Physiological  Effects  of  the  Ethylic  Alcohol  Series  on  the 
Isolated  Mammalian  Heart”  (in  “Studies  from  the  Biological 
Laboratory  of  the  Johns  Hopkins  University,”  vol.  iv,  No.  5). 
On  the  value  of  alcohol  on  various  body  functions,,  see  Gilman 
Thompson,  “ Dietetics,”  pages  205  to  232  ; Binz,  “ Pharma- 
kologie”;  Schmiedeberg,  “ Arzneimittellehre.”  The  literature  on 
the  effect  of  alcohol  on  the  functions  of  the  stomach  can  be 
found  in  the  text-books  of  Riegel,  Boas,  Ewald,  Wegele,  Pen- 
zoldt  (vol.  iv  of  “ Handbuch  d.  Therapie  ”),  Munk,and  Uffelmann. 
The  literature  is  too  great  and  the  results  are  too  uncertain  to 
permit  of  any  resume  to  be  given  here.  The  question  arises, 
“ Why  do  we  give  alcohol  in  gastric  therapeutics  ? Is  it  a food  or 
merely  a stimulant  ? In  doses  taken  ordinarily  with  the  more 
common  beverages  does  it  facilitate  or  retard  digestion  ? ” Most 
of  the  text-books  mentioned  take  the  stand  that  as  alcohol  is 
oxidized  in  the  body  it  furnishes  a considerable  amount  of  energy. 

The  question  whether  alcohol  is  a true  food-stuff,  capable  of 
serving  as  a direct  source  of  energy  and  of  replacing  a correspond- 
ing amount  of  fats  or  of  carbohydrates  in  the  daily  diet,  is  a 
matter  of  controversy.  Reichert  (“Therapeutic  Gazette,”  Feb.  15, 
1890)  concludes  that  moderate  doses  of  alcohol  do  not  affect  the 
total  amount  of  heat  produced  in  the  body  of  a dog.  As  it  is 
nearly  completely  oxidized  in  the  body,  and  gives  off  considerable 
heat  in  the  process,  the  fact  that  the  total  heat  production  remains 
unaltered  indicates  that  the  oxidation  of  alcohol  protects  an  isody- 
namic amount  of  food-materials  in  the  body  from  consumption, 
thus  acting  as  a food-stuff  capable  of  replacing  other  elements  of  the 
food.  Opposed  diametrically  to  these  results  are  those  of  Miura 
(“  Zeitschr.  f.  klin.  Medicin,”  1892,  vol.  xx,  p.  137),  whose  obser- 
vations were  made  on  his  own  metabolism,  after  he  had  brought 
himself  into  a condition  of  nitrogen  equilibrium  upon  a mixed 
diet.  Then  for  a time  a portion  of  the  carbohydrates  was  omitted, 
and  its  place  substituted  by  an  isodynamic  amount  of  alcohol.  The 
result  was  a loss  of  proteid  from  the  body,  proving  that  the  alcohol 
had  not  protected  the  proteid  tissue  as  it  should  have  done  if  it 
acts  as  a food.  In  a third  period  the  old  diet  was  resumed,  and 
after  nitrogen  equilibrium  had  again  been  established,  the  same 
proportion  of  carbohydrates  was  omitted  from  the  diet,  but  alco- 
hol was  not  substituted. 

When  the  diet  was  poor  in  proteid,  it  was  found  that  less  proteid 


EFFECT  OF  ALCOHOL  ON  METABOLISM. 


289 


was  lost  from  the  body  when  alcohol  was  omitted  than  when  it 
was  used,  indicating  that  so  far  from  protecting  the  tissues  of  the 
body  by  its  oxidation,  the  alcohol  exercised  a directly  injurious 
effect  upon  proteid  consumption.  Recent  experimental  investiga- 
tions (Rosemann,  “ Ueber  d.  Einfluss  des  Alkohols  auf  den  mensch- 
lichen  Stoffwechsel,”  “ Zeitschr.  f.  Diatet.  u.  physikal.  Therapie,” 
von  Leyden  u.  Goldscheider,  Bd.  1,  p.  138)  confirm  Miura’s  results, 
namely,  that  alcohol  is  no  proteid  saver,  but  protects  the  fats  from 
consumption.  Further  researches  will  have  to  show  whether  and 
how  it  protects  the  oxidization  of  non-nitrogenous  constituents  of 
the  body — the  fats. 

Professor  W.  O.  Atwater,  from  experiments  on  the  effect  of  alco- 
hol on  metabolism,  conducted  in  a thoroughly  scientific  and  sys- 
tematic manner  at  the  Wesleyan  University,  concludes  : 

1.  The  alcohol  is  oxidized — that  is,  burned — as  completely  as 
bread,  meat,  or  any  other  food. 

2.  In  the  oxidation  all  the  potential  energy  of  the  alcohol  was 
transformed  into  heat  and  muscular  power.  In  other  words,  the 
body  made  the  same  use  of  the  energy  of  the  alcohol  as  of  that 
of  sugar,  starch,  and  other  ordinary  food  materials. 

3.  The  alcohol  protected  the  material  of  the  body  from  consump- 
tion just  as  effectively  as  the  corresponding  amounts  of  sugar  and 
starch — that  is  to  say,  whether  the  body  was  at  rest  or  at  work,  it 
held  its  own  just  as  well  with  the  one  as  with  the  other. 

According  to  Atwater,  alcohol  is  not  a tissue  builder,  but  it  can 
and  does  serve  as  fuel.  The  amount  used  in  his  experiments  per 
day  was  equal  to  about  2 y2  ounces  of  absolute  alcohol — about  as 
much  as  would  be  contained  in  five  or  six  ounces  of  whisky  or  in 
a quart  of  claret  or  Rhine  wine.  (Extract  from  “ Report  to  Mid- 
dletown (Conn.)  Scientific  Assoc.”;  the  experiments  have  not  yet 
been  published.) 

It  is  emphasized  that  alcohol  is  not  a desirable  food  for  common 
use ; for  in  saving  the  non-nitrogenous  bodies  (the  fats)  from  con- 
sumption— an  observation  which  agrees  well  with  the  practical 
experiences  concerning  the  habitual  use  of  alcohol — it  is  very 
probable  that  alcohol  acts  as  a weak  protoplasmic-  poison.  Miura 
( loc . cit.)  has  already  suggested  such  an  influence;  also  Romeyn  (see 
Maly’s  “ Yahresbericht  d.  Thierchemie,”  1887,  p.  400),  Stammreich 
(“  Inaug.  Dissert.,”  Berlin,  91),  and  A.  Schmidt  (“  Centralbl.  f.  d. 
Med.  Wiss.,”  1875,  No.  23).  The  work  of  these  four  experimenters 
showed  an  increased  albumin  breakdown,  which  in  Miura  and 


290 


DIETETICS  OF  ALCOHOLIC  BEVERAGES. 


Stammreich’s  observations  continued  for  two  days  after  the  use  of 
alcohol  had  been  stopped.  The  results  of  Atwater  do  not  support 
the  assumption  that  alcohol  may  be  used  as  a food  ; they  indicate 
that  it  protects  the  oxidation  of  the  fats.  Saving  the  fats  from 
consumption,  even  if  it  could  be  accomplished  without  injurious 
collateral  effects,  is,  from  a therapeutic  standpoint,  only  very  rarely 
desirable  (emaciation,  tuberculosis).  But  if  it  is  accompanied  by 
increased  destruction  of  the  proteids  of  the  body,  then  alcohol  is 
not  a dietetic  aid  for  the  advancement  of  nutrition. 

Therapeutically,  there  is  still  conceded  to  alcohol  a stimulating 
and  an  antipyretic  influence. 

Concerning  the  effects  of  moderate  amounts  of  alcohol  on  diges- 
tion by  pepsin-hydrochloric  acid,  and  on  salivary  and  pancreatic 
digestion,  we  believe  the  following  abstract  of  Chittenden  and 
Mendel’s  experiments  (“  American  Journal  of  Medical  Sciences,” 
January  to  April,  1896)  to  be  a clear  representation  of  this  matter: 

One  can  not  define  with  mathematical  exactness  the  action  of  a 
given  percentage  of  absolute  alcohol  on  pepsin  proteolysis,  since 
variation  in  the  attendant  conditions,  i.  e.,  the  relative  amounts  of 
pepsin,  acid,  and  proteid,  together  with  the  period  of  digestion,  the 
digestibility  of  the  particular  proteid,  etc.,  are  prone  to  modify  the 
final  result.  Thus,  with  a weak  gastric  juice,  where  the  amount  of 
ferment  present  is  small,  and  digestive  action  consequently  slow, 
or  where  the  proteid  material  used  is  difficult  of  digestion,  the  re- 
tarding effect  of  a given  percentage  of  alcohol  is  far  greater  than 
when  the  digestive  fluid  is  more  active  ; that  is,  when  it  contains 
more  pepsin.  Further,  this  difference  of  action  is  more  pronounced 
the  larger  the  percentage  of  alcohol  present.  The  following  gen- 
eral conclusions  were  drawn  from  artificial  digestive  mixtures. 

First.  It  is  plainly  manifest  that  in  the  presence  of  small  amounts 
of  alcohol  (one  to  two  per  cent,  of  absolute  alcohol)  gastric  diges- 
tion may  proceed  as  well  or  even  better  than  under  normal  circum- 
stances. In  fact,  many  of  their  experiments  show  a slight  increase 
in  digestive  power  when  the  mixture  contained  one  or  two  per 
cent,  of  absolute  alcohol.  This  increased  digestive  action,  though 
slight,  occurred  too  frequently  to  be  the  result  of  mere  accident, 
and  apparently  indicates  a tendency  for  alcohol,  when  present 
in  small  quantity,  to  slightly  increase  the  digestive  action  of 
pepsin-hydrochloric  acid;  or,  in  other  words,  to  stimulate  the 
ferment  so  that  it  can  accomplish  somewhat  more  than  it  other- 
wise could  do.  As  the  percentage  of  alcohol  is  raised,  retardation 


ACTION  OF  ALCOHOL  ON  PANCREATIC  DIGESTION.  29 1 

or  inhibition  becomes  more  noticeable,  although  ordinarily  it  is  not 
very  pronounced  until  the  digestive  mixture  contains  five  to  ten 
per  cent,  of  absolute  alcohol.  With  15  to  18  per  cent,  of  absolute 
alcohol  digestive  action  may  be  reduced  one-quarter,  or  even  one- 
third  ; the  exact  amount  of  retardation,  however,  being  especially 
dependent  upon  the  activity  of  the  gastric  juice  and  upon  the 
natural  digestibility  of  the  proteid  material.  It  is  to  be  remem- 
bered, however,  that  18  per  cent,  of  absolute  alcohol  would  be 
equivalent  to  36  per  cent,  of  proof-spirit;  so  that,  if  we  could 
assume  the  contents  of  the  human  stomach  at  a given  period  to 
contain  one-third  proof-spirit,  it  might  perhaps  be  considered  that 
digestive  action  would  be  retarded  to  the  extent  of  25  to  35  per 
cent.,  provided  the  gastric  juice  present  in  the  stomach  was  of 
fair  strength  and  the  proteid  matter  of  ordinary  digestibility. 
Such  percentages  of  proof-spirit,  however,  are  not  likely  to  be 
long  present  in  the  stomach,  and  it  is  perhaps  idle  to  speculate  on 
such  hypothetical  cases.  We  may  in  this  connection,  however, 
again  emphasize  the  fact  that  the  stronger  the  gastric  juice  and  the 
more  digestible  the  proteid  food  undergoing  digestion,  the  less  re- 
tardation will  a given  percentage  of  alcohol  produce ; while,  on 
the  other  hand,  the  weaker  the  gastric  juice  and  the  more  indi- 
gestible the  proteid,  the  greater  will  be  the  inhibition  caused  by  a 
given  percentage  of  alcohol.  In  other  words,  those  variations 
which  must  naturally  exist  in  the  stomach  contents  of  different  in- 
dividuals, both  in  health  and  disease,  will  lead  to  different  degrees 
of  retardation  in  the  presence  of  given  percentages  of  absolute 
alcohol.  It  would,  therefore,  be  unwise  to  make  a general  specific 
statement  regarding  the  action  of  a given  percentage  of  alcohol. 
Under  definite  conditions,  however,  as  Chittenden’s  experiments 
plainly  show,  the  presence  of  a definite  amount  of  alcohol  always 
leads  to  essentially  the  same  results. 

In  order  to  prevent  any  misinterpretation  of  these  results,  we 
would  again  call  attention  to  the  fact  that  we  are  dealing  here  with 
only  one  of  the  four  questions  that  need  to  be  answered  before  we 
can  hope  to  fully  understand  the  influence  of  alcohol  on  gastric 
digestion  as  a whole.  Thus,  the  results  afford  plain  evidence  of 
the  influence  of  alcohol  on  the  digestive  or  solvent  power  of  the 
gastric  juice  ; but  we  should  not  be  justified  in  arguing  that  exactly 
the  same  results  would  follow  from  the  introduction  of  alcohol  into 
the  living  stomach.  The  action  of  a given  percentage  of  alcohol 
on  proteolysis  alone  would  be  essentially  the  same  in  the  stomach 


292 


DIETETICS  OF  ALCOHOLIC  BEVERAGES. 


as  in  a beaker,  provided  the  alcohol  was  not  absorbed  into  the 
blood  and  thus  removed  from  contact  with  the  digestive  mixture, 
and  provided  it  did  not  exert  any  influence  on  the  character  of  the 
gastric  juice  secreted.  But  it  is  easily  conceivable  that  a percent- 
age of  alcohol  which  does  not  interfere  with  solution  of  the  proteid 
food-stuffs  may  so  modify  the  amount  or  character  of  the  secretion 
that  digestion  might  be  greatly  stimulated  or  greatly  retarded. 
Further,  as  already  stated,  the  presence  of  alcohol  in  the  stomach 
may  so  affect  absorption  and  peristalsis  that  the  rate  of  digestion 
may  be  modified  from  this  cause  ; hence  the  results  above  recorded 
are  to  be  used  only  in  drawing  conclusions  as  to  the  effect  of  vari- 
ous percentages  of  alcohol  on  the  purely  chemical  process  of  gastric 
digestion,  i.  e .,  on  pepsin-proteolysis. 

In  conclusion,  it  is  to  be  noted  that  Chittenden’s  results  are 
more  or  less  in  accord  with  what  has  been  previously  published 
concerning  the  action  of  alcohol  on  gastric  digestion.  Thus, 
Bikfalvi  found,  in  artificial  digestive  experiments,  that  alcohol,  even 
in  small  quantities,  retards  normal  gastric  digestion.  Klikowicz 
found  that  the  presence  of  five  per  cent,  of  alcohol  in  the  digestion 
of  egg-  and  serum-albumin  led  to  somewhat  variable  results, 
although,  as  a rule,  there  was  an  indication  of  a slight  stimulation 
of  proteolytic  action.  In  the  presence  of  ten  per  cent,  of  alcohol 
there  was  always  marked  retardation,  while  fifteen,  twenty,  and 
thirty  per  cent,  of  alcohol  checked  digestion  to  a marked  degree. 

Roberts  found,  by  artificial-digestion  experiments,  that  in  the 
presence  of  less  than  ten  per  cent,  of  proof-spirit  there  was  no 
appreciable  retardation.  With  ten  per  cent.,  retardation  was  only 
barely  detectable.  With  twenty  per  cent,  there  was  quite  distinct 
but  still  only  a slight  retardation.  Above  this  point,  however,  the 
inhibitory  effect  of  alcohol  increased  rapidly.  (Refer  to  the  tables 
of  Roberts  at  the  end  of  this  chapter.)  That  the  action  of  a digestive 
ferment  may  be  both  stimulated  and  retarded  by  the  same  sub- 
stance, according  to  the  quantity  present,  has  been  already  demon- 
strated ; hence  there  is  no  inconsistency  in  the  above  results  with 
alcohol.  The  same  action  has  likewise  been  observed  with  yeast- 
cells. 

Action  of  Alcohol  on  Pancreatic  Digestion. — In  view  of  the 
position  which  pancreatic  digestion  occupies  in  the  digestive  proc- 
ess, it  is  readily  seen  that  it  is  more  desirable  to  ascertain  the 
influence  of  small  quantities  of  alcoholic  liquors  than  large 
amounts,  since  absorption  must  naturally  lead  to  a decided  dimi- 


EFFECT  OF  ALCOHOL  ON  ABSORPTION. 


293 


nution  of  alcohol  before  it  can  normally  become  mixed  with  the 
pancreatic  juice  and  partially  digested  food-material  in  the  small 
intestine.  Hence,  more  stress  was,  as  a rule,  laid  upon  the  influence 
of  small  percentages  of  the  various  fluids  experimented  with,  and 
only  occasionally  the  action  of  large  quantities  was  tried. 

The  results  with  absolute  alcohol  indicate  that  the  proteolytic 
ferment  of  the  pancreatic  juice  is  more  sensitive  to  absolute  alcohol 
than  the  ferment  of  the  gastric  juice.  Retardation  of  digestive 
action  is  more  pronounced,  even  with  small  amounts  of  alcohol. 
Further,  as  in  the  case  with  pepsin,  the  weaker  the  digestive  powers 
of  the  pancreatic  juice,  the  greater  the  retarding  action  of  absolute 
alcohol.  When  the  amount  of  alcohol  present  in  the  digesting 
mixture  is  less  than  one  per  cent,  the  retardation  of  the  digestive 
action  is  very  slight,  provided  the  ferment  is  fairly  vigorous  in  its 
action. 

Action  of  Alcohol  on  Salivary  Digestion. — In  the  first  set  of 
experiments  on  salivary  digestion  Chittenden  determined  the  time 
it  took  to  reach  the  achromic  point.  By  this  method  he  found 
that  absolute  alcohol  has  very  little  influence  upon  the  amylolytic 
or  starch-digesting  power  of  neutral  saliva.  Only  when  the  saliva, 
added  to  the  digestive  mixture,  is  diluted  in  the  proportion  of 
1 : 30,  does  the  presence  of  even  ten  per  cent,  of  alcohol  have  any 
measurable  influence,  and  then  only  to  retard  the  appearance  of 
the  achromic  point  two  minutes.  As  this  percentage  of  absolute 
alcohol  is  equal  to  at  least  twenty  per  cent,  of  proof-spirit,  it  fol- 
lows that  pure  alcohol  free  from  admixture  is  practically  without 
influence  upon  the  digestion  of  farinaceous  food  by  the  saliva. 

By  the  second  method,  which  was  to  determine  the  amount  of 
maltose  formed,  he  found  that  small  amounts  of  absolute  alcohol 
may  actually  cause  an  increased  formation  of  maltose.  On  the 
other  hand,  the  presence  of  ten  or  fifteen  per  cent,  of  absolute 
alcohol  leads  to  a distinct  retardation  in  the  formation  of  sugar, 
although  the  inhibition  is  not  very  great  considering  the  amount 
of  alcohol  present.  This  retardation  of  the  secondary  action 
of  the  ferment  is  perhaps  suggested  by  the  slight  delay  in  the 
appearance  of  the  achromic  point  in  the  presence  of  ten  per  cent, 
of  absolute  alcohol. 

Effect  of  Alcohol  on  Gastric  Peristalsis. — We  have  personally 
made  a number  of  observations  concerning  this  special  point  on 
three  healthy  students  with  normal  stomachs  by  means  of  our 
method  of  graphically  registering  the  gastric  peristalsis  on  the 


294 


DIETETICS  OF  ALCOHOLIC  BEVERAGES. 


kymographion  (“  New  York  Med.  Journal,”  June  22,  1895).  These 
students  were  teetotalers,  and  to  exclude  the  influence  of  suggestion 
the  alcohol  was  poured  into  the  stomach,  diluted,  through  a tube, 
and  sometimes  water  was  used  in  place  of  alcohol.  The  subject 
was  at  no  time  aware  of  what  was  being  used.  It  was  found  that 
alcohol,  when  contained  in  gastric  contents  up  to  six  per  cent., 
exerts  no  appreciable  effect  on  the  motility  one  way  or  the  other ; 
but  beyond  this  the  peristalsis  begins  to  show  evidence  of  im- 
pairment. 

The  presence  of  twenty  to  twenty-five  per  cent,  of  alcohol  leads 
to  a very  distinct  retardation  and  reduction  of  the  tonicity  in  the 
gastric  movements,  which  seems  to  last  in  its  effects  from  two  to 
three  hours.  Even  after  the  alcohol  is  thoroughly  washed  out  of 
the  stomach  the  peristalsis  continues  to  be  retarded. 

In  dogs  the  identical  results  were  obtained,  except  that  at  five  to 
six  percent,  a short  period  of  peristaltic  unrest  was  observed  before 
the  marked  inhibition  developed.  The  inhibition  of  the  peristalsis 
when  the  gastric  contents  contain  twenty  to  twenty-five  per  cent, 
of  alcohol  occurs  quite  regularly,  and  is  not  the  result  of  mere 
accident.  It  is  probably  due  to  a direct  poisoning  effect  on  the 
muscularis,  similar  to  the  poisoning  effect  on  the  heart-muscle 
observed  by  us  (Hemmeter,  “ Studies  from  the  Biological  Labora- 
tory,” loc.  cit .).  This  amount  of  alcohol  must  be  in  the  organ  at 
least  ten  minutes  before  the  peristaltic  inhibition  sets  in. 

Effect  on  Absorption. — The  effect  of  alcohol  on  the  rate  of 
absorption  from  the  stomach  is  a different  question  from  the 
absorbability  of  the  substance  itself.  There  is  a general  unanimity 
that,  owing  to  its  rapid  diffusibility,  alcohol  is  promptly  absorbed 
from  mucous  surfaces.  At  the  same  time  the  experiments  of 
von  Mehring  suggest  that  the  absorption  of  substances  soluble  in 
alcohol  may  be  facilitated  by  the  latter;  for  example,  that  peptone 
or  maltose  taken  in  alcohol  may  be  absorbed  more  rapidly  than 
when  taken  in  water.  Exact  experimental  facts  concerning  this 
matter  are  wanting. 

In  large  doses  alcohol  hinders  absorption  by  the  direct  damage 
it  does  to  the  cylindrical  surface  epithelium. 

Among  gastro-enterologists  the  impression  prevails  that  alcohol 
and  alcoholic  beverages  are  capable  of  promoting  the  appetite;  and 
probably  for  this  purpose  and  for  its  stimulating  effect  we  are  justi- 
fied in  giving  it.  Summing  up  the  physiological  action,  so  far  as 
we  are  concerned,  it  may  be  said  : (1)  The  effect  of  moderate  doses 


EFFECT  OF  MALT  LIQUORS  ON  GASTRIC  DIGESTION.  2Q5 

of  alcohol  on  metabolism  is  that  it  not  only  fails  to  protect  proteid 
oxidation,  but  actually  increases  it.  Oxidation  of  fat  is  probably 
inhibited.  (2)  That  on  pepsin  hydrochloric  acid  it  acts  favorably 
in  quantities  equal  to  one  to  two  per  cent,  of  absolute  C2H0O, 
but  beyond  that  it  gradually  inhibits  this  action.  (3)  On  pan- 
creatic digestion  it  acts  unfavorably.  (4)  On  salivary  digestion  it 
acts  favorably,  increasing  the  formation  of  maltose  when  present 
in  amounts  not  exceeding  five  per  cent.  (5)  On  the  peristalsis  it 
has  no  influence  until  the  amount  exceeds  six  per  cent.,  when  it 
begins  to  inhibit  the  motility.  (6)  Its  effect  on  the  rate  of  absorp- 
tion is  unknown. 

In  pathological  conditions  the  effects  of  alcohol  are  undeniably 
different,  its  stimulating  and  temperature-depressing  influence  mak- 
ing it  of  value  in  continued  fevers.  In  pathological  cases,  wher- 
ever the  amount  of  free  HC1  is  altered,  either  in  hyperchylia  or 
achylia  gastrica,  Chittenden’s  deductions  do  not  hold  good.  In 
hypochylia,  or  subacidity,  alcohol  may  be  of  some  service  in  stimu- 
lating the  mucosa  to  more  prolific  secretion,  but  in  hyperchylia  it 
irritates  the  already  very  much  excited  gland-cells  still  further.  In 
achylia  with  entire  absence  of  secretion,  digestion  is  considerably 
reduced  by  alcohol.  Speaking  generally,  alcohol  might  be  dis- 
pensed with  as  a therapeutic  and  dietetic  agent  if  it  were  not  for 
its  appetizing,  stimulating,  and  antipyretic  qualities.  In  hyper- 
acidity and  hypersecretion,  in  ulcer  and  all  chronic  affections  with 
augmented  secretion,  alcohol  is  contraindicated.  In  atonic  stom- 
achs with  retention  and  stagnation  of  contents  and  pronounced 
impairment  of  motility  alcohol,  in  our  experience,  acts  as  a poison. 
Symptoms  of  vertigo,  nausea,  and  even  tetany  are  directly  trace- 
able to  the  introduction  of  whisky  or  wine  under  such  conditions. 
In  our  opinion  these  results  are  brought  about  by  substances 
already  existing  in  these  types  of  stomach  diseases,  which  are 
prevented  from  entering  the  circulation  by  a protective  action  of 
the  gastric  mucosa,  which  does  not  absorb  them.  The  addition  of 
alcohol  renders  these  toxins  absorbable.  Healthy  stomachs  not 
rarely  exhibit  a certain  adaptation  to  alcohol,  and,  naturally,  upon 
such  organs  the  agent  has  a different  effect  than  upon  the  stomach 
of  a teetotaler. 

Beer  has  a very  little  therapeutic  utility ; by  reason  of  its  weight 
it  is  contraindicated  in  all  conditions  weakening  the  gastric  wall. 
Riegel  holds  that  it  is  well  to  permit  its  use  in  simple  hyperacidity. 
It  contains  a certain  amount  of  nutritious  matter,  and  should, 


296 


DIETETICS  OF  ALCOHOLIC  BEVERAGES.* 


therefore,  not  be  forbidden  if  the  patient  craves  it,  provided  the 
motor  power  is  good.  Even  the  absorption  of  less  bulky  wines  is 
attended  by  an  excretion  of  water  into  the  stomach  (von  Mehring, 
loc.  cit.),  which  may  favor  stasis  of  liquids  and  furtherance  of 
existing  dilatation. 

The  following  is  a table  by  Roberts  (“  Lectures  on  Dietetics  and 
Dyspepsia  ”),  showing  the  effects  of  various  percentages  of  malt 
liquors  on  gastric  digestion  : 


Proportion  of  Malt  Liquors  in 
the  Digesting  Mixture. 

Time  in  which  Digestion  was  Completed 
(Normal,  One  Hundred  Minutes). 

Ale, 

Burton. 

Light  English 
Table  Beer. 

, Lager  Beer. 

Ten  percent., 

1 15  minutes,  . . 

100  minutes,  . . 

100  minutes. 

Twenty  per  cent., 

140  “ 

115  “ • • 

115  “ 

Forty  per  cent. 

200  “ . . 

140  “ 

140  “ 

Sixty  per  cent  , 

Embarrassed,  . 

180  “ 

180  “ 

The  digesting  mixture  contained  two  gm.  of  dried-beef  fiber, 
0.15  percent,  of  hydrochloric  acid  (HC1),  and  one  c.c.  of  glycerin, 
extract  of  pepsin,  and  varying  quantities  either  of  wines  or  malt 
liquors,  and  filling  up  to  100  c.c.  with  water. 

The  following  table  gives  the  effects  of  various  percentages  of 
hock,  claret,  and  champagne  upon  peptic  digestion  (Roberts) : 


Proportion  of  Hock,  Claret,  or 
Champagne  in  the  Digesting 
Mixture. 

Time  in  which  Digestion  wtas  Completed 
(Normal,  One  Hundred  Minutes). 

Hock. 

Claret. 

Champagne. 

Ten  percent., 

100  minutes,  . 

. . 100  minutes,  . . 

90  minutes. 

Twenty  per  cent., 

115 

, . | 140  “ 

100  “ 

Forty  per  cent., 

150  “ 

. . 180  “ . . 

130 

Sixty  per  cent. 

Embarrassed, 

. Embarrassed,  . 

180  “ 

In  cases  of  gastric  disease  where  great  general  debility  commands 
liberal  alcoholic  stimulation,  particularly  if  the  gastric  motor  func- 
tion be  impaired,  it  is  best  to  administer  the  stimulant  by  rectal 
enema.  It  may  have  been  observed  that  most  of  the  enemata  have 
provided  for  this  emergency,  and  contain  more  or  less  wine. 

Sir  Wm.  Roberts  points  out  that  in  the  plan  of  the  dietary  of 
the  civilized  races,  arrived  at  slowly,  as  the  result  of  an  immense 
experience,  we  seem  to  detect  two  apparently  contradictory  aims — 


LAVAGE  AND  THE  GASTRIC  DOUCHE. 


297 


namely,  on  the  one  hand,  to  render  food,  by  preparation  and 
cooking,  as  digestible  as  possible;  and,  on  the  other  hand,  to 
control  the  rate  of  digestion  by  the  use  of  certain  accessory  articles 
with  food,  such  as  alcoholic  beverages.  In  reality  these  objects 
are  not  contradictory,  but  cooperative  to  a beneficial  end.  For,  to 
express  the  problem  in  another  way,  it  may  be  said  that  we  render 
food,  by  preparation,  as  capable  as  possible  of  being  completely 
exhausted  of  its  nutrient  properties  ; and,  on  the  other  hand,  to 
prevent  this  nutrient  matter  from  being  wastefully  hurried  through 
the  body  we  make  use  of  agents  which  abate  the  speed  of  diges- 
tion. This  combination  of  appliances  renders  our  plan  of  feeding 
more  elastic,  more  adaptable  to  variety  of  individual  health  and 
constitution,  and  to  variety  of  external  conditions. 

If  this  view  of  digestive  retardation  in  the  stomach  be  well 
founded,  the  stomach  becomes  in  some  degree  a storage  organ  for 
food — like  the  crop  of  birds,  the  paunch  of  ruminants,  the  dilata- 
ble cheeks  of  monkeys,  and  the  pouch  of  the  pelican. 

This  classical  writer  on  dietetics  expresses  himself  similarly  on 
the  importance  of  preparing  the  food  in  such  a way  that  it  tastes 
good  (Sir  William  Roberts,  loc.  cit .,  “ The  Eulogium  of  the  Pal- 
ate ”).  Even  Bunge,  the  well-known  physiologist,  who  is  a pro- 
nounced teetotaler,  declares  that  we  are  justified  in  the  use  of  any 
food  or  drink  if  for  no  other  reason  but  that  it  gratifies  the  palate, 
provided  it  does  no  harm  ; but  the  substitution  of  harmless  food 
and  drink  for  alcohol  is  strongly  urged. 


CHAPTER  IV. 

LAVAGE  AND  THE  GASTRIC  DOUCHE. 

The  technics  of  lavage — the  indications  for  and  against  it — have 
been  treated  in  the  section  on  the  Stomach-tube.  In  brief,  lavage 
is  indicated  (a)  where  the  exit  of  the  chyme  from  the  stomach  is 
hindered  by  a mechanical  obstruction,  giving  rise  to  decomposi- 
tions. To  this  class  belong  all  forms  of  dilatation  except  those 
depending  on  simple  atony,  for  here  we  are  not  dealing  with  any 
obstruction  to  the  outflow,  but  with  a lowering  of  the  peristalsis, 
which  is  not  markedly  benefited  by  lavage.  Dilatations  that  indi- 


20 


298 


LAVAGE  AND  THE  GASTRIC  DOUCHE. 


cate  lavage  are  those  due  to  cicatricial  stenosis,  or  neoplasm  of  the 
pylorus  and  duodenum,  and  impairment  of  motor  function  in 
consequence  of  carcinoma,  sarcoma,  syphilitic  and  tuberculous 
gastritis,  simple  atrophic  gastritis,  myasthenia,  contractions  caused 
by  acids,  alkalies,  or  other  chemicals.  The  benefit  derived  from 
lavage  must  vary  with  the  stage  at  which  the  treatment  is 
undertaken.  In  cases  of  cicatricial  stenosis  of  mild  and  incipient 
character  the  dilatations  have  been  cured  by  lavage,  probably 
because  a compensatory  hypertrophy  of  the  musculature,  develop- 
ing gradually,  enabled  the  organ  to  expel  the  chyme.  In  these 
gastrectasias  the  stomach,  after  the  systematic  lavage  treatment,  no 
longer  contained  food  and  HC1  in  large  quantities  in  the  morning. 
The  stools  and  the  quantity  of  the  urine  became  normal,  and  the 
patients  could  tolerate  an  ordinary  diet.  But  such  cases  must, 
even  after  recovery,  avoid  overloading  the  stomach,  as  this  has 
been  known  to  bring  about  relapse.  The  compensatory  hyper- 
trophy of  the  musculature,  although  it  may  last  for  years,  in  these 
cases  is  not  a permanent  condition,  and  in  our  experience  often 
gives  way  to  a subsequent  atrophy  and  return  of  all  the  symptoms 
of  stagnation. 

( b ) The  second  main  indication  is  where  foreign  or  irritating 
collections  are  mixed  with  the  gastric  contents,  which  sooner  or 
later  interfere  with  digestion.  These  collections  may  consist  of 
abnormally  augmented  gastric  juice,  of  gastric,  pharyngeal,  and 
esophageal  mucus,  and  of  bile.  In  hypersecretion  lavage  is  best 
carried  out  with  sodium  bicarbonate,  and  thereafter  with  argentic 
nitrate  or  bismuth  subnitrate.  The  pyrosis,  distention,  and  consti- 
pation are  much  relieved  thereby.  In  cases  of  much  accumulation 
of  mucus,  warm  alkaline  and  saline  solutions  are  preferable ; for  in 
the  gastritis  mucosa  the  HC1  secretion  is  lost,  and  common  salt  is 
a stimulant  to  that  secretion — if  there  be  any  secreting  glandular 
cells  left.  I have  found  that  sulphocarbolate  of  zinc,  in  the  strength 
of  one  grain  to  one  ounce  of  water,  will  check  excessive  secretion  of 
mucus  in  chronic  gastritis.  It  is  used  in  the  intragastric  spray  after 
previous  lavage.  Toxic  products  of  complex  nature  may  accumulate 
in  the  organ,  in  consequence  of  carcinoma,  uremia,  and  diabetes  mel- 
litus;  here  lavage  is  also  indicated.  During  the  lavage  one  should 
always  have  a second  glass  vessel,  holding  one  liter,  into  which  the 
outflow  discharges,  so  that  it  may  be  ascertained  each  time  how 
much  is  regained.  It  is  very  dangerous  to  wash  out  the  stomach 
with  medicated  and  antiseptic  solutions  without  ascertaining 


THE  GASTRIC  DOUCHE. 


299 


whether  all  the  solution  flows  out  again.  Even  with  simple  water, 
overloading  of  the  stomach  can  not  be  avoided  except  by  measur- 
ing the  outflow.  In  a paper  published  in  the  “ Practitioner”  (1892, 
No.  4)  W.  Soltau  Fenwick  reports  three  cases  of  poisoning  from 
leaving  antiseptic  solutions  in  the  stomach.  In  one  case  (“  Schmidt’s 
Jahrbucher,”  1883,  Bd.  cxcvm,  p.  28)  death  was  caused  in  six  days 
by  leaving  a two  to  three  per  cent,  solution  of  boric  acid  in  the 
stomach.  Fenwick  also  makes  a strong  plea  against  the  indiscrim- 
inate use  of  antiseptics  within  the  stomach,  for  the  alimentary  canal 
is  endowed  with  the  power  of  absorbing  not  only  the  poisonous 
products  of  the  bacteria,  but  also  most  of  the  substances  which  are 
introduced  to  destroy  them  (W.  S.  Fenwick,  “ Disorders  of  Diges- 
tion in  Infancy,”  etc.,  p.  141). 

Tetany  has  been  observed  after  lavage  by  Bouveret  and  Devic, 
who  collected  twenty-one  cases  (“  Revue  de 
Med.,”  February,  1892).  In  all,  thirty-four  such 
cases  of  tetany  of  gastric  origin  have  been  re- 
ported, though  not  all  due  to  lavage.  Ewald 
reported  two  cases  that  are  of  interest — one  a 
male,  aged  forty-five,  who  died  from  a sud- 
den, copious,  esophageal  hemorrhage  two  days 
after  he  had  sought  relief  by  introduction 
of  the  esophageal  sound.  There  were  symp- 
toms of  mediastinal  tumor  or  aneurysm.  The 
second  patient  died  suddenly  while  he  was  intro- 
ducing the  tube  himself ; the  autopsy  showed 
a dissecting  aneurysm  at  the  beginning  of  the 
ascending  aorta,  still  within  the  pericardium. 

Frerichs  and  Penzoldt  have  reported  similar 
cases.  Every  new  patient  should,  therefore,  be 
examined  for  abnormal  conditions  within  the 
thorax  before  lavage. 

The  Gastric  Douche. — By  douching  the  stom- 
ach, is  meant  an  internal  irrigation  with  water 

....  T . Fig.  26.— Recurrent 

under  high  pressure.  It  was  first  practised  at  gastric  needle 

.,  ...  . , . Spray  or  Douche. 

Kussmaul  s clinic,  and  described  later  by  Mal- 
branc  (“  On  the  Treatment  of  Gastralgias  by  the  Internal  Gastric 
Douche,”  etc.,  “ Berlin,  klin.  Wochenschr.,”  1878,  No.  4).  It  does 
not  differ  essentially  from  ordinary  lavage  except  in  the  fact  that 
the  funnel  or  vessel  into  which  the  water  is  poured  is  held  at  least 
one  meter  above  the  cardia.  Rosenheim  improved  and  revived 


300 


LAVAGE  AND  THE  GASTRIC  DOUCHE. 


the  method,  after  it  had  been  disregarded  for  twelve  years,  by  de- 
vising a special  douching  tube  with  numerous  very  small,  lower 
openings  instead  of  one  or  two  large  ones.  Water  that  is  allowed 
to  run  into  the  stomach  through  such  a tube  under  high  pressure 
strikes  the  walls  with  many  currents  of  considerable  impetus.  The 
central  or  terminal  opening  in  Rosenheim’s  douche  tube  is  larger 
than  the  lateral  ones,  and  permits  of  an  easy  outflow.  Dr.  F.  B. 
Turck,  of  Chicago,  has  devised  a stomach  needle  douche  with  a 
separate  outflow  tube ; it  also  produces  an  intragastric  shower 
(Fig.  26),  and  is  a useful  instrument. 

Rosenheim  recommends  the  douche  for  nervous  dyspepsia  and 
chronic  gastritis,  with  or  without  impaired  motility.  If  the  douch- 
ing was  done  with  solution  of  sodium  chlorid  an  increase  in  the 
HC1  production  could  be  ascertained;  whereas  nitrate  of  silver 
caused  a reduction  of  the  secretion  (“  Berlin.  Klinik,”  1894,  Heft 


71).  Riegel  speaks  well  of  argentic  nitrate  applied  in  this  manner 
for  all  irritative  states  of  secretion  ( loc . cit.,  p.  300). 

Fleiner  has  called  attention  to  the  fact  that  he  and  Kussmaul 
could  incite  a feeling  of  hunger  by  douches.  These  clinicians 
increased  the  effect  by  irrigating  the  gastric  mucosa  with  solutions 
of  bitter  tonics  : hops  and  quassia  were  experimented  with. 

In  severe  cases  of  anorexia  we  have  tried  this  method  with  infu- 
sions of  gentian  and  cinchona,  and  were  pleased  with  the  effects. 
Einhorn  has  invented  an  intragastric  spray  (Fig.  27),  which  is  rec- 
ommended for  disinfection  of  the  mucosa,  to  produce  an  astringent 
or  an  anesthetic  effect.  It  is  surprising  what  a trifling  amount  of 
cocain  is  necessary  to  relieve  a gastralgia  when  used  in  this 
manner.  For  gastric  erosions  the  nitrate  of  silver  spray  (1  : 1000) 
is  frequently  curative.  For  excessive  secretion  of  mucus  zinc 
sulphocarbolate,  one  grain  to  one  ounce  of  water,  can  be  recom- 


ELECTRICITY  IN  THE  TREATMENT  OF  GASTRIC  DISEASES.  30 1 

mended.  The  gastric  douche  and  spray  should  be  applied  only 
in  an  empty  stomach.  Motor  impairment  of  nervous  origin  is 
occasionally  much  improved  by  alternately  douching  with  warm 
(ioo°  C.)  and  cold  water. 

Electricity  in  the  Treatment  of  Gastric  Diseases. — The  effect 
of  electricity  on  the  various  functions  of  the  stomach  has  been 
already  referred  to  under  the  consideration  of  the  motor  function 
and  will  be  further  described  under  the  various  diseases  in  which 
it  is  recommended.  The  results  of  physiological  experiment  and 
of  clinical  experience  are  largely  contradictory.  Physiological 
experiments,  when  conducted  by  medical  men,  are  frequently 
inexact  and  misleading.  It  requires  special  physiological  labora- 
tory training  of  years  to  control  the  technics  of  vivisection  and 
general  experimentation.  In  the  experiments  of  medical  men  on 
the  physiological  effects  of  electricity  it  is  not  difficult  to  find 
numerous  defects  in  the  physics  and  physiology  of  the  methods 
used,  the  conduct  and  the  execution  of  the  experiment,  etc.,  which 
render  their  results  invalid  from  the  outset;  so  that  it  is  useless 
to  go  into  the  literature  of  the  history  of  gastric  electrotherapy 
exhaustively.  Many  experimenters  fail  to  give  the  details  and 
conditions,  the  kind  of  cell  used,  the  number  of  milliamperes,  the 
number  of  faradic  stimulations  to  the  minute,  the  kind  of  electrode, 
the  distance  of  primary  from  secondary  coil.  Control  experiments 
are  wanting  to  ascertain  whether,  in  the  same  animal,  peristalsis 
could  not  be  observed  per  se  without  stimulation  by  electricity,  or 
whether  the  stimulation  may  not  have  been  purely  mechanical,  not 
electrical. 

From  a clinical  standpoint  it  is  not  necessary  to  demonstrate 
that  electricity  can  produce  changes  in  the  chemistry,  resorption, 
and  motility  of  the  stomach  in  order  to  justify  its  employment; 
for  there  may  be,  and  probably  are,  influences  exerted  by  elec- 
tricity upon  the  nutrition  of  living  cells  which  as  yet  escape  our 
methods  of  analysis.  The  effect  of  electrical  stimulation  of  the 
cells  of  spinal  ganglia,  as  seen  and  determined  by  micrometric 
measurement,  and  consisting  in  a loss  of  bulk  mainly  in  the 
nuclei,  was  first  described  by  C.  F.  Hodge,  in  the  “ American  Jour, 
of  Psychology  ” for  May,  1888,  and  May,  1889.  Judging  from  these 
experiments,  which  were  conducted  with  exemplary  accuracy  and 
regard  for  physiological  detail,  it  is  reasonable  to  presume  that,  in 
some  way  or  other,  the  metabolism  of  muscle-,  gland-,  and  nerve- 
cells  of  the  stomach  may  be  influenced  by  electricity.  The 


302 


LAVAGE  AND  THE  GASTRIC  DOUCHE. 


demonstration  of  this  is  a future  prospect ; at  present  the  main 
reason  why  we  employ  this  agent  is  simply  because  we  know  that 
in  certain  diseases  it  is  of  much  benefit.  Physiology  may  come  to 
our  aid  later  on,  and  tell  us  why  it  is  that  these  results  are  pro- 
duced. From  the  work  done  by  medical  physiologists  so  far,  no 
clear  deductions  are  possible. 

The  electrical  stimulation  of  the  vagus  in  a subject,  forty-five 
minutes  after  execution,  which  was  carried  out  by  Beynard  and 
Loye  (“  Progres  Medicale,”  1885.  No.  29),  and  produced  a secre- 
tion of  gastric  juice,  has  strengthened  the  belief  that  the  vagus 
contains  gastric  secretory  fibers.  Ziemssen  (“  Klinische  Vortrage,” 
No.  12,  1887),  Rossi  (“  Lo  Sperim.,”  1881),  and  Hoffmann,  who 
experimented  at  Riegel’s  clinic  (“  Berlin,  klin.  Wochenschr.,”  1889, 
No.  12),  all  arrived  at  the  conclusion  that  electricity  promoted  the 
secretion  of  gastric  juice. 

The  results  of  investigations  concerning  the  influence  of  the 
two  kinds  of  currents — the  constant  and  the  interrupted — differ 
widely.  Einhorn  was  of  the  opinion  that  the  faradic  current  pro- 
moted secretion  and  the  galvanic  impeded  it  (“  Deutsche  med. 
Wochenschr.,”  1893;  also  “ Zeitschr.  f.  klin.  Med.,”  Bd.  xxiii). 
The  experiments  of  Hoffmann  ( loc . cit.)  suggested  that  the  galvanic 
current  favored  an  increased  secretion,  while  Bocci’s  results  with 
intragastric  faradization  would  have  us  believe  that  in  animals  the 
interrupted  current  can  augment  both  peristalsis  and  secretion 
(“  Lo  Sperimentale,”  Giugno,  1881). 

Concerning  the  effect  of  electricity  on  the  motor  function  we 
might  quote  a few  experimenters.  Schillbach  (“  Virchow’s  Arch.,” 
Bd.  cix,  p.  284)  produced  strong  contractions  at  the  site  of  the 
anode  by  applying  the  galvanic  current  to  the  intestines  of  a rabbit. 
Von  Ziemssen  (loc.  cit .),  Bocci  (loc.  cit.)y  Ludwig,  and  Weber  have 
stated  that  the  faradic  as  well  as  the  galvanic  current  applied 
directly  to  the  stomach  cause  contraction  of  the  same  in  animals. 
Fubini  (“  Centralbl.  f.  med.  Wiss.,”  1882,  No.  33)  concluded  that 
electricity  accelerates  intestinal  peristalsis  ; he  experimented  on 
Vella’s  double  intestinal  fistula.  Two  Americans,  Rockwell  and 
Beard  (“  Phila.  Medical  and  Surgical  Reporter,”  1868,  No.  20),  were 
among  the  first  to  employ  electricity  in  the  treatment  of  nervous 
dyspepsia. 

In  Pepper’s  case  of  spontaneous,  visible,  gastric  peristalsis 
(‘‘Phila.  Med.  Times,”  1871,  p.  274)  no  peristaltic  movements 
could  be  produced  by  applying  electricity  percutaneously.  Kuss- 


EFFECT  OF  ELECTRICITY  ON  GASTRIC  PERISTALSIS. 


303 


maul,  in  1877,  stated  that  “ the  therapeutic  results  obtained  by 
Fiirstner  in  gastrectasias  did  not  prove  that  an  actual  peristalsis 
was  produced  by  the  current,  but  they  were  probably  due  to  con- 
traction of  the  abdominal  muscles”  (“  Archiv  f.  Psychiatrie  u.  Ner- 
venkrankh.,”  1878,  p.  205).  Canstatt  first  suggested  treating  dila- 
tations by  placing  one  electrode  in  the  esophagus,  the  other  on  the 
stomach ; and  Duchenne  first  actually  applied  this  method  (both 
the  latter  quoted  from  Kussmaul,  loc.cit .).  In  1877  Kussmaul  {Joe. 
cit.)  began  introducing  intragastric  electrodes,  made  by  inserting  a 
copper  wire  in  a stomach-tube,  the  wire  terminating  in  a little  ex- 
posed knob  which  came  in  direct  contact  with  the  inner  gastric 
surface. 


Fig.  28. — Rectal  Electrode. 


Bardet  improved  this  method  by  a similar  electrode,  which,  how- 
ever, did  not  come  in  contact  with  the  mucosa  in  one  spot  only,  but 
by  a quantity  of  water  previously  taken  it  was  distributed  over  the 
entire  surface  (Bardet,  “ Bull.  Gen.  de  Therap.,”  1884).  Ziemssen 
then  employed  a similar,  device,  but  Einhorn  completed  the 
evolution  of  the  intragastric  electrode  by  originating  a soft,  very 
plastic,  deglutable  instrument,  the  end  of  which  is  inclosed  in  an 
ovoid,  perforated,  hard-rubber  cap.  Ewald  prefers  Einhorn’s  elec- 
trode a little  more  rigid,  so  that  it  can  be  pushed  into  the  stomach 
and  need  not  necessarily  be  swallowed.  The  thickness  of  the  rub- 
ber tube  in  Ewald’s  modification  is  1^  mm.  Rosenheim  (loc.  cit.), 
Wegele  (“  Therap.  Monatshefte,”  April,  1895),  Charles  G.  Stockton 


304 


LAVAGE  AND  THE  GASTRIC  DOUCHE. 


(“  A New  Gastric  Electrode,”  “ Medical  Record,”  Nov.  9,  1889), 
and  F.  B.  Turck  have  later  devised  electrodes  for  this  purpose  which 
represent  no  advance  over  those  mentioned.  The  thin-wired  elec- 
trode of  Einhorn  (Fig.  29)  possesses  the  advantage  that  it  can  be 
swallowed  by  those  not  used  to  the  stomach-tube,  to  which  they 
must  become  accustomed  in  case  Wegele’s,  Stockton’s,  or  Rosen- 
heim’s electrode  is  employed.  The  inclosing  tube  of  Einhorn’s 
instrument  is  really  too  thin,  however,  for  in  our  experience  it  rap- 
idly wears  through  near  the  connection  with  the  hard-rubber  end- 
cap,  and  we  consider  Ewald’s  modification  safer,  more  durable,  and 
of  easier  introduction. 

These  results  correspond  in  the  main  with  those  previously  pub- 
lished by  Meltzer  (“  New  York  Med.  Jour.,”  June  15,  1895),  whose 
experiments  were  conducted  with  great  care,  and  from  a physio- 
logical aspect  are  beyond  reproach.  We  should  have  preferred 
knowing  how  many  vibrations  to  the  second  Meltzer  used,  since 
we  have  assured  ourselves  that  when  too  many  stimulations  to  the 
second  are  thrown  into  a muscle,  particularly  an  involuntary  mus- 
cle, it  will  not  contract  at  all ; whereas  the  same  muscle  will  con- 
tract if  a smaller  number  of  stimulations  be  used  (judged  by  the 
Kronecker  interrupter  and  a Jacquet  chronograph).  These  facts 
were  first  stated  in  an  article  in  the  “ New  York  Med.  Jour.”  (Hem- 
meter,  “ Recording  Motor  Functions  of  the  Stomach,”  “ New  York 
Med.  Jour.,”  June  22,  1895,  p.  772).  We  used  an  intragastric  deg- 
lutable  rubber  bag  (see  illustrations,  plate  iv),  which  had  small 
brass  knobs  extended  at  any  desirable  location,  and  when  the  bag 
was  distended  by  blowing  it  up  within  the  stomach  the  end  elec- 
trodes pressed  directly  against  the  mucosa — usually  one  at  the 
pylorus  and  one  in  the  fundus  ; the  bag  was  in  connection  with  a 
tambour  or  manometer  recording  on  the  Ludwig  kymographion. 
We  have  already  briefly  stated  that  we  were  unable  to  produce  any 
contraction  of  the  human  or  animal  stomach  with  the  strongest 
currents  to  be  obtained  from  one  Grove  cell  prepared  anew  for 
each  experiment,  and  the  distance  of  the  primary  from  the  second- 
ary coil  equal  to  zero  when  both  electrodes  were  within  the  stom- 
ach touching  the  mucosa.  We  have  elsewhere  given  our  studies 
on  the  resistance  which  fresh  human  gastric  mucosa  offers  to  the 
constant  current,  and  in  the  main  can  confirm  Meltzer  that  percu- 
taneous and  direct  faradization  of  the  stomach  and  intestines  can 
produce  no  contraction  of  these  parts.  Not  every  current  which, 
according  to  magnetic  needles  or  the  milliamperemeter,  actually 


EFFECT  OF  ELECTRICITY  ON  GASTRIC  PERISTALSIS.  305 

penetrates  the  gastric  wall  causes  contraction.  For  instance,  with 
one  electrode  within  the  stomach  of  man  or  dog,  and  another  on 
the  gastrocnemius,  the  skeletal  muscle  may  contract  vigorously 
and  the  stomach  remain  passive.  Again,  in  human  subjects  the 
factors  of  natural  peristalsis  occurring  under  the  nervous  tension 
due  to  the  experiment,  and  of  suggestion,  can  not  be  satisfactorily 
eliminated. 

In  a recent  publication  Einhorn  has  attempted  to  disprove  the 
experiments  of  Meltzer,  but,  as  far  as  can  be  judged  from  the  report 
of  the  former  (in  the  “ Archiv  f.  Verdauungskrankheiten,”  Bd.  n, 
p.  454),  the  experiments  were  not  conducted  along  the  same  lines 
nor  with  the  same  regard  for  physiological  detail  as  those  of 
Meltzer.  Einhorn  gives  brief  synopses  of  eighteen  experiments, 
twelve  of  which  were  made  with  frogs,  with  which  Meltzer  did  not 
work,  and  from  the  results  of  which  conclusions  regarding  the 
mammalian  stomach  can  not  be  safely  drawn.  Three  animals  were 
rabbits  ; in  these  the  stomach  is  always  full  of  ingesta,  unless 
starved.  Two  were  rats;  one  only  was  a dog  ; the  latter  was  the 
animal  with  which  Meltzer  mainly  worked.  Nor  is  it  evident  that 
Einhorn’s  results,  as  stated  by  him,  contradict  those  of  Meltzer  in 
salient  points.  Taking,  for  instance,  the  last  experiment  with  the 
dog,  Einhorn  made  three  kinds  of  stimulations  with  the  double 
electrode  : (i)  on  the  serous  (peritoneal)  surface,  near  the  fundus — 
contraction  ; (2)  on  the  peritoneal  surface  over  the  pylorus — strong 
contraction ; (3)  opening  of  the  stomach, — one  electrode  against 
the  mucosa,  the  other  on  the  peritoneal  layer  outside  ; a weak 
current  causes  slight  peristaltic  contractions. 

Meltzer  does  not,  in  his  original  paper,  deny  any  of  these 
possibilities ; even  the  contraction  of  the  third  experiment  was 
witnessed  by  him  when  the  inner  electrode  on  the  mucosa  was 
placed  near  the  outer  one  on  the  serosa.  But  with  bipolar  internal 
stimulation — i.  e.,  with  both  electrodes  on  the  mucosa — even  Ein- 
horn does  not  claim  to  have  obtained  any  peristalsis  of  consider- 
able tonicity.  We  incline  to  the  opinion  that  satisfactory  evidence  has 
not  yet  been  furnished  that  internal  electric  stimulation  can  influ- 
ence secretion  or  motility  either  way.  This  conclusion  has  been 
reached  after  years  of  experimenting  on  both  functions  in  the  Bio- 
logical Laboratory  of  the  Johns  Hopkins  University. 

In  a recent  reply  to  Einhorn’s  criticism,  Meltzer  accepts  the 
explanation  of  the  former,  concerning  the  difficulty  of  penetration 
of  the  electric  current  to  the  muscular  layer  (Boas’  “ Archiv  f. 


\o6 


LAVAGE  AND  THE  GASTRIC  DOUCHE. 


Verdauungskrankh.,”  Bd.  hi,  Heft  2,  S.  133).  This  maybe  caused, 
according  to  Einhorn,  by  the  mucosa  being  a bad  conductor  as  well 
as  by  its  being  a very  good  conductor — leading  the  current  away 
from  the  point  of  contact.  We  have  shown  conclusively  that  the 
fresh  normal  human  mucosa  is  a poor  electric  conductor.  Einhorn, 
however,  assumes  that  the  mucosa  conducts  so  well  that  the  cur- 
rent does  not  reach  the  muscularis,  because  it  moves  in  the  direc- 
tion of  least  resistance — in  the  glandular  layer  itself.  Tests  made 
with  the  mucosa  peeled  off  from  the  other  layers  of  the  stomach  of 
a dog  under  narcosis,  with  the  milliamperemeter  in  the  circuit, 
show  that  the  fresh  mucosa  is  practically  a non-conductor. 

Indications  for  the  Employment  of  Electricity  and  Manner  of  Appli- 
cation.— Direct  gastric  faradization  is  recommended  for  dilatations 
due  to  relaxation  of  the  musculature,  but  not  to  stenosis,  whether 
these  cases  are  associated  with  reduced  secretion  or  not.  Relaxa- 
tions of  the  cardia  or  pylorus  are  benefited  by  the  faradic  current. 
Sensory  disorders  (gastralgia)  are  successfully  treated  with  direct 
galvanization.  Rosenheim  (loc.  cit.)  believes  that  the  galvanic 
current  is  more  effective  in  debility  of  the  peristalsis.  In  all 
symptoms  of  sensory  irritation  he  prefers  the  constant  current 
also,  but  in  secretory  disturbances  he  has  ceased  to  use  electricity; 
and  we  agree  with  him  that,  in  the  latter  class,  more  can  be 
accomplished  by  medicated  douches  and  adapted  acid  or  alkaline 
and  bitter  tonic  medicines  than  with  electricity.  Brock  confirms 
the  good  effect  of  galvanism  on  the  course  of  gastric  neuroses 
(“  Therap.  Monatshefte,”  June,  1895),  though  he  is  not  so  enthusi- 
astic as  Einhorn. 

According  to  Goldschmidt,  there  are  no  distinct  differences 
between  the  effects  of  direct  galvanization  and  direct  faradization  ; 
but  nevertheless  he  recommends  the  former  for  the  painful,  the 
latter  for  the  functional  disturbances  of  the  stomach.  In  contrast 
with  those  mentioned,  von  Ziemssen  prefers  the  percutaneous  to  the 
direct  intragastric  application  ; his  reasons  are  not  very  convincing, 
in  the  light  of  Meltzer’s  and  Goldschmidt’s  experiments.  The 
electric  brushing  of  the  skin  of  the  abdomen,  breast,  and  back, 
urged  by  von  Ziemssen,  seems  to  be  a great  stimulus  for  nervous 
energy  in  neuropathic  cases. 

In  this  country,  Allen  A.  Jones  (“  Med.  Rec.,”  June  13,  1891), 
Charles  G.  Stockton  (“  Med.  Rec.,”  1889,  p.  530),  and  D.  D.  Stewart 
(“  Therap.  Gazette,”  1893,  p.  744)  have  published  clinical  obser- 
vations on  the  intragastric  employment  of  electricity,  and  there 


HYDROPATHIC  AND  ORTHOPEDIC  METHODS. 


307 


is  a fairly  uniform  agreement  that  the  class  of  gastric  neuroses, 
particularly  the  sensory  neuroses,  nervous  vomiting,  and  anorexia, 
are  special  indications  for  electricity  in  the  form  of  the  constant 
current,  and  that  the  direct  intragastric  method  is  to  be  preferred 
to  the  percutaneous. 

In  simple  atony  and  atonic  dilatations  (but  not  in  those  depend- 
ent upon  pyloric  obstruction)  the  preference  is  to  be  given  to  the 
direct  faradic  current.  The  manner  of  application  is  simple  ; the 
anode  is,  as  a rule,  swallowed,  and  forms  the  intragastric  pole. 
The  cathode  must  have  the  shape  of  a conveniently  broad  and  long, 
felt-covered  plate  (Fig.  30),  which,  after  it  is  dipped  in  warm  water,  is 
placed  for  ten  minutes  on  the  epigastrium  ; thereafter  passed  slowly 
up  and  down  over  the  spinal  column  from  the  cervical  to  the  sacral 
region.  The  meter  should  always  be  in  the  circuit,  in  case  the 
galvanic  current  is  used,  and  the  strength  of  the  current  be  about 
twenty-five  milliamperes.  The 
electric  bath,  or  electricity 
applied  when  the  body  is 
immersed  in  a saline  bath,  has 
its  advantages  in  gastric  neu- 
roses. 

For  more  complete  literature 
of  the  subject  the  reader  is  re- 
ferred to  the  writings  of  Kuss- 
maul  (loc.  cit.),  Einhorn  (loc. 
cit.,  and  Einhorn,  “ Berlin,  klin. 

Wochenschr.,”  1891,  No.  23; 
also  “ Zeitschr.  f.  klin.  Med.,”  1893,  xxm,  p.  369),  and  Goldschmidt 
(“  Deutsches  Archiv  f.  klin.  Med.,”  Bd.  xv,  p.  295).  The  latter 
investigator  worked  under  Moritz,  whose  capital  experiments  on 
the  motility  we  have  already  abstracted.  Goldschmidt  concludes 
that  the  “ direct  faradization  and  galvanization  of  the  stomach 
(distance  of  primary  from  secondary  coil  = zero,  duration  fifteen 
to  twenty-five  minutes)  has  only  an  unimportant  and  inconstant 
influence  on  the  peristalsis,  and  on  secretion  it  has  no  influence 
whatever.” 

Hydrotherapeutic  and  Orthopedic  Methods. — Hydriatic  pro- 
cedures are  much  lauded  by  German  and  French  gastro-enterolo- 
gists.  Most  of  these  methods  can  influence  the  stomach  only 
indirectly  and  secondarily,  and  therefore  are  of  greater  utility  in 
functional  disturbances  than  in  the  organic  gastric  diseases.  These 


308 


LAVAGE  AND  THE  GASTRIC  DOUCHE. 


methods  may  be  divided  into  (i)  general  or  systemic,  (2)  special 
or  local  hydrotherapic  treatments.  The  method  to  employ  depends 
more  upon  the  state  of  general  health  and  the  condition  of  the  ner- 
vous system  than  upon  any  local  condition.  Wherever  hydriatic 
treatment  becomes  necessary,  it  is  imperative  to  send  the  patient 
to  some  well-managed  institution,  as  most  of  the  procedures  can 
not  be  executed  at  home.  Among  the  methods  most  employed 
are  the  various  local  and  general  douches — viz.,  fan  douche;  cold, 
hot,  graduated,  Scotch,  and  French  douches.  Among  these  we  have 
tried  the  Scotch  douche  most  frequently  in  gastric  myasthenia.  It 
consists  of  a stream  of  moderate  intensity  directed  against  the  epi- 
gastrium for  three  or  four  minutes.  But  during  this  time  the  tem- 
perature of  the  water  is  changed  every  ten  or  twenty  seconds  from 
28°  to  8°  R.,  or  vice  versa;  it  is  much  lauded  by  von  Ziemssen 
and  Rosenthal  (“  Magenneurosen,”  etc.,  Wien,  1886).  There  are, 
besides,  many  kinds  of  fine  sprays,  and  the  sponge,  sea-salt,  pour, 
dash,  shower,  shallow,  vapor,  and  sitz-baths  ; also  a variety  of 
packs,  fomentations,  and  compresses  (see  Baruch,  “ Hydro- 
therapy ”).  A local  application  which  is  very  soothing  in  gas- 
tralgic  affections  is  the  so-called  Priessnitz  pack,  which  consists 
simply  of  a towel  folded  together  to  the  size  of  six  by  ten  inches, 
and  dipped  into  hot  or  cold  water,  wrung  out  so  that  there  is  no 
dripping  from  it,  and  then  applied  to  the  epigastrium ; a layer  of 
oiled  silk  or  gutta-percha  paper  is  laid  over  it  and  the  whole  is 
snugly  secured  and  held  in  place  by  a broad  flannel  bandage 
passed  around  the  body.  As  a matter  of  fact,  most  patients  feel 
relieved  and  free  from  pain,  but  how  the  quieting  effect  is  pro- 
duced is  a matter  of  conjecture. 

In  the  treatment  of  gastric  ulcer  hot  cataplasms  are  very  service- 
able. We  are  in  the  habit  of  using  spongiopiline  dipped  into  hot 
water  and  applied  to  the  epigastrium  after  the  excess  of  water  is 
pressed  out. 

The  orthopedic  appliances  used  in  the  treatment  of  gastric  diseases 
are  often  only  imperfect  substitutes  for  the  more  lasting  effects  of 
proper  operations.  They  consist  of  contrivances  to  support  the 
stomach  in  gastroptosis,  or  to  keep  up  a floating  kidney  and 
prevent  its  interfering  with  the  gastric  or  intestinal  peristalsis. 
Where  the  abdominal  muscles  have  become  so  relaxed  that  they 
seem  to  drag  the  viscera  downward  instead  of  supporting  them,  a 
condition  found  in  obesity  (Hangebauch  = pendulous  abdomen), 
the  Landau  abdominal  corset,  for  both  sexes,  has  proven  of  un- 


INDICATIONS  FOR  GASTRIC  MASSAGE. 


309 


doubted  usefulness  in  many  cases  in  the  author’s  practice.  Ab- 
dominal gymnastics  are  the  most  effective  prophylaxis  against 
these  conditions. 

Gastric  Massage. — Von  Ziemssen  (“  Ueber  d.  physik.  Behandl. 
chronischer  Magen-  und  Darmleiden,”  Leipzig,  1888,  p.  29)  and 
Rosenheim  (loc.  cit .,  p.  146)  consider  massage  a very  subordinate 
means  of  treatment  for  stomach  diseases.  Ewald  (loc.  cit.),  Boas 


Fig.  31. — Massage  of  the  Stomach  in  Dilatation  or  Gastroptosis.— 

(Penzoldt  and  Stintzing,  “ Handbuch  d.  Therapie”  etc.) 

(loc.  cit.),  and  Riegel  (loc.  cit.),  however,  believe  that  there  is  some- 
thing of  value  in  the  treatment.  The  best  study  of  gastric  massage 
was  published  by  Zabludowsky  (“  Berlin,  klin.  Wochenschr.,”  1886, 
No.  26)  and  Cseri  (“  Wien.  med.  Wochenschr.,”  1889).  The  technic 
of  massage  differs  according  to  the  object  to  be  accomplished.  If 
it  is  intended  as  a passive  exercise  to  strengthen  the  musculature, 
it  is  best  done  on  an  empty  stomach,  in  bed  before  breakfast.  But 
if  the  massage  is  expected  to  assist  in  the  expulsion  of  chyme,  it 


3io 


GASTRIC  MASSAGE. 


should  be  undertaken  three  to  four  hours  after  the  principal  meals. 
Massage  can  not  be  properly  performed  except  on  the  uncovered 
skin.  Indications  for  massage  are  given  in  the  disturbances  of  the 
motor  function's,  viz.:  (i)  Those  depending  on  myasthenia  or 
atony;  (2)  depending  on  a stenosis  of  moderate  degree;  (3)  cases 
of  reduced  secretion  and  chronic  gastritis;  (4)  gastroptosis  or  pro- 
lapse of  the  stomach  ; and  (5)  certain  cases  of  nervous  inhibition 
of  peristalsis.  In  cancer,  ulcer,  hematemesis,  all  acute  inflamma- 
tions in  or  around  the  organ,  in  excessive  dilatation,  distention,  or 


Fig.  32. — Massage  for  Improving  Gastric  Tonicity. — {Penzoldt  and  Stintzing, 
“ Handbuch  d.  Therapie etc.) 


contraction,  and  in  all  cases  of  intragastric  putrefaction,  massage  is 
contraindicated. 

Massage  of  the  stomach  and  colon  is  generally  practised  with  a 
view  to  support  and  strengthen  the  expulsive  power  of  these 
organs  ; secondarily,  its  use  may  promote  the  nutrition  of  the 
mucosa  and  favor  the  resorption  of  infiltrations. 

The  technic  varies  with  the  indication.  For  improving  the 
muscular  tone  of  the  empty  stomach  the  masseur  places  himself 
to  the  right  of  the  patient,  who  must  lie  on  his  back  with  knees 
slightly  flexed.  First  movement  ( a ) : Insert  the  left  hand  slowly 


TECHNICS  OF  GASTRIC  MASSAGE. 


311 

and  gradually  deeply  under  the  left  arch  of  the  false  ribs,  under 
and  past  the  edge.  To  increase  the  pressure,  gently  press  the 
right  hand  firmly  on  the  left.  Second  movement  ( b ) : Now  describe 
small  circles  with  the  hands  thus  arranged,  progressing  slowly 
from  the  pylorus  to  the  fundus.  Third  movement  (r) : Perform 
strong  vibratory  movements  toward  the  depth  with  the  finger-tips, 
white  a and  b are  being  executed.  F'ourth  movement  (d) : Knead 
the  stomach  between  thumb  and  four  fingers,  and  in  conclusion 
execute  stroking  passes,  with  extended  four  fingers,  from  left  to 
right. 


Fig.  33. — Massage  of  the  Stomach  and  of  the  Colon. — ( Penzoldt  and  Stintzing , 
“ Handbuch  d.  Therapie etc.) 


Massage  of  the  full  stomach  is  undertaken  with  a view  to  mix  its 
contents  thoroughly  or  to  aid  in  forcing  them  into  the  duodenum. 
Zabludowski  (loc.  cit.)  advises  the  pressing  of  the  stomach  against 
the  spinal  column,  dividing  it  into  halves;  by  compressing  the 
half  nearest  the  pylorus,  he  widens  the  latter  by  wedging  the 
chyme  through  it  into  the  duodenum.  This  is  justifiable  only 
where  it  is  sure  that  the  chyme  is  comparatively  fresh,  and  not  in  a 
state  of  putrefaction.  The  author  has  repeatedly  experimented 
with  Zabludowski’s  method,  and  frequently  failed.  It  is  doubtful 


312 


GASTRIC  MASSAGE. 


whether  the  contents  of  very  dilated  stomachs  can  be  expressed 
into  the  duodenum  by  massage. 

Combination  of  Massage  and  Medicated  Irrigations  of 
Stomach  and  Colon. — When  solutions  of  chemicals  are  poured 
into  the  stomach  or  swallowed,  they  exert  a more  prompt  and 
lasting  effect  if  the  organ  is  subjected  to  gentle  massage  during 
the  time  these  solutions  are  in  it.  In  case  there  has  been  retention 
of  ingesta  and  processes  of  putrefaction,  the  stomach  must  first  be 
thoroughly  cleansed  by  lavage.  If  the  solutions  contained  active 
chemicals  they  must  be  removed  after  the  massage  by  careful  irri- 
gation with  plain  water. 

This  treatment  is  indicated  in  hyperacidity  with  alkaline  solutions, 
in  sub-  or  anacidity  with  diluted  HC1  and  all  conditions  of  chronic 
hyperemia,  excepting  the  active  processes  given  above  as  contra- 
indications. In  states  of  relaxation  of  muscular  tonus  and  in 
hyperesthesia  and  gastralgia  we  have  observed  most  gratifying 
improvement  where  other  methods  had  proved  futile. 

The  technics  of  the  method  are  simple : in  some  cases  the  patient 
may  be  permitted  to  drink  the  medicated  solutions,  but  it  will  gener- 
ally be  preferable  to  pour  them  in  through  the  tube,  especially  when 
lavage  is  indicated  before  the  procedure.  The  taste  of  some  of  the 
drugs  that  are  necessary,  prevents  drinking  the  solutions,  or  it  may 
be  requisite  that  the  mouth  or  esophagus  be  protected  from  the 
agents.  As  soon  as  the  solution  is  in  the  stomach,  the  patient 
occupying  the  dorsal  recumbent  position,  with  the  knees  flexed,  the 
masseur  begins  with  gentle  but  deeply  penetrating  compression  of 
the  epigastrium  and  hypogastrium  with  palmar  surface  of  the  fingers. 
Thereupon  stroking  of  the  stomach  region  from  above  downward ; 
from  left  to  right,  and  reversely ; next  follow  circular  friction  move- 
ments of  the  stomach  especially,  but  also  over  the  entire  abdomen. 
During  the  massage  the  dorsal  position  should  be  exchanged  with 
the  right  and  left  lateral  position.  The  medicines  inside  the  organ 
will  in  this  manner  be  extensively  and  thoroughly  brought  in  con- 
tact with  the  gastric  walls,  and  it  is  conceivable  that,  through  the 
increased  circulation  effected  thereby,  absorption  is  favored  in  a 
manner  not  otherwise  obtainable.  The  duration  of  this  method 
should  not  exceed  ten  minutes  with  indifferent  substances,  and 
only  five  minutes  if  chemicals  with  a decided  effect  are  used.  The 
agents  that  have  been  employed  are  the  following : In  anacidity 
and  achylia , HC1  2:  1000;  also  normal  salt  solutions  and  one  per 
cent,  of  ichthyol.  In  anorexia , solutions  of  the  tinctures  of  Colombo, 


MINERAL  SPRINGS.  3 I 3 

calisaya,  quassia,  gentian,  and  hops.  In  hyperacidity , the  natural 
alkaline  mineral  waters,  such  as  Saratoga  Vichy,  or  per  cent, 
solution  of  Carlsbad  salts.  Jaworski’s  antacid  solution  is  useful 
here,  and  also  suspensions  of  bismuth  and  solutions  of  nitrate  of 
silver  i : 1000.  In  hypersecretion  the  same  solutions  as  in  hyper- 
acidity are  applicable  ; but  in  addition  to  these  we  have  employed 
tannigen,  four  grams  to  one  liter,  rendered  soluble  by  bicarbonate 
of  sodium.  The  substances  applicable  in  gastric  fermentation  have 
been  recorded  in  the  chapter  on  Motor  Insufficiency. 


CHAPTER  V. 

MINERAL  SPRINGS. 

The  Uses  and  Abuses  of  Natural  Mineral  Waters  in  Diseases  of  the 
Digestive  Orga  ns . * 

With  such  a wealth  of  valuable  mineral  springs  in  this  country 
it  is  difficult  to  understand  the  large  annual  exodus  of  Americans 
to  foreign  water  resorts.  We  fear  the  fault  rests  with  the  Ameri- 
can physician,  not  the  American  waters.  Few  native  physicians 
give  to  the  selection  and  adaptation  of  proper  mineral  waters 
the  consideration  it  deserves;  whereas  in  German,  French,  and 
English  practice  this  forms  a common  and  important  factor.  Ac- 
cording to  Baruch,  even  American  doctors  resident  at  the  springs 
do  not  insist  upon  precision  in  proper  drinking,  diet,  hydrotherapy, 
or  exercise. 

The  surpassing  virtues  of  our  American  mineral  waters  can  be 
attested  only  by  making  an  individualizing  selection  of  the  waters 
for  each  case,  after  establishing  the  diagnosis. 

Too  much  empiricism,  too  much  fashion  and  sport,  too  much 
alcohol,  and  not  sufficient  peace  and  quiet  of  mind  exhibit  them- 
selves at  our  American  springs. 

Without  a diagnosis — not  to  speak  of  test-meals — we  have  known 

* In  the  preparation  of  this  chapter  we  have  availed  ourselves  of  the  Analyses  of  the 
Mineral  Springs  of  the  United  States  as  given  in  the  records  of  the  Department  of  the 
Interior  (Agriculture),  Washington,  D.  C.  ; and  in  the  description  of  the  physiological 
effects  of  the  various  springs  we  have  followed  the  works  of  Flechsig,  S.  Baruch,  Lud- 
wig, and  G.  Thompson  in  reference  to  waters  with  which  we  have  no  personal  experience. 

21  « 


3H 


MINERAL  SPRINGS. 


of  numerous  instances  where  the  waters  of  springs  were  ordered. 
Systematic  mineral-water  treatment  should  be  recommended  only 
after  the  institution  of  careful  chemical  and  physical  examinations. 

In  reference  to  the  abuse  of  mineral  waters,  we  limit  our- 
selves to  their  misuse  in  gastric  diseases.  We  would  exclude, 
first,  all  cases  of  motor  insufficiency  of  any  kind,  whether  of  the 
simple  atonic  or  the  stenotic  form,  whether  with  pronounced  dilata- 
tion or  not,  because  we  know  that  water  is  not  absorbed  from 
the  stomach,  and  hence  can  only  aggravate  (by  its  weight)  the 
myasthenia  and  dilatation.  Where,  however,  the  various  saline 
and  alkaline  waters  can  be  readily  obtained,  they  serve  admirably 
for  lavage.  The  sodium  chlorid  spring-water  is  beneficial  in  sub- 
or  anacidity,  and  the  alkaline  waters  whenever  hyperchylia  is 
associated  with  dilatation. 

In  neoplasms  of  the  stomach,  particularly  in  carcinoma,  mineral- 
water  treatment  is  harmful.  For  ulcer,  the  Carlsbad  springs  have 
been  much  lauded  by  Leube  and  others;  but  we  coincide  with 
Ewald  in  the  opinion  that  the  same  or  perhaps  more  rapid  effects 
would  have  been  obtained  in  such  cases,  had  patients  taken  the 
rest  cure  at  home.  Rest,  diet,  and  effective  local  treatment  are 
the  things  most  needed,  and  these  can  be  obtained  much  more 
readily  at  home  than  elsewhere.  For,  after  all,  as  far  as  gastric 
sufferers  are  concerned,  the  most  important  things,  even  at  the 
springs,  are  rest  to  body  and  stomach  in  particular,  diet,  suitable 
food,  good  cooking,  etc. 

In  acute  gastritis  mineral  waters  are  useless.  There  remain  still 
to  be  considered  the  neuroses  of  secretion  and  motility.  All  secre- 
tory neuroses  are,  more  or  less,  indications  for  mineral-water  treat- 
ment, particularly  those  in  which  an  excessive  amount  of  HC1  is 
formed,  with  which  the  alkaline  waters  combine,  at  the  same  time 
exerting  a very  desirable  astringent  effect  on  the  mucosa;  for  these, 
such  waters  as  the  Saratoga  Vichy  are  applicable.  In  achylia  of 
nervous  origin  the  saline  waters  might  rationally  be  tried ; but 
where  the  glandular  elements  are  destroyed  they  can  not  restore 
the  secretion,  although  they  may  aid  in  dissolving  mucus  and  keep- 
ing the  membrane  cleaner  than  otherwise.  In  the  motor  neuroses, 
if  dependent  upon  hyperchylia  or  hypersecretion,  the  alkaline  waters 
may  benefit  by  removing  the  causes,  as  stated  above ; but  in 
insufficiency  of  the  pylorus  and  cardia  we  have  neither  heard  of 
nor  seen  improvement. 

The  proper  field  for  these  waters  is  undoubtedly  chronic  gas- 


INDICATIONS  FOR  THE  USE  OF  MINERAL  WATERS. 


315 


tritis.  With  their  judicious  use  much  good  can  be  effected.  It 
should  not  be  overlooked,  however,  that  there  may  be  a chronic 
gastritis  with  normal  or  excessive  acidity  ; here  the  alkaline  waters 
are  to  be  preferred  to  the  salines.  In  chronic  gastritis  with  achylia 
only  salines  of  mild  concentration  are  useful;  for  the  powerful 
saline  (NaCl)  waters,  such  as  Carlsbad  (Miihlbrunnen),  may  un- 
doubtedly cause  an  injurious,  alkaline,  irritative  transudate  from 
the  mucosa  if  retained  in  the  stomach. 

In  chronic  gastritis  the  still  or  the  carbonated  saline  waters 
undoubtedly  are  beneficial,  by  their  stimulating  effect  on  the  secre- 
tions. Gastric  sufferers  should  drink  their  spring-water  preferably 
warm.  Cold  spring-water  should  be  rendered  tepid  by  the  addition 
of  warmed  water  from  the  same  spring.  All  waters  which  are  to 
act  on  the  stomach  are  tolerated  better  warm  than  cold. 

In  uncomplicated  hyperacidity  and  hypersecretion  the  alkaline 
or  the  mixed  alkaline  saline  springs  are  beneficial.  In  this  country 
the  Saratoga  Vichy  is  the  most  available.  Alkaline  waters  also 
benefit  peptic  ulcer  cases  when  there  have  been  no  hemorrhages 
for  some  time,  because  they  neutralize  the  acid  excess  and  actually 
lessen  the  activity  of  secretion.  Waters  containing  sodium  sul- 
phate are  applicable  to  the  treatment  of  secondary  gastritis. 

According  to  Stille  and  Maisch  there  are,  indeed,  two  classes  of 
patients  who  require  the  use  of  very  different  mineral  waters.  The 
first  is  composed  of  that  large  body  of  invalids  in  whom  there  exists 
no  organic  change  of  structure,  but  whose  functions  are  merely 
weakened  or  clogged  by  the  strain  of  business,  the  exhaustion 
of  pleasure,  excesses  in  eating  or  drinking,  or,  in  this  country 
especially,  by  the  manifold  errors  committed  in  the  preparation 
and  consumption  of  food  and  the  disregard  of  hygienic  rules  in 
their  habits  of  living.  The  second  consists  of  that  smaller  but 
still  numerous  class  of  persons  who,  besides  being  more  or  less 
injured  by  the  causes  of  ill  health  just  enumerated,  have  been 
affected  with  definite  diseases,  and  especially  rheumatism,  gout, 
calculous  disorders,  cutaneous  eruptions,  scrofula,  syphilis,  dia- 
betes, paralysis,  uterine  disorders,  etc.  Of  these  two  classes  the 
former  is  benefited  most  by  a visit  to  the  less  mineralized  springs, 
while  the  latter  requires  a course  of  active  medicinal  treatment 
such  as  the  stronger  mineral  waters  afford.  In  both  classes  of 
patients,  but  particularly  in  the  first,  the  action  of  the  waters  is 
only  one  out  of  many  influences  that  combine  to  restore  their 
health.  Toward  that  end  a total  change  of  habits  is  one  of  the 


3j6 


MINERAL  SPRINGS. 


most  influential  agencies  in  very  many  cases.  Escape  from  the 
anxieties  and  fatigue  of  business,  from  the  excitement  of  fashion- 
able life,  the  mental  tension  of  political  and  professional  pursuits, 
the  worrying  annoyances  of  domestic  affairs,  endured,  perhaps,  in 
a large  city,  with  all  its  enervating  social  duties,  its  Babel-like 
sounds,  and  its  polluted  atmosphere, — escape  from  these  alone 
ought  to  suffice  to  restore  the  disturbed  balance  of  health.  When 
we  consider  how  much  more  probable  must  this  result  become 
when  fatigue,  anxiety,  contention,  wearisome  routine,  and  foul  air 
are  exchanged  for  repose  and  peace  in  the  midst  of  novel  scenes 
and  new  associates,  and  freedom  from  the  onerous  conventionali- 
ties of  fashionable  life,  different  apartments,  food,  and  occupation, 
it  may  even  seem  doubtful  whether,  after  all,  some  other  new  resi- 
dence would  not  profit  the  invalid  as  much  as  the  frequented 
springs.  But  there  are  two  reasons  against  this  conclusion  : the 
one  is  that,  with  many  persons,  relief  would  be  impossible  without 
an  exercise  of  the  faith  which  gives  potency  to  waters  as  well  as  to 
other  remedial  agents;  and  the  other  is  that  even  the  purest  of 
these  waters,  systematically  used,  especially  in  conjunction  with 
bathing  and  regular  exercise,  do,  in  a greater  or  less  degree,  depu- 
rate the  system  through  the  kidneys,  bowels,  and  skin,  and  by  a 
gentle  but  sustained  action  gradually  remove  effete  products  of 
tissue-change  from  the  system  and  free  the  organs  from  the 
poisons  that  tainted  them.  Judiciously  used  under  the  advice  of  a 
competent  physician,  these  almost  neutral  waters  and  the  milder 
saline  springs  are  capable,  in  a few  weeks,  of  changing  the  languid, 
indifferent,  pale,  and  feeble  invalid  into  the  lively  and  energetic 
leader  of  the  gay  crowd.  Such  rapid  transformations  are  frequently 
witnessed,  especially  at  the  hot  springs  of  Virginia,  the  Bedford 
springs,  Pa.,  at  some  of  the  Saratoga  springs  (though  in  the  last- 
mentioned  place  routine  hygienic  treatment  becomes  more  difficult 
because  of  numerous  side  temptations),  and  certain  European 
springs,  such  as  Wildbad,  Gastein,  and  Pfeffers,  none  of  which 
contains  any  considerable  proportion  of  mineral  ingredients.  But 
these  waters,  whether  drunk  warm  or  cold,  if  they  are  largely 
used,  act  as  organic  purgatives,  and  increase  materially  the  total 
amounts  of  solids,  and  especially  of  urea,  excreted  with  the  urine, 
without  causing  the  debility  which  an  equal  discharge  from  the 
bowels  would  occasion. 

Alkaline  Waters. — The  chief  ingredients  of  these  waters  are 
the  alkaline  carbonates,  especially  the  carbonate  of  sodium.  They 


ALKALINE  WATERS. 


3*7 


also  contain  varying  amounts  of  the  carbonates  of  lime,  mag- 
nesium, lithium,  sodium  chlorid,  etc.,  and  many  of  them  are 
strongly  charged  with  carbonic  acid  gas.  Although  it  is  probable 
that  the  other  saline  constituents  may  contribute  to  the  total  phys- 
iological effects  of  these  waters,  they  owe  their  main  therapeutic 
activity  to  the  alkaline  salts  they  contain.  The  temperature  of 
these  springs  is  also  a point  worthy  of  consideration.  In  a general 
way  it  may  be  said  that  the  physiological  action  of  these  waters  is 
like  that  of  any  alkaline  salt,  plus  the  effect  produced  by  the  circu- 
lation of  large  quantities  of  water  in  the  system.  The  carbonate 
of  sodium  neutralizes  free  acids  or  fermentation  products  in  the 
stomach,  whether  taken  during  or  after  meals.  According  to 
Brunton  and  Sidney  Ringer,  the  stronger  alkaline  waters,  if  taken 
before  meals,  increase  the  secretion  of  gastric  juice.  This,  in  the 
author’s  experience,  is  doubtful.  The  fact  is,  distilled  water  will 
also  cause  a secretion  of  gastric  juice  in  the  normal  stomach,  but 
will  not  neutralize  the  acid  thus  secreted,  as  the  alkaline  waters 
must  invariably  do.  This,  however,  is  not  an  effective  way  of 
treating  anacidity.  For  this  condition  the  treatment  is  given  in 
the  clinical  part.  The  carbonic  acid  set  free  by  the  decomposi- 
tion of  the  carbonates  in  the  stomach  and  the  sodium  chlorid 
usually  present  in  these  waters  act  as  a stimulant  to  the  gastric 
mucous  membrane,  promoting  secretion  and  counteracting  any 
disturbing  influence  exerted  by  the  carbonate.  The  free  carbonic 
acid  frequently  contained  in  waters  of  this  class,  by  its  stimulating 
effects  on  gastric  peristalsis,  accelerates  digestion,  and  thereby 
increases  the  desire  for  food. 

It  would  appear,  therefore,  that  the  alkaline  waters  have  a wide 
range  of  usefulness.  They  seem  to  be  especially  indicated  in 
gastric  affections  in  which  there  is  an  excessive  production  of 
hydrochloric  acid,  as  in  acid  dyspepsia,  atony  of  the  gastric 
mucous  membrane,  and  gastric  ulcer.  In  all  catarrhal  conditions 
of  the  stomach  they  are  most  serviceable,  but  a free  and  prolonged 
use  lowers  the  nutrition,  except  in  case  of  waters  containing 
chlorid  of  sodium. 

The  names  of  a few  of  the  more  important  Alkaline  Waters 
are  here  appended  : 

Vichy,  in  France;  Ems  and  Fachingen,  in  Germany;  Saratoga 
Vichy  (rich  in  C02),  New  York;  St.  Louis  Springs,  Michigan 
(poor  in  C02);  Bethesda  Springs,  Wisconsin.  Other  sodium 
chlorid  waters,  containing  also  some  carbonates  and  C02,  are: 


MINERAL  SPRINGS. 


Hathorn,  Congress,  and  Kissengen  Springs,  in  Saratoga,  New  York  ; 
Homburg,  Wiesbaden,  Kissingen,  and  Selters,  in  Germany;  Bour- 
bonne,  in  France. 

All  alkaline  waters  contain  more  or  less  carbon  dioxid,  and  their 
most  important  ingredients  are  the  alkaline  carbonates.  They 
also  contain  sodium  chlorid  and  sometimes  sodium  sulphate.  In 
some,  one  variety  of  salts,  in  others,  another  preponderates.  Gen- 
erally speaking,  the  European  waters  are  richer  in  alkalies  than 
are  the  American. 

Alkaline  waters  are  useful  in  uric  acid  diathesis  and  lithemic 
conditions,  gout,  chronic  rheumatism,  obesity,  hepatic  engorgement, 
gall-stones,  hyperacidity,  gastric  ulcer,  and  catarrhs  of  the  mucous 
membranes,  especially  of  the  stomach,  respiratory  tract,  and 
bladder. 

Alkaline  Sulphur  Waters. — Richfield  Springs,  Sharon  Springs, 
and  Avon  Springs,  in  New  York;  Greenbrier  White  Sulphur 
Springs,  in  West  Virginia;  Harrogate,  in  England;  Neuendorf 
and  Meinberg,  in  Germany;  Aix-la-Chapelle,  in  Rhenish  Prussia. 

Those  waters  containing  sulphureted  hydrogen  in  addition  to 
other  ingredients  are  used  moderately  in  gout,  chronic  rheumatism, 
obesity,  and  chronic  eczema.  They  are  often  supplemented  by  a 
course  of  chalybeate  waters. 

Alkaline  and  saline  purges  contain  a high  percentage  of  sodium 
and  magnesium  sulphates.  These  waters  are  often  called  “ bitter 
waters.”  Such  are  Piillna,  in  Bohemia  (the  strongest  of  all  and 
one  of  the  oldest  known)  ; Carlsbad  (Sprudel),  in  Bohemia  ; Marien- 
bad  (Kreuzbrunnen),  in  Bohemia;  Friedrichshall,  in  Germany; 
Franz  Josef,  in  Austria;  Kissingen  Bitter  Water,  in  Bavaria  ; Hun- 
yadi  Janos,  in  Hungary;  Rubinat  Condal  Spring  and  Villacabras, 
in  Spain ; Crab  Orchard  and  Estill  Springs,  in  Kentucky ; Bedford 
Springs,  in  Pennsylvania ; Epsom,  in  England ; some  of  the  Sara- 
toga waters.  These  waters  are  useful  to  counteract  indiscretions 
in  diet  and  congestion  of  the  liver.  The  Rubinat  water  is  effective 
and  possesses  the  advantage  of  being  less  disagreeable  than  many 
of  the  others.  Villacabras  water  is  a Spanish  sodium  sulphate, 
strongly  purgative  water,  obtained  not  far  from  Madrid. 

These  waters  should  be  taken  either  very  cold  or  in  a half-pint 
of  very  hot  water.  If  drunk  lukewarm,  their  taste  is  nauseous 
and  may  excite  emesis.  We  advise  that  these  powerful  waters 
be  entirely  avoided  where  there  is  any  distinct  organic  disease 
of  the  stomach. 


SALINE  WATERS. 


319 


Various  other  zvaters  are  the  Alum  Springs,  in  Virginia  ; Oak 
Orchard  Acid  Spring,  in  New  York;  Bourboule,  in  France,  which 
contains  arsenic.  Roncegno  water  is  a ferruginous  arsenical  water 
from  the  Tyrolean  province  of  Trent. 


COMPARATIVE  CHART  ILLUSTRATIVE  OF  ALKALINE  WATERS.— 
[Baruch.) 


One  Pint  Contains  : 

American. 

European. 

Sodium 

Carbonate. 

Carbonic  Acid 
Gas. 

Temperature. 

Other  Prominent 
Constituents. 

Vichy  (Grand 
Grible  Spring) , 

Grs. 

Cub.  in. 

Fahr. 

Ojo  Caliente  Spring, 

France,  .... 

26 

14 

105.8° 

Sodium  chlorid,  4 grs.; 
sodium  sulphate,  2 
grs.  ; potassium  car- 
bonate, 2 grs. 

Sodium  chlorid,  4 grs.; 
sodium  sulphate,  1 gr. 

New  Mexico,  . . 

Fachingen  Spring, 

14 

IOO° 

Saratoga  Vichy 

Germany,  . . . 

19 

32 

50° 

Sodium  chlorid,  4 grs.; 
calcium  carbonate,  2 
grs. 

Spring,  New  Y ork, 

Ems  (Kesselbrun- 
nen  Spring), 

II 

48 

5o° 

Calcium  and  magnesium 
carbonates,  17  grs.; 
sodium  and  potassium 
chlorids,  18  grs. 

St.  Louis  Spring, 

Germany,  . . . 

IO 

6 

1150 

Sodium  chlorid,  7 grs.; 
calcium  carbonate,  1 
gr\ 

Michigan,  . . . 

7 

1 

5o° 

Calcium  and  magnesium 
carbonates,  6 grs.; 
calcium  sulphate,  7 
grs. 

Saline  Waters. — This  class  may  be  conveniently  subdivided 
into,  first,  waters  containing  chiefly  the  chlorid  of  sodium;  and, 
second,  waters  containing  large  quantities  of  the  sulphates  of 
sodium  and  magnesium — the  so-called  “bitter  waters”  of  German 
authors. 

The  Sodium  Chlorid  Waters. — These  waters  contain,  besides 
large  quantities  of  sodium  chlorid,  a certain  proportion  of  other 
chlorids,  especially  those  of  lime  and  magnesium,  and  small 
amounts  of  alkaline  and  earthy  sulphates  and  carbonates,  iodids 


320 


MINERAL  SPRINGS. 


and  bromids.  Carbonate  of  iron  is  sometimes  present  in  consid- 
erable quantity.  The  gases  consist  for  the  most  part  of  carbonic 
acid,  which  renders  the  water  more  agreeable  to  the  palate  and 
more  readily  absorbed.  Some  of  these  waters  are  heavily  charged 
with  sulphureted  hydrogen.  They  occur  both  as  cold  and  ther- 
mal springs,  and  may  be  utilized  both  for  drinking  and  bathing 
purposes. 

The  physiological  action  of  these  waters  is  chiefly  attributable 
to  the  presence  of  sodium  chlorid.  This  salt,  as  is  well  known,  has 
a stimulating  effect  upon  all  the  mucous  membranes  of  the  body, 
especially  that  of  the  gastro-intestinal  tract.  In  the  stomach  it  dis- 
solves the  mucus,  increases  the  secretion  of  gastric  juice,  thereby 
promotes  the  digestion  of  albuminous  substances,  and  excites  peris- 
talsis. In  the  intestines  it  stimulates  the  flow  of  pancreatic  juice 
and  bile,  and,  owing  to  its  well-known  influence  on  the  process  of 
osmosis,  promotes  the  absorption  of  food.  Intestinal  peristalsis  is 
also  increased,  and,  if  the  sodium  chlorid  is  present  in  large  quan- 
tity, the  water  may,  in  its  effects,  be  laxative  and  even  purgative. 
Some  authors  have  regarded  this  purgative  action  as  representing 
the  chief  therapeutic  virtues  of  these  waters,  but,  according  to 
Flechsig,  it  is  subordinate  in  importance  to  the  effect  of  the  sodium 
chlorid  on  the  blood.  He  states  that  this  salt  exerts  considerable 
influence  on  the  process  of  tissue  metabolism,  augmenting  the 
metamorphosis  of  nitrogenous  matters  and  increasing  the  oxida- 
tion of  albuminous  substances,  as  is  shown  by  the  increased  quan- 
tity of  solids  in  the  urine.  The  iodids  and  bromids  contained  in 
some  of  these  waters  are  usually  present  in  such  very  minute 
amounts  that  it  is  doubtful  whether  they  contribute  to  their  thera- 
peutic action ; at  any  rate,  it  is  impossible  to  separate  their  effects 
from  those  of  the  sodium  chlorid. 

The  therapeutic  indications  of  sodium  chlorid  waters,  as  based 
upon  their  physiological  action,  are  sufficiently  obvious.  Their 
stimulating  effects  upon  the  mucous  membranes  have  been  utilized 
in  the  treatment  of  catarrhal  processes,  especially  in  the  stomach, 
duodenum,  and  bile-ducts;  and  in  chronic  intestinal  catarrh 
associated  with  constipation,  their  use  has  been  highly  com- 
mended. 


BITTER  OK  PURGATIVE  WATERS. 


321 


COMPARATIVE  CHART  ILLUSTRATIVE  OF  SALINE  WATERS.— 

[Baruch.) 


American. 

European. 

Sodium 

Chlorid. 

Carbonic 
Acid  Gas. 

)nk  Pin* 

it 

E = 

<L> 

H 

r Contains: 

Other  Prominent 
Constituents. 

Homburg  (Eliza- 
bethbrunnen), 

Grs. 

Cub.  in. 

Fahr. 

Grains. 

Ballston  Artesian 
Lithia  Well,  New 

Germany,  . . . 

79 

48 

50° 

Chlorids  of  calcium  and. 
magnesium,  15  ; cal- 
cium carbonate,  11. 

York, 

Wiesbaden  (Koch- 
brunnen),  Ger- 

93 

53 

Magnesium  and  calcium 
carbonate,  34  ; potas- 
sium chlorid,  4;  lithium 
carbonate,  0.7. 

Hathorn  Spring, 

many,  .... 

52 

17 

155° 

Chlorid  of  potassium,  1 ; 
calcium  carbonate,  3. 

Saratoga,  New 

York, 

Bourbonne  (Fon- 
taine Chaude), 

64 

47 

47° 

Calcium  and  magnesium 
carbonates,  28. 

Congress  Spring, 

France,  .... 

46 

1490 

Calcium  chlorid,  5 ; cal- 
cium sulphate,  6. 

Saratoga,  New 

York, 

Kissingen  (Rak- 

50 

49 

52° 

Calcium  and  magnesium 
carbonates,  21 ; sodium 
bromid,  1. 06. 

Kissengen  Spring, 

oczi),  Germany, 

44 

42 

51° 

Potassium  chlorid,  2 ; 
calcium  carbonate,  8. 

Saratoga,  New 

York, 

42 

45 

0 

0 

Calcium  and  magnesium 
carbonates,  26 ; sodium 
carbonate,  8 ; lithium 
carbonate,  0.64. 

Selters,  Germany, 

17 

30 

62° 

Sodium  carbonate,  6. 

Saratoga  Seltzer 

Sodium  carbonate,  2;  cal- 
cium and  mignesium 
carbonates,  10. 

Spring,  New  York, 

17 

5o° 

Bitter  or  Purgative  Waters. — This  name  has  been  applied  to 
waters  characterized  by  a high  percentage  of  the  sulphates  of 
sodium  and  magnesium.  They  also  contain  considerable  quanti- 
ties of  the  sulphates  of  lime,  and  the  carbonates  of  lime  and 
magnesium,  though  rarely  small  amounts  of  carbonic  acid  gas. 
Carbonate  of  sodium,  however,  is  seldom,  if  ever,  found  in 
them. 

The  chief  physiological  action  of  these  waters  is  comprised  in 
the  stimulating  effect  which  they  exert  upon  the  mucous  mem- 
branes of  the  gastro-intestinal  tract.  They  give  rise  to  a profuse 


322 


MINERAL  SPRINGS. 


watery  secretion  of  a serous,  or  even  mucous,  character,  and  thus 
act  as  purgatives.  If  taken  in  large  quantities,  they  frequently 
produce  gastric  and  intestinal  disturbances,  and  their  protracted 
use  is  apt  to  be  followed  by  atony  of  the  intestines  and  intestinal 
catarrh.  It  is  as  yet  a matter  of  speculation  whether  this  purga- 


COMPARATIVE  CHART  ILLUSTRATIVE  OF  BITTER  AND  PURGATIVE 
WATERS. — {Baruch.') 


One  Pint  Contains: 

American. 

European. 

Sodium 

Sulphate. 

Magnesium 

Sulphate. 

Carbonic 
Acid  Gas. 

Temperature. 

Other  Prominent 
Constituents. 

Grs. 

Grs. 

Cub.  in. 

Fahr. 

Crab  Orchard, 
Foley's  Spring, 

Piilln  a,  Bohemia, 

124 

93 

Chlorid  of  magne- 
sium, 16 grs.;  mag- 
nesium carbonate, 
6 grs. 

Kentucky,  . . 

Friedrichshall, 

7 

25 

Calcic  carbonate,  7 
grs. ; potassium  sul- 
phate, 1 gr. 

Estill’s  Springs, 
Irvine  Springs, 

Germany,  . . 

41 

39 

5 

46° 

Sodium  chlorid,  67 
grs.;  magnesium 
chlorid,  31  grs.; 
calcic  sulphate,  II 
grs. 

Kentucky,  . . 

Carlsbad  (Spru- 

32 

Calcic  carbonate,  4 
grs.;  sodium  chlo- 
rid, 2 grs. 

Bedford  Springs, 

del),  Bohemia, 

19 

8 

162° 

Sodium  carbonate,  9 
grs.;  sodium  chlo- 
rid, 8 grs. 

Pennsylvania, 

Marienbad 
(Kreutzbrunnen) , 

10 

9 

58° 

Chlorid  of  sodium,  I 
gr. ; calcium  sul- 
phate, 2 grs. 

Harrodsburg 
Spring,  Saloon 
Spring,  Ken- 

Bohemia, . . 

36 

15 

53° 

Sodium  carbonate,  8 
grs.;  sodium  chlo- 
rid, II  grs. 

tucky,  .... 

28 

Calcic  sulphate,  10 
grs.;  sodium  chlo- 
rid, I gr. 

tive  action  is  due  to  the  increased  exudation  of  fluids,  or  whether 
it  results  from  the  stimulation  of  intestinal  peristalsis,  as  is  assumed 
by  Flechsig  and  others.  Owing  to  the  increased  peristalsis,  the 
passage  of  food  through  the  intestines  is  accelerated  ; and  in  con- 
sequence of  the  diminished  absorption  of  nutriments  engendered 


SULPHURETED  WATERS. 


323 


by  this,  a loss  of  weight  and  disappearance  of  the  fatty  tissue 
results. 

It  follows  from  the  above  considerations  that  the  use  of  these 
waters  is  restricted  to  cases  in  which  we  desire  to  stimulate  the 
intestinal  secretions,  as  in  chronic  constipation  occurring  in  ple- 
thoric persons,  engorgements  of  the  abdominal  and  pelvic  viscera, 
hemorrhoids,  etc.  They  also  prove  serviceable  in  cases  of  obesity, 
as  part  of  a treatment  of  denutrition.  On  the  other  hand,  their 
use  is  contraindicated  in  anemic  persons,  and  where  there  is  great 
irritability  of  the  stomach  and  intestines,  with  a tendency  to 
diarrhea. 

American  waters  of  this  class  are  somewhat  weaker  in  sulphates 
of  sodium  and  magnesium  than  the  European,  but  the  quantity  of 
purgative  salts  present  in  the  former  is  quite  sufficient  to  produce 
active  therapeutic  effects.  All  these  waters  contain  a considerable 
amount  of  sodium  chlorid,  which  contributes  essentially  to  their 
physiological  action. 

The  Bedford  Spring  (Pa.)  water  is  especially  to  be  recommended 
on  account  of  its  mildness.  It  is,  in  our  opinion,  of  no  advantage 
when  spring-waters  possess  an  excessively  large  percentage  of 
drastic  salts.  In  a concentrated  solution  magnesium  chlorid  acts 
as  a cellular  poison  on  the  superficial  gastric  and  intestinal  epithe- 
lium when  used  for  weeks.  Bedford  Mineral  Magnesia  Spring  has 
also  a mildly  diuretic  effect;  its  laxative  effect  is  not  experienced 
until  at  least  500  c.c.  are  taken  in  twelve  hours. 

Sulphureted  Waters. — The  constituent  imparting  to  these 
waters  their  distinguishing  characteristic  is  the  sulphureted  hydro- 
gen which  they  contain  in  greater  or  lesser  amount.  With  this 
gas  we  find  associated  a varying  quantity  of  sulphur  combinations, 
such  as  the  sulphids  of  potassium,  sodium,  calcium,  and  magne- 
’ sium.  They  also  contain  the  alkaline  and  earthy  sulphates  and 
carbonates,  the  chlorid  of  sodium,  and  the  sulphates  and  carbonates 
of  iron  ; and  these  are  frequently  present  in  large  quantities,  and 
certainly  play  a not  unimportant  part  in  the  therapeutic  action  of 
these  waters.  According  to  Daland,  “ a sulphur  spring  of  moderate 
strength  contains  not  less  than  twelve  cubic  inches  of  sulphureted 
hydrogen  in  the  gallon,  though  many  springs  contain  so  small  an 
amount  that  therapeutically  they  are  inert,  and  the  good  effects 
observed  are  due  to  the  influence  of  the  increased  use  of  water, 
change  of  scene  and  climate,  cessation  of  work,  regular  meals,  good 
hygiene,  and  hope — all  of  which  contribute  strongly  to  restore 


324 


MINERAL  SPRINGS. 


health  at  all  springs.”  Many  of  the  sulphur  waters  are  thermal, 
and  are  chiefly  employed  in  baths. 

Regarding  the  physiological  action  of  sulphur  waters  on  the 
system,  nothing  positive  can  be  said.  Various  plausible  theories 
have  been  proposed  to  account  for  their  curative  effects  in  the 
diseases  for  which  they  are  employed.  It  is  claimed  that  their 
chief  action  is  exerted  on  the  intestinal  canal,  where  they  stimulate 
the  functions  of  the  glands,  augmenting  secretion  and  producing 
laxative  effects.  When  administered  for  prolonged  periods  they 
give  rise  to  gastro-intestinal  disorders  and  exert  a debilitating 
influence  upon  the  blood,  heart,  and  lungs,  as  evidenced  by  anemia, 
cardiac  weakness,  etc.  According  to  Leichtenstern,  the  sulphureted 
hydrogen  absorbed  into  the  blood  is  rapidly  converted  into  sul- 
phuric acid,  and  is  therefore  devoid  of  any  specific  effect,  unless 
present  in  very  large  amounts.  On  the  other  hand,  Stifft  concludes 
that  the  sulphureted  hydrogen  has  a specific  excitant  action  upon 
the  sensitive  fibers  of  the  pulmonary  branches  of  the  pneumogas- 
tric  and  upon  the  respiratory,  cardiac,  and  vasomotor  centers,  its 
prolonged  use  giving  rise  to  paralysis  from  overstimulation.  In 
this  way  he  explains  the  action  of  the  sulphur  waters  upon  the 
respiratory  and  circulatory  systems,  upon  tissue-metabolism,  and 
upon  the  secretory  and  excretory  functions. 

These  waters  have  been  administered  internally  in  passive  con- 
gestion of  the  abdominal  and  pelvic  viscera,  especially  in  plethoric 
persons ; in  enlargements  of  the  liver  and  spleen  ; hemorrhoids  ; 
chronic  intestinal  catarrh;  and  chronic  poisoning  by  metals.  In  the 
form  of  baths  they  have  been  recommended  in  gout  and  chronic 
rheumatism,  but  their  curative  effect  in  these  cases  is  attributable 
to  the  elevated  temperature  of  the  waters  rather  than  to  any 
specific  action  of  the  sulphureted  hydrogen  or  other  constituents. 
At  many  baths  the  internal  or  local  use  of  the  waters  is  combined 
with  inhalation  of  the  gases  or  of  the  nebulized  waters ; and  this 
method  has  been  found  useful  in  the  treatment  of  chronic  catarrhs 
of  the  pharynx,  larynx,  and  bronchi.  Sulphureted  waters  are,  in 
our  estimation,  worthless  as  a therapeutic  agent  in  gastro-intestinal 
diseases. 

Sulphureted  waters  are  abundantly  represented  in  the  United 
States.  In  Virginia  they  are  particularly  well  represented — vide 
Jordan’s  White  Sulphur  Springs,  Frederick  County  ; Greenbrier 
White  Sulphur  Springs,  Roanoke  Red  Sulphur  Springs,  Yellow 
Sulphur  Springs,  Montgomery  County,  Va.,  and  many  others  in 


CHALYBEATE  WATERS. 


325 


other  States.  There  is  certainly  no  necessity  for  traveling  to 
Aachen-Baden  (near  Vienna),  Leuk,  or  Weilbach  to  use  waters  of 
this  type. 

The  following  chart  illustrates  the  superiority  of  the  sulphur 
waters  of  America : 


COMPARATIVE  CHART  ILLUSTRATIVE  OF  SULPHURETED 
WATERS. — {Baruch.) 


One 

Pint  Contains: 

American. 

European. 

Sulphureted 

Hydrogen. 

Sulphids. 

Temperature. 

Other  Prominent 
Constituents. 

Cub. 

in. 

Grs. 

Fahr. 

Sandwich  Spring,  On- 

Neundorf, Germany, 

i.:8 

o-55 

53° 

Calcium  and  magnesium 
sulphates.  10  grs. 

tario,  Canada,  . . 

Aix-le-Bains, 

52° 

Chlorid  of  magnesium,  19 
grs.;  calcium  sulphate, 
15  grs. 

France,  

0.82 

1080 

Calcium  carbonate,  1 gr. 

Sharon  Spring.  White 
Sulphur  Spring, 

New  York,  . . . 

Harrogate,  Eng- 

0  28 

00 

0 

Calcium  and  magnesium 
sulphates,  24  grs. 

Paroquet  Spring, 

land,  

053 

1-54 

Sodium  chlorid,  86  grs.; 
potassium  and  magne- 
sium chlorids,  10  grs. 

Kentucky,  . . . 

3 75 

Sodium  chlorid,  39  grs. 

Meinberg,  Germany, 

0.61 

0 67 

00 

0 

Sodium  sulphate,  6 grs. 

Salt  Sulphur  Spring, 
Iodin  Spring,  W. 

Virginia,  .... 

Sodium  sulphate,  3 grs.; 
calcium  sulphate,  8 grs. 

Chalybeate  Waters. — A large  number  of  mineral  springs  con- 
tain the  salts  of  iron,  but  the  quantity  present  is  frequently  so 
small  as  to  be  practically  devoid  of  therapeutic  effects.  In  the 
class  under  consideration  only  waters  containing  a sufficient  quan- 
tity of  chalybeates  to  be  of  value  in  the  treatment  of  disease  will 
be  mentioned. 

Iron  salts  usually  occur  in  the  form  of  the  carbonate  or  sulphate. 
Other  constituents,  which  are  sometimes  present  in  large  amounts, 
are  the  alkaline  carbonates  and  sulphates,  the  earthy  carbonates, 
sodium  chlorid,  alum,  and  sulphuric  acid.  Alum  often  exists  in 
considerable  quantities,  especially  in  the  chalybeate  springs  of 
Virginia. 


326 


MINERAL  SPRINGS. 


Chalybeate  waters  containing  the  carbonate  of  iron  are  clear, 
odorless,  have  a slight  inky  taste,  and  are  highly  charged  with 
carbonic  acid  gas,  which  renders  them  palatable.  They  are  chiefly 
employed  for  drinking  purposes.  The  sulphate-of-iron  waters 
have  a marked  astringent  taste,  which  sometimes  proves  an  objec- 
tion to  their  use.  This  astringency  may  be  decidedly  increased  by 
the  presence  of  alum. 

The  following  chart*  illustrates  the  superior  quality  of  some 
American  chalybeate  springs  : 


CHALYBEATE  WATERS. — [Baruch. ) 


One  Pint  Contains: 

American. 

European. 

Sulphates 
of  Iron. 

Carbonates 
of  Iron. 

Carbonic 
Acid  Gas. 

Other  Prominent 
Constituents. 

Brighton,  England, 

I 80 

Calcium  sulphate,  4 grs. 

Church  Hill  Alum 

Springs,  Virginia, 

Spa  (Buhon),  Bel- 

19 8 

Magnesium  and  calcium 
sulphates,  22  grs. ; alu- 
minium sulphate,  9 grs. 

gium,  

0.67 

71.6 

Small  amounts  of  calcium 
carbonate  and  alumina. 

Rock  Enon  Springs, 

Virginia,  .... 

Schwalbach  (Stahl- 
brunnen),  Ger- 

1.78 

Calcium  and  magnesium 
sulphates,  2 grs.  ; cal- 
cium and  sodium  carbon- 
ates, alumina. 

Vichy  Springs,  New 

many,  

50.2 

Calcium  carbonate,  I gr. ; 
manganese  carbonate 
0. 10  gr. 

Almaden,  Cal.,  . 

St.  Moritz  (Grande 
Source),  Switzer- 

O.60 

29.8 

Sodium  carbonate,  17  grs.; 
calcium  carbonate,  3 grs  ; 
magnesium  sulphate,  I 
gr.;  sodium  chlorid,  4 
grs. 

land,  

39  2 

Sodium  carbonate,  1 gr.; 
calcium  carbonate,  6 
grs.;  sodium  sulphate, 
1 gr. 

Estill  Springs,  Ken- 

tucky,   

4-15 

Calcium  carbonate,  I gr.; 
magnesium  sulphate,  I 
gr- 

* These  charts  make  no  claim  to  completeness.  Boas  has  suggested  a more  extensive 
enumeration  of  the  German  chalybeate  springs  in  this  book  (see  Review  on  Hemmeter’s 
“ Diseases  of  the  Stomach,”  “ Deutsche  med.  Wochenschrift,”  April  14, 1898,  No.  15  ; 
* ‘ Literaturbeilage,”  No.  10,  p.  58).  This,  however,  can  not  fairly  be  considered 


INDICATIONS  FOR  THE  USE  OF  ACIDULOUS  WATERS.  327 

The  physiological  action  of  chalybeate  waters  is  essentially 
similar  to  that  of  all  iron  compounds;  they  promote  constructive 
metamorphosis,  increasing  the  number  of  red  corpuscles  in  the 
blood  and  stimulating  all  the  body-functions.  For  internal  use 
the  waters  containing  the  carbonate  of  iron  are  preferable,  since 
they  are  less  apt  to  disturb  the  stomach,  and  are  more  easily 
assimilated,  owing  to  the  carbonic  acid  gas  present.  According 
to  the  character  of  the  case,  it  may  be  necessary  to  select  an  iron 
water  containing  alkalies,  sodium  chlorid,  sulphate  of  sodium  and 
magnesia,  or  alum. 

The  chalybeate  waters  have  been  recommended  in  anemia, 
chlorosis,  and  all  conditions  attended  with  anemia,  such  as  hysteria 
and  neurasthenia  ; chronic  endometritis,  dysmenorrhea,  amenorrhea, 
chronic  gonorrhea,  and  spermatorrhea;  chronic  affections  of  the 
kidneys,  diabetes  mellitus,  chronic  gastritis,  nervous  dyspepsia, 
chronic  diarrhea,  etc. 

Among  the  iron  and  alum  springs,  Bedford  Alum  Spring  has 
been  found  remarkably  efficacious  by  Baruch  in  chronic  diarrhea, 
which  had  resisted  both  private  and  hospital  treatment. 

The  contraindications  to  their  use,  as  given  by  Flechsig,  com- 
prise all  febrile  and  congestive  conditions  and  advanced  organic 
diseases  of  the  lungs,  liver,  and  kidneys.  The  sulphate-of-iron 
waters  are  excellent  astringents  and  disinfectants,  and  have  been 
highly  recommended  in  chronic  diarrhea,  gastric  ulcer,  etc. 

Acidulous  Waters. — These  waters  owe  their  therapeutic  prop- 
erties to  the  large  quantity  of  carbonic  acid  gas  they  contain,  the 
solid  constituents  being  present  only  in  small  amounts.  As  has 
been  stated,  many  alkaline  and  saline  waters  contain  considerable 
quantities  of  C02;  but  its  effects,  whatever  they  may  be,  are  com- 
pletely subdued  by  those  of  the  mineral  ingredients.  In  the  acid- 
ulous waters,  however,  the  carbon  dioxid  is  the  chief  therapeutic 
agent,  and  for  this  reason  it  becomes  necessary  to  discuss  them 
as  a separate  class  of  mineral  waters. 

The  physiological  action  of  carbonated  waters  is  comprised  in  a 
gentle  stimulative  effect  upon  the  mucous  membrane  of  the 
stomach,  promoting  peristalsis,  and  thereby  a more  rapid  evacua- 
tion of  its  contents.  The  pulse  and  respiration  are  said  to  be 


within  the  range  of  our  work.  We  can  not  even  do  justice  to  our  native  mineral  springs. 
For  fuller  information  we  must  refer  to  the  works  quoted  in  the  beginning  of  this 
chapter. 


328  IMPORTANT  MEDICINAL  AGENTS  IN  GASTRIC  THERAPY. 

slightly  accelerated,  and  a large  quantity  of  urine  is  excreted.  It 
seems,  however,  that  this  diuretic  effect  is  not  attributable  to  the 
carbonic  acid  gas,  as  is  assumed  by  some  authors,  but  rather  to  the 
large  quantities  of  water  which  the  patient  is  able  to  imbibe  with- 
out distress,  for  the  quantity  of  the  gas  absorbed  into  the  blood 
through  the  walls  of  the  stomach  is  certainly  too  small  to  produce 
systemic  effects. 

The  acidulous  waters  have  been  chiefly  recommended  in  gastric 
disorders,  especially  those  of  neurotic  origin;  and,  owing  to  their 
agreeable  taste,  they  form  excellent  table  waters.  They  relieve 
nausea,  increase  the  appetite,  and  aid  digestion  by  stimulating  the 
secretion  of  HC1.  On  account  of  their  stimulating  effect  upon  the 
peripheral  cutaneous  nervous  system,  they  have  also  been  employed 
as  baths. 


CHAPTER  VI. 

IMPORTANT  MEDICINAL  AGENTS  IN  GASTRIC  THERAPY. 

HC1  is  given  in  the  absence  or  diminution  of  the  normal  secre- 
tion mainly  for  three  purposes  : (1)  To  supplement  gastric  prote- 
olysis; (2)  to  act  as  an  antiseptic;  (3)  as  a tonic  and  stomachic. 

To  these  effects,  that  we  have  in  mind  in  supplying  PI  Cl,  may 
be  added  its  influence  as  a regulator  of  the  gastric  peristalsis ; 
and  that  it  brings  the  insoluble  calcium  and  magnesium  salts  of  the 
ingesta  into  solution ; in  fact,  all  of  the  objects  and  functions  that 
are  recognized  as  physiological  to  the  HC1  (see  p.  49)  may  be  at 
least  partially  accomplished  by  supplying  it  in  sufficient  quantity. 

The  HC1  deficit — i.  e .,  the  amount  of  decinormal  HC1  solution 
that  must  be  added  until  the  reaction  of  the  chyme  shows  free 
HC1 — should  be  determined  when  the  reactions  for  free  HC1 
turn  out  negative.  In  one  case  the  deficit  may  be  very  slight, 
in  another  very  considerable.  Slight  deficits  generally  yield 
readily  to  treatment  by  diet  and  lavage,  often  without  adminis- 
tration of  HC1 ; large  deficits  may  be  a sign  of  atrophy  and 
never  yield  to  HC1  therapy,  no  matter  how  much  is  given.  But 
the  question  arises,  Can  it  be  supplied  in  sufficient  quantity  ? 
The  simple  presence  of  free  HC1  does  not  contraindicate  the 


LOSS  OF  HCl  SECRETION  DISPOSES  TO  ILL  HEALTH.  329 


administration  of  the  acid.  Positive  reaction  to  Congo  paper  and 
phloroglucin-vanillin  indicates,  it  is  true,  that  MCI  is  secreted  in 
excess  of  what  is  required  to  combine  with  the  food.  In  healthy 
digestion  it  is  always  found  that  this  excess  amounts  on  the 
average  to  30  c.c.  of  a decinormal  solution  of  NaOH  after  an  Ewald 
test-meal  (in  Baltimore) ; and  it  seems  to  be  what  is  necessary  or 
advantageous,  not  for  digestive  purposes  (for  even  with  a large 
excess  of  HCl  it  is  not  the  rule  for  all  the  proteid  matter  to  be 
digested  in  the  stomach),  but  for  destroying  the  exuberance  of 
micro-organisms  swallowed  with  the  food.  The  frequently  quoted 
cases  without  any  gastric  secretion  whatever  who  succeed  in 
maintaining  their  nitrogen  equilibrium, — and  we  have  seen  many 
such, — and  the  experiment  with  the  dog  (Kaiser  and  Czerny) 
whose  weight  was  kept  up  although  the  largest  portion  of  the 
stomach  was  removed,  and  the  total  extirpations  of  the  stomach 
by  Schlatter,  Brigham,  and  others,  constitute  but  a weak  argu- 
ment against  the  therapy  of  HCl.  For  although  such  patients 
manage  to  get  along  fairly  well,  it  is  only  under  the  most  careful 
diet  and  by  taking  very  little  exercise  that  they  maintain  their 
health.  Permanent  and  perfect  health  with  total  absence  of  gastric 
secretion  is  rarely  observed,  except  in  those  who  are  able  to  rest 
much  and  have  their  food  prepared  with  great  care.  These  facts 
must  not  be  overlooked  in  the  work  of  von  Noorden  (“  Ueber  die 
Ausnutzung  der  Nahrung  bei  Magenkranken,”  “ Zeitschrift  f.  klin. 
Med.,”  1890,  Bd.  xvii),  which  demonstrated  that  absolute  and  per- 
manent deficiency  of  gastric  juice  may  be  accompanied  by  perfect 
health.  This  health  is  perfect  under  the  conditions  mentioned,  but 
when  they  are  taxed  by  work  or  the  diet  is  not  the  usual  one,  suffer- 
ing becomes  manifest.  If  achylia  gastrica  could  really  exist  without 
any  subjective  or  objective  disturbance,  how  is  it  that  so  many  of 
these  patients  consult  the  stomach  specialists  and  are  reported  by 
them  in  literature?  When  we  must  work  for  our  living  and  can  not 
have  the  benefit  of  the  dietetic  kitchen  at  all  times,  we  must  have 
an  active  gastric  juice  to  partially,  at  least,  disinfect  and  dissolve  our 
food,  and  a person  who  secretes  no  gastric  juice  is  or  soon  becomes 
a patient.  In  a recent  article  on  Achylia  Gastrica  by  F.  Martius  and 
O.  Lubarsch  (published  by  T.  Deuticke,  Leipzig,  1897),  the  authors 
arrive  at  the  conclusion  that  neither  simple  achylia  nor  that  depen- 
dent upon  atrophy  of  the  mucosa  (anadenia)  can  bring  about  severe 
anemic  or  cachectic  conditions  unless  motor  insufficiency,  atrophy 
of  the  intestinal  mucosa,  or  general  diseases  (tuberculosis,  lues, 
22 


330  IMPORTANT  MEDICINAL  AGENTS  IN  GASTRIC  THERAPY. 

infections,  etc.)  are  added.  Even  if  this  is  true,  generally  speaking 
it  does  not  disprove  the  statement  that  absence  of  HC1  in  the  gas- 
tric secretion  compels  the  individual  to  lead  the  life  of  a patient. 
But  over  and  beyond  this,  Flint  (, loc.cit .),  Fenwick  (“The  Lancet,” 
1877),  Quinke  (“  Samml.  klin.  Vortrage,”  No.  ioo,  1876),  Nothnagel 
(“  Deutsch.  Arch.  f.  klin.  Med.,”  Bd.  xxiv,  1879),  Osier  (“  Amer. 
Jour.  Med.  Sciences,”  April,  1897),  Kinnikut  (“Amer.  Jour.  Med. 
Sciences,”  October,  1887),  also  Rosenheim  and  G.  Meyer  (both  in 
article  on  “Achylia,”  by  Martius  and  Lubarsch),  have  described 
cases  of  pernicious  anemia  in  which  atrophy  of  the  gastric  mucosa 
was,  at  the  autopsy,  found  to  be  the  only  organic  disease  existing. 
It  is  conceivable  that  the  intestine  can  not  persistently  digest  an 
amount  of  proteid  sufficient  to  maintain  the  nitrogen  equilibrium 
during  work ; that  it  depends  upon  a certain  part  of  this  prote- 
olysis to  be  performed  by  the  stomach  ; that  the  acid  gastric  chyme 
is  necessary  for  the  stimulation  of  the  duodenal  secretions.  It  is 
probable  that  digestion  in  the  duodenum  is  not  perfect  without  the 
acid  protoids,  which,  as  we  know,  cause  increased  diastatic  action 
of  the  pancreatic  juice  (B.  K.  Rachford,  “Am.  Journ.  Physiol.,” 
vol.  11,  p.  494,  July,  1899). 

So  I take  the  ground  that  the  supplementing  of  HC1  is  rational, 
even  if  we  can  not  supply  the  deficit,  because  the  amount  necessary 
thereto  could  not  expediently  be  administered.  If  we  can  not 
always  add  sufficient  HC1  to  make  the  chyme  distinctly  acid,  we 
can  at  least  add  enough  to  disinfect  it  and  free  it  from  a part,  the 
surplus,  of  its  germs,  and  perhaps  produce  some  of  the  preliminary 
stages  to  peptone;  for  the  acid  albumins  (syntonin)  and  propeptones 
are  absorbable,  and  those  not  absorbed,  we  believe,  are  of  some 
further  utility  in  duodenal  digestion.  This  conclusion  is  based 
upon  quantitative  analyses  of  human  duodenal  contents,  from 
cases  of  achylia  gastrica  and  from  normal  individuals.  In  some 
cases,  however,  we  are  enabled  to  add  enough  to  give  the  reaction 
of  free  HC1  to  the  chyme. 

According  to  Honigmann  and  von  Noorden  (“  Zeitschr.  f.  klin. 
Medizin,”  Bd.xm),one  part  by  weight  of  pure  HC1  is  able  to  satu- 
rate 18  parts  by  weight  of  egg-albumen  ; 100  drops  of  dilute 
hydrochloric  acid,  containing  12.5  per  cent,  of  the  absolute  HC1, 
will  suffice  to  digest  15  gm.,  or  225  gr. — little  less  than  4 drams 
of  pure  egg-albumen.  Riegel  cites  this  statement  (Joe.  cit.,  p.  258), 
evidently  to  show  how  inefficacious  100  drops  of  a 12.5  per  cent. 


DIGESTIVE  POWER  OF  THERAPEUTIC  DOSES  OF  HCl.  33 1 

solution  of  HCl  are  as  a digestive.  (The  dilute  hydrochloric  acid 
of  the  U.  S.  Pharmacopeia  is  a ten  per  cent,  solution.) 

The  conclusions  of  Honigmann  and  von  Noorden,  however,  are, 
in  our  opinion,  not  calculated  to  inspire  therapeutic  skepticism. 
An  amount  of  proteids  equal  to  4 drams  of  dried  egg-albumen  is  a 
considerable  quantity  to  be  relieved  of,  and  it  can  not  fail  to  ease 
gastric  digestion  to  give  the  acid,  even  if  it  can  do  no  more  work 
than  this.  But  then  it  is  practicable  to  give  more  than  100  drops 
of  dilute  HCl  if  necessary.  Furthermore,  the  albumen  molecule 
need  not  be  saturated  in  order  to  become  absorbable,  as  we  shall 
see.  Not  near  so  much  HCl  is  required  for  the  formation  of  acid 
albumen  as  for  that  of  hemialbumose  or  peptone. 

Riegel  himself  succeeded  in  causing  a resumption  of  secretion 
of  HCl  in  a patient  who  had  not  shown  any  for  months,  after  he 
had  taken  1.5  gm.  of  hydrochloric  acid  daily  for  fourteen  days. 
He  believes,  however,  that  diet  and  lavage  may  have  had  much  to 
do  with  the  recovery. 

Reichmann  and  Mintz  (“  Wiener  klin.  Wochenschr.,”  1892)  report 
several  cases  in  which  free  HCl  could  be  again  demonstrated  after 
it  had  been  missing  for  a prolonged  time  ; the  resumption  of  HCl 
secretion  was  attributed  by  them  to  a prolonged  dosage  with  the 
same  acid.  As  we  shall  see  in  the  chapter  on  Achylia,  this  dis- 
ease may  depend  on  a number  of  very  different  factors.  Sometimes 
there  is  no  evidence  of  pathological  change  in  the  mucosa,  and 
naturally  these  may  readily  recover  (neuroses),  even  without  HCl 
treatment. 

Professor  Biedert  claims  to  have  used  120  drops  of  dilute  HCl 
daily  for  a number  of  years,  with  much  benefit  to  his  achylia  (Biedert 
and  Langermann,  “ Diatetik  u.  Kochbuch  f.  Magenkranke,”  1895). 
Hanni  introduced  into  the  stomach  400  c.c.  of  a 2.5  : 1000 
solution  of  HCl,  containing  also  2 gm.  of  pepsin,  together  with 
an  Ewald  test-breakfast.  As  early  as  fifteen  minutes  afterward, 
when  some  of  the  test-meal  was  withdrawn,  the  free  HCl  had 
completely  disappeared  and  the  digestive  power  of  the  sample  was 
equal  to  zero  (Hanni,  “ Zeitschr.  f.  klin.  Med.,”  Bd.  xix,  Supple- 
ment^. 307);  and  Boas  cites  this  statement  to  show  that  the  diges- 
tive value  of  HCl  therapy  is  doubtful.  Now,  a patient  who  gets 
rid  of  400  c.c.  of  liquid  in  fifteen  minutes  has  hypermotility  ; so 
much  could  not  possibly  be  absorbed  in  that  short  period  (the 
stomach  does  not  absorb  dilute  HCl  solutions).  Nor  could  all 
of  1 gm.  of  absolute  HCl  which  400  c.c.  of  a 2.5  : 1000  solu- 


332  IMPORTANT  MEDICINAL  AGENTS  IN  GASTRIC  THERAPY. 

tion  contain  enter  into  combination  with  the  proteid  of  a single 
roll;  for  ioo  gm.  of  wheat  roll  contain  only  7 gm.  of  nitrogenous 
or  HCl-binding  materials.  We  know,  however,  that  1 gm.  of 
absolute  HC1  can  digest  18  gm.  of  dried  egg-albumen.  There- 
fore the  400  c.c.  had  probably  all  been  rapidly  expelled  into  the 
duodenum  before  they  could  even  be  thoroughly  triturated  with 
the  test-breakfast.  This  does  not  occur  normally,  and  we  are  not 
justified  in  drawing  conclusions  from  such  hyperkinetic  cases 
regarding  the  value  of  HC1  therapy. 

As  the  amount  of  absolute  HC1  introduced  in  Hanni’s  experi- 
ments equaled  1 gm.,  and  as  so  much  could  not  enter  into  com- 
bination with  the  proteid  of  one  roll,  or  100  gm.  of  wheat  bread, 
it  stands  to  reason  that  if  the  motility  had  not  been  so  exaggerated, 
some  of  the  HC1  would  have  been  regained.  Whenever  Hanni 
{loc.cit.,  p.  306)  succeeded  in  regaining  some  of  the  solution  of  HC1 
after  it  had  remained  in  the  stomach  forty-five  to  sixty  minutes,  or 
even  thirty  minutes  (see  cases  No.  3,  Schmid,  and  No.  4,  Hanni, 
p.  307,  loc.  cit .),  the  tests  for  HC1  were  positive  and  fibrin  was  well 
digested  by  the  filtrate.  The  experiments  of  von  Mehring,  Moritz, 
and  myself  apparently  agree  in  permitting  the  deduction  that 
fifteen  minutes  is  an  abnormally  rapid  time  for  the  expulsion  of 
400  c.c.  of  liquid  (even  if  it  were  only  water)  into  the  duodenum, 
and  whenever  there  is  a fuller  meal  given  than  a simple  test-breakfast, 
this  rapid  expulsion  does  not  occur,  because  solid  and  semisolid 
matter  can  not  be  moved  out  so  readily.  Again,  we  must  make 
allowance  for  a certain  unavoidable  nervous  tension,  and  for  the 
influence  of  suggestion,  which  takes  hold  of  patients  under  experi- 
mentation, and  which,  from  experience,  we  know  has  a decided 
influence  on  the  rate  of  peristalsis. 

A careful  series  of  analyses,  constituting  a rational  basis  for  HC1 
therapy,  is  that  of  Charles  E.  Simon  (“  The  Modern  Aspect  of 
Indicanuria,”  “ Amer.  Jour.  Med.  Sciences,”  Aug.,  1895,  p.  170). 
We  submit  a number  of  his  conclusions : 

“(1)  The  gastric  juice  possesses  antiseptic  and  germicidal 
properties. 

“ (2)  These  properties  are  referable  to  the  presence  of  free 
hydrochloric  acid. 

“(3)  A subnormal  amount  of  free  hydrochloric  acid  will  call 
forth  an  increased  degree  of  intestinal  putrefaction. 

“(4)  The  conjugate  sulphates  form  an  index  of  the  degree  of 
intestinal  putrefaction. 


INDICATIONS  AND  CONTRAINDICATIONS  TO  HCl  THERAPY.  333 

“ (5)  The  increased  intestinal  putrefaction  in  cases  of  subacidity 
and  anacidity  of  the  gastric  juice  is  largely  referable  to  an  increased 
formation  of  indol. 

“ (6)  The  elimination  of  indican  in  the  urine  may  be  regarded  as 
an  index  to  the  amount  of  free  hydrochloric  acid  present. 

“(7)  A normal  acidity  of  the  gastric  juice  is  never  associated 
with  increased  indicanuria. 

“ (8)  Cases  of  ulcer  of  the  stomach  apparently  form  an  exception 
to  this  rule,  an  increased  indicanuria  being  usually  associated  with 
hyperchlorhydria. 

“(9)  In  other  cases  of  hyperchlorhydria  a subnormal  or  normal 
amount  of  indican  is  eliminated.” 

We  therefore  recommend  hydrochloric  acid,  believing  in  its 
efficacy  in  supplementing  the  digestive  work  of  the  stomach. 
Whenever  it  is  indicated,  we  usually  give  20  drops  of  the  diluted 
HCl  (U.  S.  Pharm.)  in  2 ounces  of  water  every  half  hour,  beginning 
fifteen  minutes  before  the  meal;  then  20  drops  are  taken  during  the 
eating,  and  20  drops  one-half  hour  after  the  meal.  The  medicine 
should  always  be  taken  through  a glass  tube,  and  the  mouth 
rinsed  with  a weak  solution  of  sodium  carbonate  afterward.  As  a 
remedy  for  improving  the  appetite,  HCl  is  conceded,  even  by  those 
skeptical  of  its  digestive  power,  to  be  of  value.  For  this  purpose 
it  is  best  given  in  small  doses  diluted  with  water  (10  to  20  drops  in 
3 ounces  H20),  on  an  empty  stomach,  before  meals.  With  regard 
to  its  disinfectant  and  antifermentative  effect  I entertain  serious 
doubts,  since  it  can  not  be  given  in  sufficient  quantity  to  be  of  much 
benefit  in  that  direction  when  given  with  meals.  Whenever  there 
are  decided  fermentations  in  the  stomach,  lavage  is  the  most 
efficient  means  of  combating  it,  and  for  this  purpose  HCl  in  the 
form  of  a 6 : 1000  solution  may  be  used. 

Hydrochloric  acid  is  contraindicated  when  the  normal  gastric 
secretion  is  augmented.  We  have  observed  cases  in  which  there 
was  no  free  HCl  to  be  detected  by  Congo  paper  or  phloroglucin- 
vanillin,  but  HCl  given  per  os  produced  gastric  distress  and  pain  ; 
so  that  there  can  be  no  doubt  that  cases  of  hyperesthesia  toward 
HCl  exist  analogous  to  those  described  by  Talma  (“  Zeitschr.  f. 
klin.  Med.,”  Bd.  vm),  which  do  not  depend  upon  hyperchylia. 
One  female  patient  could  detect  whenever  8 drops  of  the  diluted 
acid  were  given  surreptitiously  in  the  meals  or  medicine,  by 
the  gastralgia  caused  thereby.  This  was  a highly  neuropathic 
case. 


334  IMPORTANT  MEDICINAL  AGENTS  IN  GASTRIC  THERAPY. 

The  amount  of  HCl  consumed  in  the  digestion  of  albumin  has 
been  very  carefully  studied  by  Fleischer.  It  takes  0.05  gm.  of  HCl 
to  transform  1 gm.  of  egg-albumen  into  acid  albumen.  As  human 
beings  frequently  take  in  150  gm.  of  egg-albumen  in  twenty-four 
hours,  it  would  require  7.5  gm.  of  pure  HCl  (or  30  gm.  of  the  25 
per  cent,  solution  of  the  laboratories)  to  transform  this  amount  into 
acid  albumin.  As  the  gastric  juice  contains  HCl  to  the  amount  of 
2 per  mille,  3 y2  liters  of  gastric  juice  would  be  required  to  digest 
that  amount  of  egg-albumen.  Many  children  consume  about  one 
liter  of  milk  daily;  this  would  require  4.5  gm.  of  pure  HCl  or  18 
gm.  of  a 25  per  cent,  solution  of  HCl  (100  gm.  of  cows’  milk  com- 
bined with  0.45  gm.  of  HCl).  These  amounts  of  HCl  would  bring 
the  ingested  albumen  only  to  the  stage  of  acid  albumin  or  syntonin  ; 
but  as  hemialbuminose  and  peptone  would  require  twice  the 
amount  of  HCl,  the  quantity  combined  with  must  eventually  be 
increased  beyond  the  figures  stated.  A portion  of  the  albuminous 
foods  passes  over  into  the  intestine,  however,  and  there  is  digested 
long  before  it  reaches  the  stage  of  hemialbuminose;  but  when  the 
transit  of  the  food  into  the  duodenum  is  obstructed,  it  is  evident 
that  enormous  quantities  of  HCl  must  be  secreted  to  digest  all  the 
albumin  that  is  taken  in.  For  a purely  physiological  reason,  it  is 
not  possible  that  the  glandular  layer  can  secrete  the  requisite 
amount.  The  absence  of  free  HCl  in  these  cases  may  be  due  to 
an  invasion  of  the  mucosa  by  the  disease  causing  the  pyloric 
obstruction.  It  is  not  impossible,  however,  that,  even  without  this 
invasion,  the  mucosa  has  become  exhausted,  its  secretory  function 
being  paralyzed. 

The  Alkalies. — Probably  the  earliest  experiments  upon  the 
effect  of  alkalies  on  the  gastric  secretion  are  those  by  Claude 
Bernard,  who  found  that  in  small  doses  they  increased  the  secre- 
tion of,  and  in  large  doses  they  neutralized,  the  gastric  juice  in 
animals. 

Leube  (in  von  Ziemssen’s  “ Handbuch,”  Bd.  vii)  stated,  as  a 
result  of  experiments  on  dogs  with  gastric  fistulae,  that  the  car- 
bonate of  soda  of  the  Carlsbad  springs  not  only  neutralized  an 
excess  of  acid,  but  could  cause  a lasting  increase  in  the  HCl 
formation  of  a diseased  mucosa. 

Du  Mesnil  (“  Deutsch.  med.  Wochenschr.,”  1892),  and  Linossier 
and  Lemoine  (Academie  de  Medecin  de  Paris,  session  of  March, 
1893)  agree  in  stating  that  when  sodium  bicarbonate  is  given 
together  with  a test-breakfast,  or  shortly  before  it,,  it  acts  as  an 


ACTION  OF  ALKALIES  ON  SECRETION. 


335 


excitant  to  the  mucosa  and  increases  the  percentage  of  HC1  formed. 
In  a case  of  hyperacidity,  however,  Du  Mesnil  found  that  the 
amount  of  HC1  was  at  once  reduced.  Indeed,  the  results  of  various 
experimenters  differ  according  to  the  normal  or  abnormal  state  of  the 
stomach  with  which  they  worked.  It  makes  much  difference,  also, 
whether  an  alkali  is  given  on  an  empty  stomach,  with  very  little  or 
no  secretion,  when  it  may  possibly  act  as  an  irritant  to  the  mucosa 
and  set  up  a secretory  reaction,  or  whether  it  is  given  at  the  height 
of  digestion  and  meets  with  free  HC1  ; it  the  latter  case  it  must  of 
necessity  combine  with  the  acid,  and  can  cause  no  further  secre- 
tion. 

It  is  unfortunate  for  the  evolution  of  truth  in  this  question — 
whether  or  not  small  doses  of  alkali  can  stimulate  secretion — that 
quite  a number  of  experimenters  (Ewald  and  Sandberg,  Leube, 
Spitzer,  etc.)  worked  with  Carlsbad  salts  or  water  instead  of  with 
a chemically  pure  simple  salt.  The  people  of  other  countries  do 
not  share  that  intense  interest  in  the  Carlsbad  and  other  springs 
with  the  physicians  of  Europe ; or  at  least  those  of  Germany  and 
Austria. 

There  are  not  a few  prominent  representatives  among  the  Ger- 
man clinicians  who  have  expressed  grave  doubts  whether  the  cures 
and  improvements  reported  are  really  due  to  the  waters  of  Carls- 
bad, but  that  the  credit  must  be  given  to  the  avoidance  of  bad  home 
influences,  the  careful  diet,  the  regular  life,  pure  air,  good  sleep, 
and  abstinence  from  alcohol  (see  pp.  3 13-3 15).  Personally,  we 
consider  it  our  duty  to  emphasize  that  the  waters  of  the  Congress 
and  Hathorn  Springs,  of  Saratoga,  N.  Y.,  and  of  the  Bedford 
Springs,  in  Pennsylvania,  have  produced  similar  marked  improve- 
ment, and,  when  this  was  not  possible,  great  alleviation  of  gastric 
symptoms  there  treated.  But  even  here  it  is  impossible  to  ignore 
the  good  which  the  strict  observance  of  the  factors  of  hygiene  and 
diet  above  mentioned  may  have  worked. 

The  natural  Carlsbad  Sprudel  salt  has  the  following  composi- 
tion, according  to  Prof.  E.  Ludwig  : 

Sodium  sulphate, 41.62  per  cent. 

Potassium  sulphate, 3.31  “ 

Sodium  bicarbonate, 36. 11  “ 

Lithium  carbonate, 0.2  “ 

Sodium  chlorid, 18.19  “ 

Sodium  borate, 0.03  “ 

Water, 0.44  “ 


336  IMPORTANT  MEDICINAL  AGENTS  IN  GASTRIC  THERAPY. 

The  artificial  Carlsbad  salt,  which,  according  to  Boas,  can  fully 
replace  the  more  expensive  natural  salt,  contains  the  following 
salts,  according  to  the  German  Pharmacopeia : 


Sodium  sulphate  (dried), 44  parts. 

Potassium  sulphate, 2 “ 

Sodium  chlorid, 18  “ 

Sodium  bicarbonate, 36  “ 


In  hyperchylia  and  hypersecretion  (in  gastric  ulcer)  it  is  given  in 
doses  of  one  to  two  dessertspoonfuls  in  of  a liter  of  water, 
to  reduce  the  excess  of  HC1  and  promote  evacuation.  In  gastritis 
it  is  also  recommended,  and  this  has  seemingly  given  the  Carlsbad 
enthusiasts  much  difficulty,  namely,  to  explain  how  the  identical 
solution  may  produce  reduction  of  the  HC1,  and  in  another  case 
promote  HC1  formation. 

We  have  studied  eight  cases  who  went  to  Carlsbad  suffering 
from  subacidity  and  from  achylia;  we  have  not,  in  a single  instance, 
observed  a return  of  secretion  where  it  was  lost  or  an  increase 
where  it  was  deficiently  formed. 

Reichmann  is  one  of  the  few  who  objected  to  applying  the  deduc- 
tions found  with  Carlsbad  water  or  salts,  on  account  of  their  com- 
plexity to  the  effects  of  pure,  simple  alkaline  salts  (“  Therapeut. 
Monatshefte,”  1895).  We  have  never  shared  the  opinions  of  thsoe 
who  believe  that  small  doses  of  alkali  given  on  an  empty  stomach 
can  produce  a reactive  secretion  of  HC1  which  may  exceed  the 
amount  necessary  to  combine  with  the  alkali  given.  We  can 
understand  that  strong  solutions  of  sodium  and  potassium  sul- 
phate, such  as  the  Carlsbad  water,  may  actually  play  the  role  of  an 
irritant,  to  which  the  mucosa  responds  in  the  form  of  an  increased 
secretion,  just  as  the  nasal  mucosa  would  do  if  a crystal  of  salt 
were  placed  in  the  nasal  passage.  Indeed,  N.  Reichmann  declares, 
after  a series  of  careful  analyses  with  Na2C03,  that  the  bicarbonate 
of  sodium  does  not  act  upon  the  secretory  inechairism  of  the  stomach , 
but  only  upon  the  juice  already  secreted , by  neutralizing  it  and  render- 
ing the  gastric  contents  alkaline  (Boas,  “ Archiv  f.  Verdauungs- 
krankh.,”  vol.  1,  p.  44). 

The  actual  therapeutic  application  of  alkalies,  therefore,  is  limited 
to  those  dyspepsias  associated  with  increased  HC1  formation,  in 
simple  neurasthenic  hyperchylia,  in  hypersecretion,  and  in  gastric 
ulcer.  They  are  indispensable  for  lavage  when  it  becomes  neces- 
sary to  neutralize  acids  and  dissolve  adherent  mucus.  The  time 


ADMINISTRATION  OF  ALKALIES. 


337 


to  give  alkalies  in  hyperacidity  is  from  one-half  to  one  hour  after 
meals,  when  the  HC1  secretion  is  quantitatively  at  its  height.  The 
sensations  of  the  patient  are  a very  good  guide,  and  the  time  can  be 
learned  by  experience;  the  alkali  should  then  be  given  a little 
previous  to  the  time  when  the  gastralgia,  eructation,  pyrosis,  and 
distention  set  in.  In  hypersecretion  there  is  a large  amount  of  HC1 
present  almost  continuously  in  the  empty  stomach,  in  addition  to 
hyperacidity  after  meals,  so  here  we  should  give  alkalies  before 
meals  in  order  to  insure  a certain  time  for  action  to  the  ptyalin  ; 
for  this  constant  secretion  a glass  of  Saratoga  Vichy,  or  simply 
sodium  bicarbonate,  5j,  in  ]/2  of  a pint  of  plain  cold  water,  before 
meals,  is  sufficient  to  permit  amylolysis.  In  ulcer  and  chronic 
gastritis  acida,  alkalies  find  application  also  (refer  to  treatment  of 
these  diseases). 

Determination  of  the  Amounts  of  Alkalies  Required. — Two  groups 
of  these  bodies  are  in  common  use:  (i)  The  alkaline  earths ; (2) 
the  alkaline  carbonates.  Of  the  first  group,  magnesia  usta  or 
calcined  magnesia,  and  the  more  expensive  magnesium  ammonium 
phosphate  are  the  favorites ; and  of  the  second,  the  sodium  car- 
bonate and  bicarbonate.  Those  alkalies  which  are  capable  of  com- 
bining with  the  largest  amount  of  HC1  are  preferable.  It  is  expe- 
dient to  avoid  excess  of  sodium  bicarbonate,  because  the  liberation 
of  C02  in  the  neutralization  may  cause  annoying  distention  of 
muscular  walls  already  infirm. 

Magnesia  usta  has  the  greatest  binding  power  for  HC1,  and  the 
reaction  is  expressed  in  the  following  equation  : 

MgO  + 2HCI  = MgCl2  + 2H20. 

Here  0.55  part  of  MgO  correspond  to  one  part  of  HC1. 

The  reaction  with  ammonio-magnesium  phosphate  is  the  fol- 
lowing : 

Mg(NH4)P04  4-  3HCI  =r  MgCl2  + NH4C1  4-  H3P04. 

Calculation  here  gives  the  result  that  1.25  parts  by  weight  of 
Mg(NH4)P04  correspond  to  one  part  by  weight  of  HC1. 

The  reaction  with  sodium  bicarbonate  is  as  follows  : 

NaHC03  4-  HC1  = NaCl  + H20  4-  C02. 

Calculation  of  the  molecular  weights  shows  that  2.3  parts  of 
NaHC03  correspond  to  one  of  HC1. 

According  to  Boas,  the  dose  of  sodium  bicarbonate  necessary  to 
counteract  a superacidity  exceeding  2.5  : 1000  is  eight  to  ten  gm., 
or  four  to  six  gm.  of  ammonio-magnesium  phosphate,  or  two  to 


338  IMPORTANT  MEDICINAL  AGENTS  IN  GASTRIC  THERAPY. 

three  gm.  of  magnesia  usta.  With  an  acidity  of  3 : 1000  HC1, 
the  NaHC03  can  be  increased  to  twelve  gm.,  the  ammonio-mag- 
nesium  phosphate  to  7.5  gm.,  and  the  magnesia  usta  to  five  gm. 
These  calculations  are  made  upon  an  amount  of  stomach  contents 
equal  to  400  c.c. ; but  as  a part  of  the  alkali  is  expelled  into  the 
duodenum,  another  part  absorbed,  and  as  the  momentary  quantity 
of  HC1  present  can  only  be  reckoned  upon,  the  figures  may  be  too 
low.  With  constipation  and  collection  of  gas  in  the  intestines  the 
preference  is  to  be  given  to  the  magnesia  salts.  Germain  See 
(“  Semaine  Medicale,”  1890,  No.  12)  recommends  the  following: 

R.  Sod.  bicarb., 

Creta  prsep. , 

Magn.  carbon., . . aa  0.2  gm.  M. 

Take  at  once. 

Boas’  formula  for  continued  excessive  secretion  is  the  following : 


Metric 

System. 

R.  Magnesise  ustse,  15.0  gr.  231.5 

Bismuth,  carbon., 

Natrii  carbon., aa  5-0  gr.  77 .2 

Ext.  belladonnse, 

Ext.  strychn., aa  o.  1-0.2  gr.  1.7.  M. 


Sig. — One  teaspoonful  three  times  daily,  half  an  hour  after  meals. 

The  amount  of  HC1  secreted  should  be  watched  and  the  alkali 
discontinued  if  it  becomes  normal. 

The  Bitter  Tonics  and  So-called  Stomachic  Remedies. — 
Experience  has  lent  belief  that  the  bitter  tonics  are  agents  which 
stimulate  the  appetite  and  the  secretory  and  motor  functions  of  the 
stomach.  They  are  represented  by  preparations  of  condurango, 
quassia,  Colombo,  gentian,  angostura,  absinthe,  nux  vomica  and 
strychnin,  creasote,  guaiacol,  orexin,  lupulin,  cetrarin,  erythrocen- 
taurin,  rheum,  resorcin,  quinia,  cinchona.  Under  certain  conditions, 
HC1,  sodium  chlorid,  and  alcohol  act  as  stomachics. 

Some  writers  class  sodium  bicarbonate  among  these  remedies, 
upon  the  supposition  that  small  doses  of  this  alkali  may  stimulate 
secretion  of  gastric  juice;  this  therapy  is,  in  our  opinion,  falla- 
cious. As  a general  rule,  these  medicines  are  useful  to  improve 
the  appetite,  and  as  anorexia  is  mostly  found  in  reduced  or  lost 
gastric  secretion,  the  effect  upon  secretion  is  apparently  the  only 
one  that  can  be  attributed  to  them.  What  the  bitter  tonics  really 
effect  and  how  they  act  is  an  unsolved  problem.  There  seems  to 
be  an  absence  of  scientific  exactness  in  many  of  the  experiments, 


ACTION  OF  BITTER  TONICS. 


339 


and  a general  diffusiveness  regarding  the  special  point  of  inquiry 
to  be  solved.  Thus,  Penzoldt  pretends  that  genuine  stomachics 
must  be  able  to  improve  all  of  the  gastric  functions  (Penzoldt, 
on  “ Salzsaures  Orexin,”  “Therap.  Monatsh.,”  1890,  No.  2).  Loss 
of  appetite  may  be  present  when  the  functional  work  is  reduced, 
and  then  bitter  tonics  would  be  indicated;  but  it  may  just  as 
well  be  present  with  normal  or  morbidly  increased  functions  when 
stomachics  would  do  harm.  For  instance,  we  have  had  many 
cases  of  anorexia  with  hyperacidity  where  the  appetite  returned 
after  the  use  of  bromid  of  strontium.  In  dilatations  with  fermenta- 
tion the  best  stomachic  is  lavage.  As  every  disturbed  function  or 
disease  requires  elucidation,  so  the  anorexia  based  thereon  demands 
its  own  adapted  treatment.  Bitter  tonics  and  allied  medications 
are,  in  general,  stimulants  to  the  mucosa,  and  although  they  have 
a large  application,  it  is  not  rational  to  use  them  empirically.  A 
sedative  or  an  antiseptic  may,  under  certain  conditions,  be  a better 
medicine  than  the  bitter  tonic  for  anorexia.  The  most  rational 
course  to  pursue  is  to  ascertain  the  exact  state  of  the  gastric  func- 
tions, and  after  the  establishment  of  the  diagnosis  attempt  to 
remove  the  cause  of  the  anorexia,  whether  it  is  depressed  motility, 
accumulation  of  mucus,  fermentation,  or  impaired  secretion.  For 
a fuller  account  of  the  physiological  effects  of  these  remedies  the 
reader  is  referred  to  recent  works  on  pharmacology  and  thera- 
peutics. 

The  most  useful  medicines  of  this  class,  in  my  experience,  have 
been  strychnin  and  condurango,  which,  according  to  the  experi- 
ments of  L.  Wolff,  have  no  appreciable  effect  on  the  rate  of 
secretion  (“  Zeitschr.  f.  klin.  Med.,”  Bd.  xvi,  S.  222).  Reichmann’s 
very  carefully  conducted  investigations  (“  Zeitschr.  f.  klin.  Med.,” 
Bd.  xiv,  Heft.  1 und  2)  brought  out  the  fact  that  some  bitter  tonics 
failed  to  cause  any  secretion  of  gastric  juice  when  distilled  water 
did;  and  whenever*  water  failed  to  produce  secretion,  the  bitter 
remedies  failed  also.  On  normal  digestive  processes  these  agents 
have  no  effect ; but  when  a juice  was  secreted  that  was  acid,  though 
not  containing  HC1,  and  if  a gastric  juice  very  weak  in  pepsin  was 
secreted,  then  the  bitter  tonics,  especially  absinthe,  were  found  to 
produce  a stronger  degree  of  acid  and  distinct  reaction  for  HC1. 
Whenever  there  was  atrophy  of  the  glandular  apparatus,  all  of 
these  remedies  failed  to  cause  a secretion  of  gastric  juice  containing 
HC1.  In  brief,  his  conclusions  are  that  the  effect  is  very  variable, 
sometimes  less  than  that  of  water;  but  sometimes  there  is  an  in- 


340  IMPORTANT  MEDICINAL  AGENTS  IN  GASTRIC  THERAPY. 


crease  of  secretion  after  the  bitter  tonic  has  become  absorbed  and 
disappeared.  They  act  best  when  given  before  meals,  and  when 
there  is  a gastric  secretion  still  present,  but  Jmuch  reduced  (hypo- 
chylia).  In  hypersecretion  Reichmann  found  that  the  acidity  was 
still  further  increased  by  bitter  tonics.  We  advise  that  the  bitter 
tonics  should  be  given  only  in  hypochylia  or  subacidity,  and  then 
one-half  hour  before  meals.  The  author’s  favorite  formula  for 
anorexia  from  hypochylia  is  the  following  : 


Metric 

System. 

B-  Strychnin,  sulphas, 0.020 

Acid,  hydrochloric,  dil. , ....  . 14.787 

Ext.  condurango  fl. , 45.361 

Elixir  gentian. , q.  s.  ad  177.442 


gr.  'A 
fgss 
f ^ iss 

f^vj.  M. 


Sig. — One-half  of  a fluidounce  in  two  ounces  of  water,  one-half  hour  before 
meals,  through  a glass  tube. 


Or— 

Metric 

System. 

B . Tinct.  nucis  vomic., 10. o fgiiss 

Essentiae  calisayae  (P.  D.  & Co.),  . 60.0  f^ij 

Elixir  gentian., q.  s.  180.0  f^vj. 

Sig. — One-half  of  a fluidounce  thrice  daily,  one-half  hour  before  meals. 


M. 


When  there  are  evidences  of  anemia  with  the  hypochylia,  the 
following  acts  satisfactorily  : 

Metric 


System. 

B- 

Quininse  sulphatis, 

I.I93 

gr.  xviij 

Strychnin,  sulphatis, 

gr-  K 

Ferri  sulphatis,  . . 

o-775 

gr.  xij 

Acid,  arseniosi.,  . 

O.OI  2-(- 

gr.  i.  M. 

Sig.- 

— Fiantpil.  No.  xij. 

One  pill  three  times  daily  (must  be  prepared  fresh  and 

not  coated). 


Boas  uses  the  following  powder  for  anorexia  : 

Metric 

System. 

B-  Ext.  strychn., 0.03-0.05 

Bismuth,  carbon., 0.50 

M.  f.  pulv.  Dent.  tal.  dos.  xx. 

SiG.  — One  powder  three  times  daily. 


gr-  | 
gr.  viij. 


Menche  has  warmly  recommended  resorcin  sublimate,  and  it 
undeniably  improves  the  appetite  in  cases  of  incipient  gastric 
fermentation.  It  has  also  a slight  sedative  action.  The  following 
is  Menche’s  formula: 


BITTER  AND  OTHER  GASTRIC  TONICS. 


341 


Metric 

System. 

R . Resorcin,  resublim. 2.0  gr.  30.5 

Acid,  mur., 1.0  gr.  15.4 

(Or,  if  it  be  indicated  in  place  of  the  HC1,  one  may  order  Natr. 
bicarb.,  8.0.) 

Aquae  destil 180.0  fg  vj 

Syr.  simpl., 20.0  3”j- 

M.  D.  et  ad  vitr.  nigr. 

SlG. — Fifteen  c.c.  (,^ss)  every  two  hours. 


The  following  formulae  are  recommended  by  Ewald  for  anorexia 
with  fermentation  : 


Metric 

System. 


R.  Tinct.  nucis  vom., 

. 25.0 

f3vi 

Resorcin,  resublim., 

. 5.0 

gr.  lxxxj 

Tinct.  amar. , 

Take  ten  to  fifteen  drops  every  two  hours. 

. 10.0 

f 3 iij- 

R.  Ext.  condurang  fl.,  

f 3 ivss 

Resorcin,  resublim. , 

SlG. — Thirty  drops  four  times  daily. 

. 4.0 

M. 


M. 


Creosote  is  a remedy  of  doubtful  efficacy  in  my  experience,  as 
it  rarely  benefits  digestion  except  in  tuberculous  patients.  Wegele 
says  ( loc . cit.f  p.  53)  that  it  will  help  if  it  is  tolerated  and  causes  no 
severe  dyspeptic  difficulties,  but  the  latter  is  just  what  it  will  do  in 
more  than  one-half  of  the  cases.  I have  my  doubts  whether  it  can 
promote  peristalsis,  as  is  asserted  by  Klemperer  (“  Centralbl.  f. 
klin.  Med.,”  1891,  No.  21),  until  enough  is  given  to  act  as  an 
irritant.  Even  when  it  is  tolerated  by  the  stomach,  the  repeated 
penetrating  eructations  are  very  annoying  to  patients.  Sommer- 
brodt  recommended  it  to  be  taken  in  capsules.  Bouchard  advises 
the  following  formula  : 

Metric 

System. 

R.  Creosot.  puriss., 13.5 

Tinct.  gent., 20.0 

Vin.  Xerens, 800.0 

Spir.  rectif. 200.0  M. 

SlG. — One-half  of  an  ounce  four  times  daily. 


Orexin  (phenyldihydrochinazolin)  has  been  strongly  indorsed  as 
a “ genuine  ” stomachic  by  Penzoldt.  In  273  cases  he  observed 
144  successful  restorations  of  appetite  and  secretion.  Its  special 
indications  are  gastric  atony  and  beginning  gastritis,  and  its  action 
is  attributed  to  its  power  of  increasing  the  secretion  of  HC1  (Pen- 
zoldt, “ Weitere  Mittheilungen  liber  Orexin basicum,”  etc.,  “ Therap. 


342  IMPORTANT  MEDICINAL  AGENTS  IN  GASTRIC  THERAPY. 

Monatshefte,”  May,  1893).  The  following  formula  is  advised  by 
Penzoldt  for  this  useful  drug: 

R.  Orexin  basic., gss,  or  2 gm. 

SiG. — Divide  into  six  powders;  inclose  in  small  wafers.  One  to  be  taken  in  a 
cup  of  bouillon  half  an  hour  before  meals,  twice  daily. 

Digestive  Ferments. — Artificial  means  of  aiding  digestion  are 
certainly  much  abused,  and  if  employed  for  long  periods,  they  fre- 
quently become,  to  a certain  extent,  injurious.  Every  organ  is 
strengthened  by  activity  and  weakened  by  lack  of  exercise.  The 
stomach  will  grow  weaker  and  weaker  the  more  artificial  gastric 
juice  is  poured  into  it,  and  the  finer  and  more  subtle  the  nourish- 
ments are  that  are  allotted  to  it.  This  agrees  in  the  main  with 
what  we  stated  under  Dietetics,  namely,  that  the  diet  should  not 
be  leveled  down  to  the  digestive  capabilities  of  the  stomach,  but 
that  digestion  should  be  leveled  up  until  it  can  deal  efficiently  with 
the  amount  of  food  required  for  the  nitrogen  equilibrium.  In 
truth,  the  indiscriminate  dosing  with  digestive  ferments  does  more 
harm  than  good.  The  stomach  is  an  organ  which  very  rapidly 
adapts  itself  to  cease  performing  the  work  that  is  done  for  it  arti- 
ficially. Then,  again,  there  is  such  a thing  as  educating  an  appa- 
rently weak  stomach  up  to  digesting  food  which  at  first  seems  in- 
digestible, and  is  taken  with  “ fear  and  trembling.”  So  we  will 
find  that  gastric  training  (gymnastics  of  digestion)  by  graded  diet 
may  favor  the  development  of  what  fragments  of  glandular  ele- 
ments may  yet  be  slumbering  in  a diseased  mucosa,  but  the  ir- 
rational use  of  ferments  may,  by  doing  all  the  work  itself,  permit 
the  gland-cells  to  go  on  to  atrophy. 

The  artificial  ferments  have  been  recommended  when  there  is  a 
deficiency  or  absence  of  the  natural  secretion.  They  may  be  con- 
sidered in  two  classes : (1)  Those  that  have  been  isolated  from  the 
mammalian  organism — viz.,  ptyalin,  pepsin,  pancreatin ; and  (2) 
those  derived  from  the  vegetable  kingdom — viz.,  the  various  dias- 
tases, papain,  bromilin.  Some  of  the  ferments  of  the  human  body 
have  not  yet  been  isolated ; these  are  the  milk-curdling  ferments  of 
the  gastric  and  pancreatic  juices  and  the  emulsifying  and  fat-split- 
ting  ferments.  There  are  ferments  in  the  succus  entericus  (invertin, 
etc.,  perhaps  a curdling  ferment)  which  we  understand  very  little. 

Ptyalin. — This  ferment  of  the  saliva  is  indicated  in  hyperacidity  and 
hypersecretion,  when  the  normal  ptyalin  may  actually  be  destroyed 
in  the  stomach.  Boas  has  shown  that  with  diminution  of  the  acidity 


SO-CALLED  AMYLACEOUS  DYSPEPSIA. 


343 


this  ferment  may,  to  a degree  at . least,  resume  its  inversion  of 
starches  into  dextrose.  With  very  intense  hyperacidity  (0.04  : 
1000)  the  ferment  appears  to  be  so  injured  that  it  can  not  be 
restored  to  function,  and  a new  supply  may  be  necessary.  Ptyalin 
is  given  in  doses  of  five  to  fifteen  grs.,  with  3j  of  sodium  bicarbonate, 
immediately  after  meals.  There  can  be  no  doubt  of  the  greater 
amount  of  dextrose  formed  with  the  aid  of  ptyalin,  and  these 
patients  are  thereby  enabled  to  eat  more  of  carbohydrates. 

Diastase. — Malt  diastase,  as  manufactured  in  the  form  of  liquid 
extract,  or  in  dry  form,  as  in  Horlick’s  diastoid,  is  serviceable 
for  the  same  purpose.  Professor  Leo,  of  Bonn  (“  Therap. 
Monatshefte,”  Dec.,  1896),  reported  to  the  Congress  of  German 
Naturalists  and  Physicians  on  taka  diastase,  an  American  product, 
which  appears  to  have  strong  starch-inverting  power,  and  to  be 
able  to  act  in  an  amount  of  acid  equal  to  0.1  per  cent.  HC1.  We 
have  assured  ourselves  that  amylolysis  is  effectually  carried  out  by 
this  taka-diastase,  but  the  addition  of  an  alkali  is  necessary,  as  with 
ptyalin,  to  render  the  effect  prompt.  Its  tastelessness  and  moderate 
price  are  in  its  favor. 

Ewald  has  found,  in  a great  many  observations,  that  absence  or 
deficiency  of  ptyalin  is  exceedingly  rare;  so  that  ptyalin  is  rarely 
required  because  it  is  secreted  in  sufficient  quantity,  but  in  some 
way  it  may  be  destroyed.  The  hygiene  of  the  mouth  should 
receive  careful  attention ; a septic  or  acid  mouth,  with  coated 
tongue  and  bad  teeth,  will  offset  any  amount  of  ptyalin.  To  treat 
“ amylaceous  dyspepsia  ” — which  is  the  objectionable  name  given 
to  symptoms  of  hyperacidity  and  hypersecretion — by  cutting  off 
the  carbohydrates  is  irrational,  because  they  can  not  be  dis- 
pensed with,  not  on  account  of  the  starch  only,  but  on  account  of 
the  proteid  which  amylaceous  foods  contain.  It  will  be  found,  from 
the  army  rations  of  men  under  service  of  various  nations,  that  the 
carbohydrate  portion  of  the  foods  is  increased  with  harder  work 
much  more  than  the  proteid  and  fat  portion  (see  tables  in  Gilman 
Thompson’s  “ Dietetics  ” and  Munk  and  Uffelmann’s  “ Ernahrung 
des  Menschen  ”).  Therefore  these  foods  should  not  be  taken  away 
because  they  may  not  be  perfectly  digested  ; but  the  cause  of  the 
indigestion  should  be,  if  possible,  removed.  If  possible,  a large 
amount  of  natural  saliva  should  be  swallowed  after  meals;  many 
times  have  we  observed  that,  with  the  simple  supply  of  additional 
saliva  caused  by  chewing  a piece  of  rubber,  starch  indigestion 
could  not  be  demonstrated  in  the  test-meal,  although  it  had 


344  IMPORTANT  MEDICINAL  AGENTS  IN  GASTRIC  THERAPY. 

existed  before.  To  Fothergill  is  attributed  the  saying  that  ferments 
are  crutches;  no  doubt  many  an  invalid  would  prefer  walking  on 
crutches  than  not  at  all.  There  are  many  crutch-walkers,  however, 
who,  by  modern  surgery,  have  been  enabled  to  throw  them  away 
and  walk  by  themselves  unaided.  Just  so  with  the  ferments  ; they 
may  be  used  with  success  temporarily,  but  the  best  thing  to  do  is 
to  discover  how  the  patient  may  digest  without  them. 

Pepsin. — There  is  no  lack  of  pepsin  preparations  in  the  market, 
and  their  digestive  powers,  as  claimed,  seemingly  have  no  limit. 
Certain  very  popular  compositions  of  pepsin  should  be  emphatic- 
ally condemned.  For  instance,  all  wines  of  pepsin  are  inefficient 
because  very  little  of  this  ferment  is  taken  up  by  alcohol.  Recently 
a preparation  was  brought  to  our  laboratory  containing  hydrastis, 
rhubarb,  pepsin,  and  pancreatin  in  one  solution,  showing  a total 
disregard  for  the  physiological  fact  that  pepsin  acts  only  in  an  acid 
and  pancreatin  in  an  alkaline  medium.  There  is  rarely  any  indi- 
cation for  the  use  of  pepsin,  for,  whenever  a test-meal  shows  free 
HC1,  pepsin  must  of  necessity  be  present  in  sufficient  amounts; 
and  even  when  HC1  is  absent,  pepsin  or  pepsinogen  are,  as  a rule, 
still  present.  Assuming  a case  in  which  the  last  vestige  of  even 
pepsinogen  secretion  has  been  lost,  the  introduction  of  the  ferment 
might  be  of  utility,  but  the  enormous  quantities  of  HC1  necessary 
to  bring  about  proper  action  of  this  pepsin  could  not  be  tolerated 
by  any  diseased  stomach  (see  chapter  on  the  Therapy  of  HC1). 
And,  again,  in  cases  where  pepsinogen  is  still  formed,  the  addition 
of  HC1  simply  will  suffice  to  convert  it  into  the  complete  ferment. 
Pepsin  is  prescribed  much  too  often;  personally,  I have  ceased 
using  it. 

Pancreatin. — Although  there  are  many  preparations  of  this  fer- 
ment, and  some  of  them  very  active,  the  substance  spoils  and  loses 
its  digestive  power  with  age.  As  it  is  an  easy  matter  to  test  its 
amylolytic  and  tryptic  power  in  artificial  digestion  experiments,  it 
is  wise  to  do  so  in  all  cases  where  much  dependence  is  placed  in 
its  action.  The  nature  and  value  of  the  substance  were  scientifically 
explained  by  Sir  William  Roberts  (“  Digestion  and  Diet,”  p.  66). 
It  can  be  obtained  in  a liquid  form  as  well  as  in  the  form  of  a dry 
powder,  from  extraction  of  the  pancreatic  gland  of  animals.  This 
ferment  is  completely  destroyed  in  the  gastric  juice.  This  is  why 
thinking  practitioners  should  not  use  both  pepsin  and  pancreatin 
together  in  the  same  solution,  because  the  medium  in  which  one 
must  act  is  opposed  to  that  of  the  other.  In  the  majority  of  cases 


PANCREATIN — INDICATIONS  FOR  ITS  USE. 


345 


where  pancreatin  is  given  empirically,  HC1  is  still  secreted  in  the 
stomach  and  the  ferment  is  destroyed.  Gilman  Thompson  ( loc . 
cit .,  p.  333)  suggests  that  the  pancreatin  be  inclosed  in  keratin  cap- 
sules. Keratin  is  unaffected  by  gastric  juice,  but  readily  dissolves, 
it  is  claimed,  in  alkaline  media.  Hence  the  pancreatin  may  pass 
through  gastric  digestion,  and  at  its  completion  pass  into  the  in- 
testine, where  the  coating  is  supposedly  dissolved  and  the  ferment 
acts  upon  the  chyle.  The  suggestion  of  Thompson  was  previously 
carried  out  by  Unna.  But  this  idea  is  not  supported  by  experi- 
ment nor  by  exact  indications  of  the  conditions  for  the  employment 
of  pancreatin.  Keratin  will  not  dissolve  in  the  duodenum  except 
very  slowly;  pills  coated  therewith  are  found  in  the  stools  during 
normal  digestion.  There  is  no  necessity  for  attempting  to  supply 
the  ferment  directly  to  the  duodenum,  since  in  the  greater  majority 
of  cases,  perhaps  all,  except  when  malignant  neoplasm,  cirrhosis,  or 
abscess  has  destroyed  the  gland,  there  is  plenty  of  pancreatic  juice 
in  that  part  of  the  bowel.  In  exceedingly  rare  cases  pancreatic 
calculi  and  diseased  states  of  adjacent  parts  may  stenose  the  duct. 
In  all  these  attempts  it  is  overlooked  that  the  reaction  of  the  nor- 
mal duodenum  is  acid  and  will  not  permit  the  solution  of  keratin. 

There  is  but  one  distinct  indication  for  the  use  of  pancreatin, 
and  that  is  permanent  deficiency  or  complete  absence  of  HC1  and 
enzyme  formation  of  the  stomach.  Experiment  and  experience 
have  conclusively  shown  that  when  pancreatic  digestion  is  started 
in  the  stomach  in  these  cases,  by  giving  the  pancreatin  with  sodium 
bicarbonate,  there  is  a more  exhaustive  utilization  of  the  proteids 
and  carbohydrates.  We  have  frequently  assured  ourselves  of  this 
fact  by  analyzing  the  stools  after  weighed  amounts  of  these  food- 
substances  had  been  ingested,  at  the  same  time  making  identical 
analyses  with  the  same  amounts  of  proteid  and  carbohydrate,  but 
with  pepsin  hydrochloric  acid  as  an  artificial  digestant ; under  the 
latter  more  food-substances  passed  through  undigested  than  when 
pancreatin  was  used. 

Pepsin  and  hydrochloric  acid  naturally  suggest  themselves  in 
atrophic  gastritis,  but  judging  from  our  observations,  pancreatin  is 
preferable.  I have  noticed  cases  in  which  there  was  a remark- 
able hypersensitiveness  to  hydrochloric  acid  even  in  doses  of  six 
drops  of  the  dilute  form,  so  that  its  use  had  to  be  dispensed  with. 
The  dose  of  pancreatin  is  from  four  to  eight  grains,  together  with 
the  same  amount  of  sodium  bicarbonate  in  form  of  compressed 
tablets ; of  these,  two  to  four  are  taken  fifteen  minutes  after  meals. 
23 


34^  IMPORTANT  MEDICINAL  AGENTS  IN  GASTRIC  THERAPY. 

Papain,  Papoid,  Papayotin . — These  ferment>containing  substances 
are  made  from  the  milky  juice  of  a tree  belonging  to  the  family  of 
Papayaceae,  native  in  Central  and  South  America. 

Bouchut  and  Wurtz  (“  Sur  la  ferment  digestiv  du  Carica  Papaya,” 
“ Compt.  Rend.,”  1879,  tome  lxxxix)  first  prepared  papain,  and  later 
Peckolt  brought  out  papayotin.  Papoid,  an  American  preparation, 
according  to  Prof.  R.  H.  Chittenden,  is  a vegetable  ferment  made 
up  of  vegetable  globulin,  albumoses,  and  peptone,  with  which  are 
associated  the  ferments  characteristic  of  the  preparation.  Papoid 
has  the  power  of  digesting  to  a greater  or  less  extent  all  forms  of 
proteid  or  albuminous  matter,  both  coagulated  and  uncoagulated ; 
its  digestive  power  is  exercised  in  a neutral,  acid,  as  well  as  alkaline 
medium.  Papoid  is  found  in  the  stools,  showing  that  it  is  not 
destroyed  in  the  alimentary  canal ; the  dose  is  from  one  to  three 
grains  after  each  meal. 

Finkler  prefers  papain  to  pepsin  for  aiding  gastric  digestion 
(“  Therap.  Gazette,”  1887,  August  15th),  and  G.  Littmann  has 
observed  good  results  with  it  in  acute  and  chronic  gastritis,  dilata- 
tions, carcinoma,  and  dyspepsia  after  chronic  ulcer  (Littmann, 
“ Munch,  med.  Wochenschr.,”  1893,  No.  29). 

Papain  seems  to  be  a variable  product  and  its  digestive  action 
not  always  the  same  (Rossbach  and  A.  Eulenberg).  It  is  an 
expensive  preparation.  Recently  a highly  concentrated  extract  of 
carica  papaya  has  been  brought  into  the  market  under  the  name  of 
caroid , which,  according  to  Chittenden,  has  even  a greater  digestive 
power  than  papoid,  and  digests  proteids,  albumins,  and  starches  in 
any  medium.  We  append  Chittenden’s  results  with  this  energetic 
ferment,  concerning  the  clinical  application  of  which  further  obser- 
vations are  necessary : 

With  0.05  per  cent,  hydrochloric  acid : 


Caroid, 

Undigested  residue. 

Proteid  digested. 
20.2  per  cent. 

Papain,  A, 

0.8959  “ 

10.9  “ 

Papain,  B, 

0-8735  “ 

13. 1 “ 

With  0.5  per  cent . sodium  bicarbonate : 

Undigested,  residue . 

Caroid, 0.4596  gm. 

Proteid  digested. 
54.3  per  cent. 

Papain,  A, 

43-4  “ 

Papain,  B, 

O.5927  “ 

41.0  “ 

If  we  examine  these  results  critically,  it  is  plain  that  the  digestive 
power  of  caroid  on  proteid  matter  is  greater  than  that,  of  the  other 


PROTEOLYTIC  FERMENT  OF  THE  PINEAPPLE. 


347 


two  preparations.  The  difference  in  digestive  strength  is  more 
apparent  in  these  experiments  with  coagulated  egg-albumen  than 
with  the  other  form  of  proteid  matter,  although  quite  marked  with 
blood-fibrin. 

2.  Starch-digesting  Poiver . — In  starch-digesting  power  caroid 
is  far  superior  to  the  other  preparations,  either  papoid  or  papain. 
The  following  experiments  will  throw  some  light  upon  this  point 

A starch  paste  was  made  from  five  gm.  of  dry  arrow-root  starch 
with  500  c.c.  of  water.  Mixtures  were  then  prepared  as  follows : 

1.  0.5  gm.  of  caroid,  -(-  90  c.c.  water  -f-  10  c.c.  of  starch  paste. 

2.  0.5  “ “ papoid,  + “ <<_)_<<  “ “ “ 

3.  0.5  “ “ papain,  A,  -f  “ “ + “ “ “ “ 

4.  0.5  “ “ papain,  B,  -j-  “ “ “ « “ “ 

These  four  mixtures  were  placed  at  40°  C.,  and  tested  from  time 
to  time  with  iodin  solution.  In  five  minutes  No.  1 had  reached  the 
achromic  point,  while  No.  2 did  not  give  the  achromic  reaction 
until  at  the  end  of  two  hours.  At  the  end  of  three  hours  Nos.  3 
and  4 still  gave  a bluish-violet  reaction  with  iodin. 

In  another  series  of  experiments  exactly  similar  to  the  above, 
except  that  each  mixture  contained  only  0.2  gm.  of  ferment,  the 
caroid  brought  about  a complete  conversion  of  the  starch  into 
bodies  non-colorable  by  iodin  in  eighteen  minutes,  while  the  others 
gave  a blue  reaction  after  two  or  three  hours. 

The  presence  of  alkalies  retards  the  diastatic  or  amylolytic  action, 
but  the  caroid  shows  throughout  very  much  greater  amylolytic 
power  than  the  other  preparations. 

The  Ferments  of  the  Pineapple. — This  fruit  contains  very  active 
proteolytic  ferments,  its  juice  being  used  in  the  production  of  the 
artificial  predigested  beef  foods  by  a prominent  American  firm. 
The  ferments  are  destroyed  by  boiling,  and  hence  are  no  longer 
active  in  the  preserved  fruit.  We  have  assured  ourselves  suffi- 
ciently of  the  proteolytic  activity  of  raw,  fresh  pineapple-juice  to 
recommend  it  in  achylia  or  subacidity,  and  to  forbid  its  use  in 
hyperacidity  and  hypersecretion,  as  well  as  in  gastritis  acida.  It 
is  allowed  mainly  because  of  its  pleasant  taste  and  because  it 
stimulates  desire  for  other  food.  The  fiber  must  be  removed  from 
the  mouth  after  chewing,  and  only  the  juice  swallowed. 


348  SURGICAL  TREATMENT  OF  ORGANIC  GASTRIC  DISEASES. 


CHAPTER  VII. 

SURGICAL  TREATMENT  OF  ORGANIC  GASTRIC  DISEASES. 

In  the  preantiseptic  time  the  stomach  was  regarded  as  a “ Noli 
me  tangere.”  Even  in  the  beginning  of  this  century  gastric 
wounds  were  considered  as  necessarily  fatal.  Larrey,  the  Surgeon- 
General  of  Napoleon,  was  one  of  the  first  to  declare,  “ Plaies  de 
Pestomac  ne  sont  pas  mortelles  dans  tous  les  cas  ” (cf.  “ Clinique 
Chirurg.,”  tome  iv,  p.  10),  which  was,  as  is  well  known,  confirmed 
by  the  notable  observations  of  our  countryman,  Beaumont,  on 
Alexis  St.  Martin.  Not  only  were  surgeons  timid  about  the  almost 
unavoidable  peritonitis,  but  there  existed  a universal  belief  that  the 
solving  and  peptonizing  action  of  the  gastric  juice  prevented  the 
wound  from  healing.  The  observation  that  undoubted  gastric 
ulcers  had  healed,  and  that  gastric  fistulse  produced  by  physiolo- 
gists in  animals  healed  spontaneously,  and  that  gastrotomy  and 
gastrostomy  performed  in  preantiseptic  years  had  not  shown  the 
corrosive  effect  of  the  gastric  juice,  paved  the  way  for  experi- 
ments by  Gussenbauer  and  von  Winiwarter,  proving  that  gastric 
wounds,  when  sutured,  healed,  as  a rule,  without  interference  from 
any  digestive  action  of  gastric  juice. 

The  first  proposition  to  treat  organic  gastric  diseases  by  operation 
was  made  by  Merrem,  who  originated  the  resection  of  the  pylorus 
(pylorectomy),  and,  after  performing  it  on  dogs,  suggested  it  for 
human  beings  (Dan’l  C.  Theodor  Merrem,  “ Animadversiones 
quaedam  chirurg.  experim.,”  etc.,  Giessse,  1810).  This  writer  men- 
tions that  a Philadelphia  surgeon  had  already  attempted  pylorec- 
tomy on  dogs  and  rabbits,  but  had  been  unsuccessful. 

Gussenbauer  and  von  Winiwarter  demonstrated  later  that 
this  operation  was  technically  feasible,  and  that  removal  of  the 
pylorus  was  not  dangerous  to  life  (“  von  Langenbeck’s  Archiv,” 
Bd.  xix,  S.  347).  They  succeeded  in  showing  that  a certain  per- 
centage of  cases  of  pyloric  carcinoma  were  indications  for  this  opera- 
tion. Czerny  and  Kaiser  confirmed  these  opinions,  and  the  latter 
managed  to  heal  and  keep  alive  a dog  from  whom  he  had  excised 
almost  the  entire  stomach.  As  a surgical  curiosity,  Haberkant 
(“  Arch.  f.  klin.  Chirurg.,”  Bd.  li,  Heft  111,  S.  484)  mentions  a total 
extirpation  of  the  stomach  by  Dr.  Conner,  of  Cincinnati,  in  a 


HISTORY  OF  GASTRIC  SURGERY. 


349 


woman  fifty  years  of  age,  who  died  before  the  esophagus  could  be 
united  to  the  duodenum.  This  operation  was  done  December  7, 
1883,  and  was  the  first  attempt  at  a total  gastrectomy  recorded. 
According  to  Rydygier,  a surgeon  named  Torelli,  in  1878,  executed 
the  first  gastric  resection  in  a man,  removing  a piece  sixteen  cm. 
long  that  had  prolapsed  from  an  abdominal  stab  wound  (“  Centralbl. 
f.  Chirurg.,”  1879,  S.  398).  In  the  same  year  Billroth  brought 
about  healing  of  a gastric  fistula  by  exposing  the  stomach  and 
suturing  it  (“  Wien.  med.  Wochenschr.,”  1881,  S.  275).  In  January, 

1881,  Billroth  executed  the  first  successful  resection  of  the  pylorus 
for  carcinoma. 

The  first  total  resection  for  ulcer  was  performed  by  Rydygier, 
and  the  first  partial  resection  for  ulcer  was  made  by  Czerny  in 

1882.  Both  were  successful.  Pean  executed  a pyloric  resection 
in  1879,  before  Billroth,  and  so  did  Rydygier  in  1880,  but  both 
were  unsuccessful.  In  the  first  publication  of  Billroth’s  resection 
(“  Wien.  med.  Wochenschr.,”  1881,  No.  6)  Wolfler  defined  the  limits 
of  the  usefulness  of  total  resection  as  existing  in  the  transition  of 
the  carcinomatous  tumors  to  the  pancreas  and  duodenum.  Cases 
in  which  the  carcinomatous  infiltration  extended  beyond  the  hepa- 
duodenal  ligament  should  be  excluded  from  resection.  From 
these  indications  the  plan  to  a second  operation  arose — “gastro- 
enterostomy,” which  is  a type  of  entero-anastomosis  (Maisoneuve), 
an  artificial  communication  between  the  stomach  and  the  jejunum, 
when  the  pyloric  obstruction,  for  reasons  given,  can  not  be 
removed.  In  1881  (September  28th)  Wolfler  performed  this 
operation  for  the  first  time;  but  the  very  next  case  (performed  by 
Billroth)  was  fatal,  the  patient  dying  with  constant  emesis  of  bile. 
The  necropsy  showed  that  the  upward  traction  of  the  jejunal  loop 
had  caused  what  is  termed  a “ spur,”  which  returned  the  duodenal 
secretions  (bile,  etc.)  into  the  stomach.  The  spur  had  divided  the 
artificial  gastro-intestinal  lumen  into  two  unequal  parts,  of  which 
the  larger  belonged  to  the  duodenal  canal,  the  smaller  to  the 
jejunal  loop  leading  away  from  the  stomach. 

As  a necessary  result  of  this  the  bile  and  pancreatic  juice  ran 
into  the  stomach,  while  nothing  could  pass  out  into  the  diminutive 
discharging  outlet.  In  one  of  Lauenstein’s  cases  (“  Verhandl.  d. 
Deutsch.  Gesell.  f.  Chirurg.,”  Thirteenth  Congress)  the  mesen- 
tery of  the  jejunal  loop,  which  had  been  drawn  up  to  meet  the 
stomach,  compressed  the  transverse  colon.  The  adducent  part  of 
the  loop  was  drawn  across  the  colon  like  a tense  ridge.  Courvoisier, 


350  SURGICAL  TREATMENT  OF  ORGANIC  GASTRIC  DISEASES. 

in  1883,  invented  another  method  calculated  to  avoid  these  diffi- 
culties. Instead  of  inserting  the  jejunum  to  the  ventral  or  an- 
terior wall  of  the  stomach,  he  made  a slit  in  the  mesentery  of  the 
transverse  colon  and  inserted  the  loop  into  the  posterior  gastric 
wall.  In  order  to  secure  the  continued  onward  flow  of  the  bile 
and  pancreatic  juice  through  the  intestine,  Courvoisier  attached 
the  adducent  part  of  the  intact  loop  to  the  stomach  for  a distance, 
then  split  the  abducent  part,  and  finally  sewed  the  wound  edges  of 
the  gastro-intestinal  opening. 

In  1885  von  Hacker  described  a similar  but  much  more 
improved  meth'od,  which  consists  in  the  following  : The  colon  and 
great  mesentery  are  raised  upward ; the  gaping  edges  of  the  slit  in 
the  mesocolon  are  attached  to  the  posterior  gastric  wall ; finally, 
the  jejunal  loop  is  attached  to  the  stomach  within  this  slit  (von 
Hacker,  “ Verhandl.  d.  Deutsch.  Gesell.  f.  Chirurg.,”  1885,  Four- 
teenth Congress). 

A third  method  of  gastro-enterostomy  was  suggested  by  Billroth 
and  Brenner  (“  Deutsche  Zeitschr.  f.  Chirurg.,”  Bd.  xxv,  p.  502). 
In  this  method  openings  are  made  both  through  the  gastrocolic 
ligament  and  mesocolon,  through  which  the  jejunal  loop  was 
drawn  up  and  sewed  to  the  anterior  gastric  wall  immediately 
above  the  greater  curvature.  Von  Hacker  has  given  these  various 
operations  very  significant  and  explicit  Latin  designations  (“  Chir. 
Beitr.  a.  d.  Erzherzogin  Sophienspital  in  Wien,”  S.  42).  These  are 
his  terms  in  English  : 

1.  Gastro-enterostomy,  anterior,  antecolonic  (Wolfler). 

2.  Gastro-enterostomy,  posterior,  retrocolonic  (von  Hacker). 

3.  Gastro-enterostomy,  anterior,  retrocolonic  (Billroth-Brenner). 

A number  of  other  modifications  must  be  passed  over,  since  we 

are  interested  only  in  the  clinical,  not  so  much  in  the  purely  sur- 
gical, aspect  of  the  subject. 

Since  the  publication  of  the  first  edition  of  this  work,  in  October, 
1897,  the  subject  of  the  “Surgery  of  the  Stomach”  has  been  re- 
viewed and  represented  in  the  “ Cartwright  Lectures,”  published  in 
the  “Phila.  Med.  Journal,”  volume  1,  pages  829, 927,  1053,  and  1 104. 
This  is  a most  comprehensive  and  conservative  representation  of 
gastric  surgery,  by  one  of  the  ablest  operators  and  surgical  philos- 
ophers of  our  country,  Prof.  W.  W.  Keen. 

A second  very  helpful  publication  bearing  directly  on  this 
subject  is  the  volume  by  Lindner  and  Kuttner — “ Die  Chirurgie 
des  Magens  und  ihre  Indicationen  einschliesslich  Diagnostik.” 


GASTROLYSIS. 


351 


The  lectures  by  Prof.  Keen  contain  references  to  most  of  the 
important  American  and  English  works,  and  the  volume  of  Lindner 
and  Kuttner,  the  German  aspect  of  the  subject,  though  this  is  by 
no  means  neglected  in  the  former. 

An  excellent  French  representation  of  surgery  of  the  stomach 
is  by  Professors  F.  Ferrier  and  Hartman,  Paris,  1899. 

VARIOUS  FORMS  OF  OPERATIONS  PRACTISED  UPON  THE 
STOMACH. 

Gastrolysis  is  the  name  of  an  operation  by  which  peritoneal 
adhesions  binding  the  stomach  to  other  abdominal  organs  and 
the  abdominal  wall  are  severed.  The  symptoms  of  gastric 
adhesions  are  variable  and  obscure,  and  the  diagnosis  is  difficult. 
The  most  constant  symptoms  are:  (1)  A long  history  of  digestive 
suffering;  (2)  persistent  pain;  (3)  persistent  vomiting;  (4) 
displacement — in  any  direction,  sometimes  even  upward.  In  one- 
third  the  cases  of  adhesions  there  is  evidence  of  existing  or  pre- 
vious gastric  ulcer. 

The  author  referred  to  a case  of  extensive  adhesions  in  the  first 
edition  of  this  work  (p.  695).  A negro,  58  years  old,  had  been 
suffering  from  the  most  intense  gastralgia,  and  vomiting  off  and 
on  for  twelve  years.  Distention  of  the  stomach  with  C02  did  not 
bring  the  stomach  forward  and  out  from  the  arch  of  the  ribs. 
The  electrodiaphany  showed  the  stomach  in  a higher  position 
than  normal.  The  gastric  contents  showed  marked  hyperacidity. 
An  operation  was  undertaken  upon  advice  of  the  writer,  the 
diagnosis  not  being  established  definitely,  but  stated  as  probably 
gastric  ulcer  with  perforation.  The  stomach  was  found  bound  to 
the  diaphragm  by  two  broad  adhesions,  to  the  transverse  colon  at 
about  its  middle,  to  the  liver  and  gall-bladder.  There  were  also 
adhesions  between  the  jejunal  loops  and  a firm  adhesion  of  the 
ascending  colon  to  the  abdominal  wall.  The  adhesions  to  the 
liver  and  gall-bladder  proved  inseparable.  No  gastric  ulcer  was 
discovered  at  the  operation,  but  an  old  cicatrix  was  found  at  the 
autopsy  two  months  after  operation. 

As  a rule,  the  operation  is  successful.  Of  Lauenstein’s  ten 
cases,  nine  recovered  (“Arch.  f.  klin.  Chir.,”  1892,  xlv,  121). 
Other  successful  operations  are  reported  by  Robson,  Naylor, 
Ferrier,  Hoffmeister,  Billroth,  Mikulicz,  and  Hahn  (“  Deutsch. 
med.  Wochenschr.,”  1894,  No.  43).  The  adhesions  may  reunite 
after  intersection  and  cause  renewed  trouble. 


352  SURGICAL  TREATMENT  OF  ORGANIC  GASTRIC  DISEASES. 

Gastrotomy  is  the  operation  of  opening  the  stomach  with  the 
object  of  removing  a foreign  body;  then  sewing  up  the  wound  in 
the  stomach,  replacing  the  viscus,  and  sewing  up  the  external 
abdominal  wound.  This  operation  must  be  looked  upon  as  very 
successful,  for,  of  18  cases  reported  by  Henry  Morris  (Ashhurst, 
“ Encyclopedia  of  Surgery,”  vol.  v,  p.  589),  14  recovered.  This 
operation  is  also  executed  with  a view  to  effecting  dilatation  of 
stricture  of  the  esophagus  from  the  stomach  side;  and,  thirdly, 
the  stomach  is  opened  for  exploratory  purposes. 

Gastrostomy  is  designed  to  rescue  a person  from  immediate 
starvation  when  there  is  a stenosis  in  the  esophagus,  either  from 
cicatricial  contraction  resulting  from  esophageal  ulcer,  syphilitic, 
tuberculous,  or  malignant  neoplasm,  or  corrosive  toxic  agents. 

Occasionally,  this  operation  may  be  required  by  tumor  outside 
the  esophagus.  Roswell  Park  (“  International  Med.  Jour.,”  Jan. 
9,  1894)  and  Stockton,  also  Whitehead,  have  done  the  operation 
for  diverticulum  of  esophagus.  The  various  methods  of  technic  of 
this  operation  are  described  in  the  articles  of  W.  W.  Keen  ( loc.cit ., 
p.  836).  Andrews,  Senn,  and  Stamm  are  American  surgeons  who 
have  described  new  methods  for  this  purpose. 

The  same  causes  affecting  the  cardia — for  instance,  carcinoma  of 
the  cardia — may  necessitate  gastrostomy.  Our  experience  is  that 
the  sooner  gastrostomy  is  performed  in  carcinoma  of  the  cardia, 
the  longer  is  the  life  sustained.  One  should  not  wait  until  noth- 
ing but  liquids  will  pass  the  stricture.  It  has  been  observed  that 
the  carcinoma  will  improve  and  show  some  tendency  toward 
healing  when  food  no  longer  passes  over  it  and  the  dilatation 
above  the  stricture  is  kept  clean  by  esophageal  lavage.  When- 
ever possible,  the  esophageal  dilatation  should  be  washed  out  daily, 
even  after  gastrostomy  has  been  performed.  In  cases  where  the 
esophageal  stricture  had  become  impassable,  it  has  occasionally  been 
noticed  that  after  gastrostomy  the  stenosis  again  became  permeable, 
and  food  could  be  swallowed  for  a while.  Witzel  has  devised  an 
oblique  entrance  of  the  fistula  into  the  stomach,  making  use  of  the 
anatomical  relations  of  the  abdominal  walls  for  that  purpose.  The 
canal  is  laid  partially  in  the  gastric  and  partially  in  the  abdominal 
walls,  being  somewhat  tortuous,  and  mostly  closed  to  food  trying 
to  come  outward  (Witzel,  “ Z.  Technik  d.  Magenfistelanlegung,” 
“ Centralblatt  f.  Chirurg.,”  1891,  No.  32).  Von  Hacker’s  technic, 
as  original  with  him,  has  been  practised  in  a number  of  cases  for 
dilating  esophageal  strictures  with  sounds  introduced  from  the 


GASTRORHHAPH  Y. 


353 


gastric  side,  when  dilatation  of  the  strictures  from  the  mouth  had 
failed.  The  unfavorable  results  of  gastrostomy — Zesas  reported 
only  19.5  per  cent,  of  so-called  recoveries  in  13 1 operations  (“Arch, 
f.  klin.  Chirurg.,”  Bd.  xxxn) — are  largely  due  to  postponing  the 
operation  until  the  general  health  is  too  low  to  assist  in  recovery. 

Mikulicz  has  formulated  his  latest  results  in  the  following  table 
(“  Arch.  f.  klin.  Chirurgie,”  Bd.  Li,  p.  9,  1895): 


GASTRECTOMY  AND  GASTROTOMY. 


Total. 

Recovered. 

Died. 

O 

2 

O 

Mortality 

Percentage 

0.0 

66.66 

IOO.00 

0.0 

For  simple  ulcer, 

For  ulcer  and  hemorrhage, 

1 

3 

1 

1 

I 

I 

0 

For  ulcer  with  perforation, 

Occlusion  of  pylorus  with  a gall-stone,  . . . 

Total, 

6 

3 

3 

50.0 

The  results  in  gastrostomy  for  esophageal  carcinoma  are  stated 
by  Mikulicz  (Joe.  cit.)  as  follows : Of  28  patients  that  survived 
the  operation  longer  than  three  weeks,  20  subsequently  died  of 
the  fundamental  disease.  The  shortest  duration  of  life  was 
three  and  one-half  weeks,  the  longest  twelve  months,  after  the 
operation.  The  average  duration  of  life  after  the  operation  was 
four  and  one-half  to  five  months. 


GASTROSTOMY. 


Total. 

Recovered. 

Died. 

Mortality 

Percentage. 

Toxic,  corrosive  stricture  of  esophagus,  . . 

9 

9 

O 

0.0 

Neurosis  (cardiospasm), 

1 

I 

O 

0.0 

Carcinoma  of  cardia  or  esophagus,  .... 

34 

28 

6 

17.64 

Total, 

44 

38 

6 

1363 

Gastrorrhaphy,  or  gastroplication,  is  an  operation  for  closure 
of  wounds  of  the  stomach.  The  term  applies  to  any  case  where 
the  stomach  is  sewed  ; it  is  generally  restricted  to  those  cases  in 
which  a limited  portion  of  the  gastric  wall  is  sutured  with  or  with- 
out excision.  The  operation  is  available  as  a means  of  reducing 
excessive  dilatations  not  complicated  by  malignant  neoplasm  and 
which  have  not  improved  under  persistent  and  careful  medical 
treatment. 


354  SURGICAL  TREATMENT  OF  ORGANIC  GASTRIC  DISEASES. 

Pylorectomy,  or  Resection  of  the  Pylorus.* — In  considering 
the  value  of  this  operation  we  must  sharply  distinguish  between 
three  types  : 

1.  Typical,  total,  or  circular  pylorectomy. 

2.  Atypical  pylorectomy,  which  consists  of  a combination  of  the 
former  with  a gastro-enterostomy. 

3.  Partial  pylorectomy. 

Typical  or  Total  Pylorectomy. — Indications  in  259  operations  were 
the  following : Carcinoma,  215  times;  ulcer  or  cicatrix,  34  times  ; 
sarcoma,  twice;  angioma  fibrosum,  once;  not  stated,  seven  times. 
In  judging  of  the  benefit  to  be  derived  from  these  operations,  we 
must  distinguish  sharply  between  (1)  the  immediate  and  (2)  the 
remote  results.  Generally  speaking,  surgeons  term  a patient 
“ recovered  ” when  he  succeeds  in  getting  over  the  effects  of  the 
operation ; this  is  the  immediate  result.  The  remote  results  are 
determined  by  the  duration  of  life  after  the  operation.  The  imme- 
diate results  of  the  259  cases  above  enumerated  are  the  following : 
Of  34  cases  of  benign  stenosis,  23  recovered;  of  215  cases  of  car- 
cinoma, 98  recovered ; both  cases  of  sarcoma  and  the  case  of 
angioma  fibrosum  recovered.  Haberkant  (loc.  cit .)  found  the  mor- 
tality for  ulcer  to  be  34.4  per  cent.,  and  for  carcinoma,  56.7  per  cent., 
in  a total  of  239  operations  performed  from  1879  to  1^94-  It  is  a 
very  important  question  for  the  clinician  whether  the  mortality  is 
becoming  less  as  time  progresses,  which  signifies  an  improvement 
in  the  technic  and  knowledge  of  the  subject.  Haberkant  arranged 
205  cases,  operated  on  from  1881  to  1894,  in  two  series  of  seven 
years  each  (from  1881  to  1888,  and  from  1888  to  1895).  In  the  first 
series  the  total  mortality  was  62.8  per  cent. ; in  the  second  series  it 
was  45.1  per  cent.  For  carcinoma  a reduction  of  the  rate  of  mor- 
tality from  65.4  per  cent,  to  42.8  per  cent.,  and  for  benign  pyloric 
stenosis  a reduction  from  42.8  per  cent,  to  27.7  per  cent.,  is  calcu- 
lated. In  1882,  of  13  cases  of  resected  carcinomata,  all  died  ; in 
1893,  of  8 cases,  all  recovered.  There  may  be  some  objection 
to  the  absolute  correctness  of  these  figures,  but  they  undoubtedly 
admit  the  belief  that  our  methods  of  diagnosis  and  operative  technic 


* For  the  statistics  and  historical  information  on  the  subject  of  the  principal  operations 
we  are  indebted  to  the  “Cartwright  Lectures,”  by  Professor  W.  W.  Keen,  “ Phila. 
Med.  Jour.,”  vol.  I,  p.  931,  and  to  an  article  by  Dr.  Haberkant  in  the  “ Arch.  f. 
klin.  Chirurg.,”  Bd.  Li,  p.  861,  1896;  to  a report  by  Prof.  J.  Mikulicz,  “Arch.  f. 
klin.  Chirurg.,”  Bd.  Li,  p.  9,  1895;  the  volume  by  Lindner  and  Kuttner  (“  Magen 
Chirurgie,”  and  the  work  of  Ferrier  and  Hartmann). 


PYLORECTOMY — RESECTION  OF  THE  PYLORUS. 


355 


are  improving.  Some  forms  of  gastric  cancer  are  much  more 
malignant  and  unfavorable  to  treatment  than  others.  In  44  cases 
in  which  microscopical  examinations  were  made,  we  found  the 
following  comparisons  : 


Nature  of  the  Gastric  Cancer. 

Number  of 
Operations. 

Recovered. 

Died. 

Scirrhus 

16 

IO 

6 

Adenocarcinoma  (epithelial  carcinoma), 

10 

5 

5 

Medullary  carcinoma, 

9 

1 

8 

Colloid  carcinoma,  

9 

7 

2 

44 

23 

21 

According  to  this  table,  colloid  carcinoma  is  the  most  favorable 
to  operation,  while  the  most  unfavorable  prognosis  is  to  be  formed 
of  medullary  sarcoma. 

The  remote  results  are  best  shown  in  the  duration  of  life  after 
the  operation,  which  is  expressed  in  the  accompanying  table  (see 
end  of  this  chapter),  from  which  it  is  evident  that  the  average 
expectation  of  life  after  pylorectomy  for  carcinoma  is  not  very  long. 
For  of  twenty-six  so-called  recoveries,  or  immediate  good  results, 
seventeen,  or  nearly  two-thirds,  died  within  one  year  after  the 
operation.  Furthermore,  of  twenty- six  (different)  cases,  twelve 
died  in  from  one  and  one-half  to  thirteen  months  from  return  of  the 
malignant  trouble  or  metastases.  One  case  of  Billroth’s  lived  five 
and  a quarter  years.  One  case  of  Kocher  (“  Centralbl.  f.  Chir.,” 
1894,  S.  221)  lived  five  years  and  four  months,  and  one  case  of  Rat- 
timmow’s  {ibid.,  S.  1014)  lived  eight  years.  Wolfler  cites  three  cases 
who  lived  over  four  years,  four  over  five  years,  one  over  six  years, 
and  two  over  eight  years.  The  boundary  of  the  pathological  tissue 
can  not  be  determined  accurately.  As  is  the  custom  in  most  malig- 
nant neoplasms  of  other  organs,  the  resection  is  made  by  cutting 
through  the  apparently  or  visibly  healthy  tissue  one  cm.  from  the 
limit  of  the  diseased  portion.  Czerny,  however,  found,  by  careful 
microscopical  examination  of  resected  pieces,  that  the  edges  of  the 
section,  made  through  apparently  healthy  tissue,  contained  cancer- 
ous alveoli ; he  therefore  advised  that  the  cut  be  made  not  one, 
but  three,  cm.  from  the  limit  of  the  carcinomatous  tissue.  Virchow 
holds  that  as  long  as  a neoplasm  is  solitary,  the  hope  for  a success- 
ful operation  must  not  be  given  up. 

Pylorectomy  is  the  only  operation  which  can  make  a definite 


356  SURGICAL  TREATMENT  OF  ORGANIC  GASTRIC  DISEASES. 

cure  or  a recovery  of  some  duration  possible;  and  although  the 
prospects  of  complete  cure  are  very  few,  we  must  hold  fast  to  the 
encouragement  which  statistics  furnish — namely,  that  more  cases 
recover  with  improvement  in  the  technic  and  the  possibility  of  early 
diagnosis.  Haberkant  ( loc . cit.,  p.  26)  takes  too  gloomy  a view  of  the 
future  of  gastric  operations  when  he  asserts  that  we  must  expect  no 
advance  in  the  curability  of  gastric  carcinoma, because,  in  his  opinion, 
patients  decide  for  the  operation  too  late,  even  after  the  diagnosis  is 
certain  ; and,  secondly,  because  it  will  be  impossible  to  diagnose 
gastric  carcinoma  at  a time  when  a cure  by  extirpation  would  be 
possible.  The  early  diagnosis  of  gastric  carcinoma,  he  emphasizes, 
is  in  almost  all  cases  impossible  (?).  The  surgeon,  as  a rule,  con- 
cludes to  operate  only  when  distinct  stenotic  symptoms  are  present, 
with  emesis,  dilatation,  and  palpable  tumor.  The  only  sign  which 
Haberkant  cites  to  be  doubtful — that  is,  the  absence  of  HC1  in  the 
gastric  contents — is  by  no  means  the  only  one  the  clinician  has  to 
be  guided  by,  as  reference  to  the  chapter  on  Diagnosis  of  Gastric 
Carcinoma  will  show.  In  justice  to  the  surgeons,  we  desire  to  say 
that  they  are  not  given  the  cases  early  enough  and  the  clinicians 
can  not  be  exempt  from  blame  for  this  delay  in  operation. 

There  can  not  be  a moment  of  doubt  about  the  feasibility  of 
operation  when  gastric  dilatation  is  manifestly  due  to  palpable 
neoplasm,  even  if  it  were  not  malignant.  But  we  generally  advise 
operation  in  case  (1)  dilatation  is  associated  with  cachexia;  (2) 
absence  of  HC1  in  the  gastric  contents;  (3)  excess  of  lactic  acid; 
(4)  presence  of  the  Oppler-Boas  bacillus.  Professor  W.  W.  Keen, 
in  quoting  these  deciding  factors  from  this  work  (“  Phila.  Med. 
Journal, ” vol.  1,  p.  932),  adds  (5)  when  age  is  passed  forty  years  ; 
(6)  when  hematemesis  is  present;  (7)  when  examination  of  blood 
shows  a diminution  in  red  corpuscles  and  hemoglobin,  and  the 
digestive  leukocytosis  is  absent.  Stenotic  symptoms,  accompanied 
by  these  signs,  are  indications  for  operation,  even  in  the  absence 
of  palpable  tumor.  Personally,  I always  urge  operation  when  the 
first  three  conditions  are  persistently  present  and  the  case  does  not 
improve  after  three  weeks  of  appropriate  treatment. 

Exploratory  laparotomy , which  Haberkant  states  to  be  the  only 
reliable  means  for  making  an  early  diagnosis  of  carcinoma,  should 
be  encouraged  by  the  internist,  not  because  carcinoma  can  be  diag- 
nosed with  certainty  thereby,  for  it  really  can  not,  as  the  stomach 
is  the  seat  of  many  kinds  of  neoplasms,  and  even  ulcer,  with  indu- 
rated edges,  may  simulate  carcinoma;  so  that  the  finding  of  a new 


HOW  MANY  PYLORIC  NEOPLASMS  ARE  OPERABLE  ? 357 

growth  does  not  include  a knowledge  of  its  exact  nature,  and  if  a 
carcinoma  of  small  size  be  at  the  posterior  side  of  the  lesser  curva- 
ture, it  may  escape  attention  even  at  autopsies  until  the  stomach  is 
removed  from  the  body.  The  article  quoted  is  an  excellent  piece 
of  work,  and  the  pessimistic  view  on  the  future  development  of 
clinical  diagnosis  need  not  discourage  the  clinician  ; for  the  prog- 
ress which  digestive  physiology,  pathology,  and  bacteriology  have 
made  in  the  last  twenty  years,  and  are  still  making,  strengthens 
the  belief  that  we  shall,  in  the  near  future,  be  able  to  make  early 
diagnoses  of  gastric  neoplasms.  Whether  they  will  be  operable  or 
not  is  another  question,  which  the  clinician  and  the  surgeon  must 
investigate  together. 

The  practitioner  should  not  be  too  guarded  in  advising  explora- 
tory laparotomy  in  cases  of  rapidly  developing  cachexia  and 
emaciation  with  the  symptoms  of  chronic  gastritis  and  absence  of 
HC1.  Tentative  treatment  should  not  be  prolonged  over  three 
weeks.  It  is  not  near  so  serious  a fault  to  have  caused  the 
opening  of  a stomach  and  found  nothing  operable,  as  to  permit  a 
case  to  continue  and  find  out,  at  the  autopsy  only,  that  it  was  a 
circumscribed  carcinoma  the  removal  of  which  might  have  pro- 
longed life  for  years.  The  author  has  been  responsible  for  three 
exploratory  laparotomies  at  which  nothing  was  found,  although 
cancer  was  suspected  in  one  and  ulcer  in  the  other  two.  The  cases 
recovered  and  were  cured  of  their  symptoms,  of  pain  and  vomiting. 
One  of  these  cases  had  vomited  a pint  of  blood  in  the  presence  of 
the  writer.  At  the  operation,  by  Dr.  J.  M.  T.  Finney,  nothing  ab- 
normal could  be  found  in  the  stomach. 

Even  after  the  diagnosis  is  certain,  much  foresight  is  necessary 
in  selecting  cases  for  operation  ; the  establishment  of  the  indication 
must  be  done  with  exactness  and  care.  That  the  mortality  from 
cancer  resections  has  sunk  from  65.4  per  cent,  in  the  period  from 
1879  to  1887  to  42.8  per  cent,  in  the  period  from  1888  to  1894,  and 
of  benign  stenosis  from  42.8  per  cent,  to  27.7  per  cent,  in  the  same 
period,  shows  that  the  importance  of  exact  “ Indicationsstellung  ” 
is  being  appreciated. 

How  many  pyloric  carcinomata  are  operable?  In  the  records  of 
the  Vienna  Pathological  Institute,  from  1817  to  1873,  Gussenbauer 
and  von  Winiwarter  found  accounts  of  542  pyloric  cancers,  of  which 
223  were  entirely  isolated,  and  172  of  these  showed  no  adhesions; 
so  41. 1 per  cent,  were  free  from  metastases,  and  37.7  per  cent,  were, 
in  addition  to  this,  free  from  adhesions — the  latter  were  suited  for 


35 8 SURGICAL  TREATMENT  OF  ORGANIC  GASTRIC  DISEASES. 

resection.  In  many  of  the  instances  where  the  necropsy  showed 
adhesions  there  must  have  been  a time  when  they  were  not  present ; 
so  that  a big  field  for  operative  therapy  is  opened.  Streit  found,  at 
the  Bern  Pathological  Institute,  that  25.9  per  cent.  (“Deutsche 
Zeitschr.  f.  Chir.,”  Bd.  xvi)  and  Kramer  (Konig,  “ Lehrb.  d.  spec. 
Chir.,”  Bd.  11)  that  33.3  per  cent,  of  pyloric  cancers  were  operable. 
The  best  statistics  state  that  from  one-quarter  to  one-third  of  these 
neoplasms  are  operable.  Adhesions  increase  the  mortality ; in 
sixty-six  cases  of  pylorectomy  in  which  records  were  kept  concern- 
ing this  point,  the  mortality  was  72.7  per  cent,  with,  and  27.2  per 
cent,  without,  adhesions.  No  immediate  recoveries  are  on  record 
where  there  were  adhesions  of  the  pylorus  with  the  transverse* 
colon,  or  with  the  colon  and  the  pancreas  together.  Two  patients 
with  tumors  of  the  curvatures  and  fundus,  although  distinctly 
ascertained  to  be  malignant  (they  were  causing  no  stenotic  symp- 
toms ; so  that  the  vicarious  digestion  of  the  intestines  maintained  the 
nitrogen  equilibrium  sufficiently),  lived  longer — not  being  operated 
— than  two  in  whom  gastro-enterostomy  was  performed.  Both 
operated  cases  had  adhesions.  In  the  non-operated  cases  there 
were  no  adhesions  found  at  autopsy — that  is  to  say,  the  average 
duration  of  life  after  the  date  of  exact  diagnosis  was  longer  in  those 
cases  of  this  type  that  were  not  operated  than  in  those  that  were. 

Can  the  secretory  and  motor  function  be  restored  after  total  ex- 
tirpation of  a malignant  tumor? 

Obalinski  and  Jaworski(“  Wien.  klin.  Wochenschr.,”  1889,  No.  5), 
Rosenheim  (“  Deutsche  med.  Wochenschr.,”  1892,  No.  49),  Kansche 
(ibid.),  and  Zawadski  and  Sohnan  (“  Deutsche  med.  Wochenschr.,” 
1894,  No.  8)  assert  that  secretion  is  not  restored  by  pylorectomy, 
but  the  last-mentioned  authors  assert  that  the  motility  may  again 
become  good.  In  cases  that  are  operated  before  a complete  de- 
struction of  the  gland-cells  has  taken  place,  the  lost  secretion  of 
HC1  has  been  observed  to  be  restored.  Rosenheim  (“  Berlin,  klin. 
Wochenschr.,”  1895,  No.  1)  and  Boas  (“  Deutsche  med.  Wochen- 
schr.,” 1895,  No.  5)  have  reported  the  only  two  cases  of  this  kind; 
so  that  it  must  be  an  extremely  rare  occurrence. 

Pyloric  stenosis  caused  by  simple  benign  adhesions  can  be  re- 
moved by  severing  the  constricting  bands.  These  adhesions  may 
cause  pain  and  hematemesis  without  gastrectasia,  as  was  shown  in 
a case  of  Hahn’s  (“Deutsche  med.  Wochenschr.,”  1894,  No.  43), 
where  laparotomy  revealed  five  adhesions  binding  the  stomach  to 
the  colon.  He  ligated  each  one  of  the  strong  bands  doubly  and 


GASTRO-ENTEROSTOMY  VERSUS  PYLORECTOMY.  359 

severed  it,  and  from  that  moment  the  patient  recovered  perfectly. 
Median  herniae  of  the  linea  alba  have  been  known  to  cause  intense 
gastric  suffering,  necessitating  operation.  Rosenheim  has  described 
such  cases,  which  were,  however,  much  benefited  by  lavage  and 
diet,  so  that  the  motor  insufficiency  was  much  improved  (“  Berlin, 
klin.  Wochenschr.,”  1897,  No.  11).  Preperitoneal  lipomata  have 
been  known  to  cause  interference  with  the  motility  and  necessitate 
surgical  interference.  Adhesions  may  reunite  after  intersection 
and  cause  renewed  trouble,  as  was  shown  in  one  case  of  Hahn’s, 
in  which  the  adhesions  were  divided  again  by  W.  Levy  two  years 
after  the  first  operation ; a few  months  after  this  Hadra  executed  a 
gastro-enterostomy,  on  Rosenheim’s  suggestion  (loc.  cit.)f  which 
gave  no  perfect  relief,  as  the  two  previous  operations  had  caused 
new  adhesions.  Referring  again  to  malignant  tumors  of  the  lesser 
or  greater  curvatures  where  good  motility  is  maintained,  and  that 
cases  of  this  kind  which  are  not  operated  may  live  a year  or  more, 
we  might  add  the  case  of  a lady  in  whom  Musser  and  Da  Costa 
diagnosed  a palpable  tumor  in  February,  1896.  Personally,  we 
determined  the  location  in  July,  1896,  when  there  was  complete 
loss  of  all  secretion  and  numerous  Oppler-Boas  bacilli  were  present 
in  the  gastric  contents.  A fragment  of  the  neoplasm  was  obtained 
in  September,  1896,  during  lavage,  clinching  the  diagnosis  of  car- 
cinoma. With  daily  lavage  with  HC1  solution  (4:  1000),  highly 
nutritious  and  concentrated  diet,  rest,  and  internal  use  of  HC1, 
condurango,  and  strychnin,  this  patient  has  gained  twelve  pounds 
in  six  months,  and  is  still  (September,  1897)  able  to  take  walks 
of  two  miles  a day — nineteen  months  after  Musser  first  diagnosed 
the  existence  of  a gastric  tumor.* 

The  number  of  authoritative  advocates  of  pylorectomy  for  benign 
stenosis  is  growing  smaller  and  smaller.  Von  Hacker  recently  again 
emphasized  that  gastro-enterostomy  is  not  used  enough  for  the 
treatment  of  cicatricial  stenoses  of  the  pylorus  and  duodenum,  and 
that  it  has  the  value  of  a radical  operation  for  many  cases  with- 
out sharing  its  dangers  (von  Hacker,  “ Magenoperationen,”  etc., 
published  by  William  Braumiiller,  Wien,  1895).  Mintz  considers 
pylorectomy  unjustifiable  for  benign  cicatricial  stenoses  (“  Zeitschr. 
f.  klin.  Med.,”  Bd.  xxv).  For  mild  stenotic  cicatrices  the  pyloro- 

* This  case  lived  eighteen  months  after  establishment  of  diagnosis  by  the  author.  At 
one  time,  July,  1896,  operation  was  strongly  advised,  but  refused.  The  great  difficulty 
with  such  cases  is  that  the  location  of  the  tumor  can  not  be  determined  with  certainty. 
Exploratory  laparotomy  is  safest  for  diagnosis. 


360  SURGICAL  TREATMENT  OF  ORGANIC  GASTRIC  DISEASES. 

plastic  operation  has  proved  sufficient.  We  shall  refer  to  this  opera- 
tion in  the  following  : 

Atypical pylorectomy  was  executed  first  in  1885,  by  Billroth.  It 
is  a combination  of  resection  of  the  pylorus  with  gastro-enteros- 
tomy  recommended  in  cases  where  carcinomata,  although  operable, 
had  so  extensively  involved  the  gastric  walls  that  after  resection  it 
was  impossible  to  suture  the  remainder  of  the  stomach  to  the  duo- 
denum, or  where  traction  upon  the  duodenum  to  meet  the  stomach 
would  produce  too  much  tension  upon  the  stitches. 

Von  Eiselsberg  executed  the  most  extensive  atypical  resection 
of  the  pylorus  in  a very  large  but  sharply  limited  carcinoma.  His 
incision  began  close  to  the  cardia  and  descended  perpendicularly 
downward,  so  that  only  a small  portion  of  the  left  fundus  remained 
(“  von  Langenbeck’s  Archiv,”  Bd.  xxxix).  Even  this  incision  was 
not  through  healthy  tissue,  and  the  stitches  tore  through,  termin- 
ating the  case  by  perforation  peritonitis.  In  twenty  cases  of 
atypical  pylorectomy  eight  died — a mortality  of  forty  per  cent. 
The  first  case  of  immediate  success  by  Billroth  succumbed  to  a 
recurrence  after  four  months.  Kronlein  performed  this  operation 
for  traumatic  cicatricial  stenosis  extending  into  the  duodenum. 

Partial  Pylorectomy  and  Partial  Resections  of  the  Gastric  Walls. — 
The  indications  are  given  by  the  round  ulcer,  both  on  the  anterior 
and  posterior  walls,  cicatrices  that  produce  interference,  or  tumors 
of  the  neighborhood  that  have  extended  to  the  gastric  wall  without 
involving  the  entire  circumference  of  the  pylorus.  Partial  pylorec- 
tomy preserves  the  valvula  pylori,  which  is  itself  rarely  the  seat 
of  gastric  ulcer.  In  a total  pylorectomy  the  sphincter  and  valve 
are  removed  entirely  and  replaced  by  a gradually  contracting 
scar.  Haberkant  records  eight  such  partial  operations — three  by 
Billroth  (reported  by  von  Hacker,  loc.  cit.),  three  by  Czerny  (“  Beitr. 
z.  klin.  Chir.,”  Bd.  ix,  1892),  one  by  Spear  (“  Centralbl.  f.  klin. 
Chir.,”  1885),  and  one  by  Schuchardt  (Twenty-third  German  Sur- 
gical Congress,  1894). 

Billroth’s  and  Spear’s  cases  all  died  ; the  three  cases  of  Czerny 
recovered.  The  indications  in  the  cases  of  the  first  two  surgeons 
were:  cicatrices,  four  times  in  the  anterior  pyloric  wall.  The  indi- 
cations in  the  last  three  cases  by  Czerny  were  : ulcer,  once  ; exten- 
sion of  sarcoma,  twice.  The  case  of  stenosing  ulcer,  operated  upon 
by  the  latter  by  this  method,  was  still  doing  well,  according  to  last 
reports,  ten  years  after  the  operation. 

The  case  of  Schuchardt’s  is  most  instructive  in  bearing  out  our 


TOTAL  GASTRECTOMY. 


361 


objection  to  Haberkant’s  assertion  that  exploratory  laparotomy  is 
the  only  reliable  means  for  early  diagnosis  of  carcinoma.  Schuch- 
ardt’s  case  had  two  open  ulcers,  only  one  of  which  was  discov- 
ered when  the  stomach  was  opened,  located  at  the  lesser  curvature 
and  removed  by  excision  of  a piece  as  large  as  a 25-cent  piece. 
Although  no  peritonitic  symptoms  appeared,  death  occurred  under 
progressive  cachexia  in  fourteen  days.  The  necropsy  showed  a 
second,  much  larger  ulcer,  which,  in  Haberkant’s  ( loc . cit. , p.  514) 
own  words,  was  not  only  inoperable,  but  could  not  even  be  pal- 
pated. If  a very  large  ulcer  can  not  be  palpated  when  the  stomach 
is  exposed,  exploratory  laparotomy  is  not  infallible  as  a diagnostic 
method  ; it  may  desert  us  like  our  clinical  methods.  The  oldest 
resections  of  the  gastric  wall  are  by  Billroth  (“  Wien.  med.  Wochen- 
schr.,”  1881,  p.  275)  and  Esmarch  (quoted  by  Wolfler,  loc.  cit),  for 
the  repair  of  fistulae. 

Rupp  resected  a subserous  leiomyoma  of  the  anterior  wall  near 
the  cardia  in  this  way  (“  von  Langenbeck’s  Arch.,”  Bd.  xl,  p.  756). 
The  number  of  partial  resections,  including  both  those  of  the 
pylorus  and  of  the  anterior  gastric  wall,  amount  to  fifteen  opera- 
tions ; eight  were  cured,  seven  were  fatal,  giving  a mortality  of 
46.6  per  cent. 

Total  Gastrectomy. — In  1897  Schlatter  reported  the  first  com- 
plete gastrectomy  anatomically  proved  as  such  (“  N.  Y.  Med. 
Rec.,”  December  25,  1897,  lii,  909).  The  operation  was  performed 
September  6,  1897.  The  patient  lived  one  year  and  two  months, 
dying  October  29,  1 898.  Death  was  due  to  multiple  carcinomatous 
metastases,  and  was  not  ascribed  to  inanition.  Brigham  (“  Boston 
Med.  and  Surg.  Jour.,”  May  5,  1898)  reported  a complete  removal  of 
the  entire  stomach  for  carcinoma,  and  anastomosing  the  duodenum 
to  the  esophagus  by  the  Murphy  button.  Brigham’s  case  was 
still  doing  well  in  June,  1899.  MacDonald  (“Jour.  Am.  Med. 
Assoc.,”  September  3,  1898)  and  Richardson  (“Boston  Med.  and 
Surg.  Jour.,”  October  20,  1898)  have  reported  successful  gas- 
trectomies. A case  of  gastrectomy  reported  by  Summa  and  Ber- 
nays  (“Jour.  Am.  Med.  Assoc.,”  February  12,  1898)  died  thirty-six 
hours  after  operation.  W.  W.  Keen  (loc.  cit)  concludes  that 
abstention  from  such  extensive  operations  is  the  wiser  course  to 
pursue.  The  author  has  already  pointed  out  that  nothing  new  has 
been  added  to  our  knowledge  of  the  physiology  of  the  stomach 
by  Schlatter’s  investigations  (Hemmeter,  “New  York  Med.  Record,” 
liii,  p.  409,  March,  1898).  That  digestion  and  metabolism  would 
24 


362  SURGICAL  TREATMENT  OF  ORGANIC  GASTRIC  DISEASES. 

go  on  normally  for  a limited  time  in  the  absence  of  the  stomach 
was  known  long  before  Schlatter’s  operation. 

Gastro-enterostomy. — In  the  beginning  of  this  chapter  we 
described  the  various  (three  main)  types  of  this  operation  that 
have  been  suggested.  Which  of  these  types  of  operation — Wolf- 
ler’s,  von  Hacker’s,  Billroth-Brenner’s,  or  any  of  the  other  methods 
described  in  modern  text-books  on  abdominal  surgery — is  to  be 
selected  is  a matter  to  be  decided  by  the  surgeon.  But  we  would 
remark  in  parenthesis  that  the  physiological  rotation  of  the  full 
stomach  around  its  long  axis,  whereby  the  large  curvature  is  turned 
anteriorly  and  the  smaller  posteriorly,  which  is  asserted  by’Tiede- 
mann,  has  been  confirmed  by  no  other  experimenter.  Betz  and 
Lesshaft  (“Virchow’s  Arch.,”  1882,  vol.  lxxxvii)  have  opposed 
the  view.  In  many  hundreds  of  experiments  on  the  full  stomachs 
of  animals  for  the  study  of  the  peristalsis  we  have  never  observed 
it,  and  even  if  it  were  observed  when  the  abdomen  is  opened,  it 
could  not  then  be  considered  physiological.  The  hypothetical 
gastric  rotation  has  been  adduced  as  an  objection  to  Wolfler’s 
anterior  antecolonic  operation,  on  the  ground  that  the  artificial 
lumen  between  stomach  and  intestine  was  compressed  by  bring- 
ing the  loop  between  the  abdominal  wall  and  the  stomach  dur- 
ing this  rotation.  Von  Hacker’s  method  does  avoid  spur  for- 
mation, and  thereby  retroflux  of  duodenal  contents  into  the 
stomach,  and  also  compression  of  the  transverse  colon  by  the  in- 
serted jejunal  loop.  In  addition  to  this  the  entire  intestinal  canal 
remains  unchanged  in  its  natural  anatomical  relations.  Von  Hacker 
himself  states  that  the  mortality  is  not  materially  reduced  by  his 
method.  The  functional  results  are  claimed  by  most  German  sur- 
geons to  be  better  with  von  Hacker’s  operation.  Chlumskij  col- 
lected, in  all,  550  gastro-enterostomies  (“  Zeitschr.  f.  klin.  Chir.,” 
1898,  xx,  231).  According  to  his  table,  the  mortality  in  231  cases 
operated  by  the  Wolfler  method  was  38.09  per  cent.;  of  152  cases 
by  the  von  Hacker  method,  32.52  per  cent.  In  the  latter  method 
the  escape  of  gastric  contents  into  the  intestine  is  facilitated  by 
gravity. 

Results. — In  388  cases  Haberkant  found  the  total  mortality  to  be 
41.5  per  cent.  For  gastro-enterostomy  for  carcinoma  it  was  43.5 
per  cent. ; for  ulcer,  25.5  per  cent.  One  of  the  indications  of  gastro- 
enterostomy is  the  simple  atonic  dilatation.  Four  such  operations 
are  reported,  one  of  which  (Selenkow)  died  and  the  remaining 
three  (Renton,'  von  Kleef,  and  Jeannel)  recovered  and  the  func- 


PYLORO PLASTIC  SURGERY. 


363 


tional  result  was  good.  Concerning  the  remote  results,  it  is  self- 
evident  that  in  carcinoma  they  can  not  be  of  long  duration,  as  the 
growth  is  left  intact ; nevertheless  the  table  at  the  end  of  this  article 
shows  ten  cases  in  which  the  recovery  lasted  over  a year.  A sin- 
gular gastro-enterostomy  is  that  reported  by  Hahn  (“  Berlin,  klin. 
Wochenschr.,”  1894,  p.  1097).  The  operators  were  convinced  that 
the  neoplasm  was  a carcinoma  ; the  patient  lived  seven  years  after 
the  operation  without  complaints,  the  tumor  always  being  palpable. 
This  case  will  always  remain  a doubtful  one. 

Robert  F.  Weir  has  attempted  to  prove  statistically  that  gastro- 
enterostomy keeps  patients  with  pyloric  carcinoma  alive  as  long  as 
pylorectomy,  whereas  the  mortality  is  in  the  proportion  of  twelve 
per  cent,  for  the  former  to  fifty-two  per  cent,  for  pylorectomy. 

Haberkant’s  statistics  of  a much  larger  number  of  cases  show 
a mortality  of  54.4  per  cent,  for  resection  to  43.5  per  cent,  for  gas- 
tro-enterostomy. But  then  many  cases  have  formerly  been  resected 
that  would  in  the  present  advanced  state  of  knowledge  not  have 
been  operated.  Pylorectomy  gives  a better  prospect  for  more  last- 
ing recovery  than  gastro-enterostomy.  Of  forty-seven  cases  recov- 
ered from  pylorectomy,  twenty-two  lived  longer  than  one  year  after 
the  operation;  but  of  fifty-eight  cases  of  gastro-enterostomy,  only 
twelve  lived  longer  than  one  year.  With  the  exception  of  Hahn’s 
doubtful  case,  there  is  no  gastro-enterostomy  in  which  the  recovery 
lasted  longer  than  two  years  ; but  of  Haberkant’s  collected  success- 
ful pylorectomies,  twelve  lived  longer  than  two  years. 

Pyloroplastic  Surgery  (Pyloroplasty). — This  operation  was 
first  devised  by  von  Heinecke,  in  March,  1886.  The  first  operation 
was  a success.  In  February,  1887,  Mikulicz  rediscovered  and 
applied  the  method  independently  of  von  Heinecke.  The  opera- 
tion, which  is  applicable  to  some  pyloric  cicatrices,  is  carried  out 
by  slitting  open  the  scars  longitudinally  in  the  line  of  the  pyloric 
lumen  and  pulling  the  wound-edges  apart  by  hooks  inserted  in  the 
middle  ; then  they  are  reunited  by  sutures  transversely.  Graphi- 
cally, the  procedure  is  expressed  thus  : 


Cases  have  been  reported  in  which  pyloroplastic  surgery  was 
attempted,  and,  failing,  a pylorectomy  had  to  be  done  (Lobker, 


364  SURGICAL  TREATMENT  OF  ORGANIC  GASTRIC  DISEASES. 

“ Verhandl.  des  XXI.  Deutsch.  Chir.  Kongresses,”  1,  60).  Czerny 
reported  a case  in  which  resection  had  to  be  done  because  the  scar 
was  so  rigid  it  could  not  be  unfolded  (“  Beitrage  z.  klin.  Chir.,”  Bd. 
ix,  1892,  p.  678).  The  cases  that  recover  from  a successful  opera- 
tion of  this  kind  are,  as  a rule,  cured  permanently  ; no  return  of 
pyloric  stenosis  has  been  reported. 

Up  to  1894  (inclusive),  5 1 operations  of  this  type  have  been  com- 
piled, 40  of  which  were  successful  and  11  fatal,  making  a mortality 
of  21.5  per  cent.  In  44  instances  where  the  indication  was  stated, 
there  were  7 peptic  ulcers  and  37  cicatricial  stenoses  ; but  of  these 
37  scars,  14  were  produced  by  corrosive  poisons.  The  combined 
tables  of  Bavton  and  Bull  (“New  York  Med.  Rec.,”  May  25  and 
June  8,  1889)  contain  28  cases,  with  a mortality  of  31.1  per  cent. 

Digital  Divulsion  of  the  Pylorus. — Loreta’s  operation  consists 
of  a simple  gastrotomy  and  subsequent  gradual  expansion  of  the 
pylorus,  by  introducing  first  one  and  then  two  fingers  ; the  dilat- 
ing forceps  has  been  used  for  the  same  purpose.  Hahn  recom- 
mended that  the  anterior  wall  of  the  stomach  should  be  invaginated 
upon  the  finger  and  carried  into  the  opening  of  the  pylorus.  The 
dangers  of  the  procedure  consist  in  (i)  rupture  or  production  of 
hemorrhages  by  lesions  of  the  gastric  wall,  (2)  frequent  return  of 
the  stenosis. 

According  to  Bull  (“  Centralbl.  f.  Chir.,”  1890,  S.  149),  Loreta 
himself  has  had  the  return  occur  in  three  cases.  Haberkant  ( loc . 
cit.)  has  compiled  31  cases  of  Loreta  operations,  with  19  cures  and 
12  deaths — a mortality  of  38.7  per  cent.  Three  of  the  fatal  opera- 
tions were  for  carcinomata. 

Novara  had  to  execute  a resection  after  divulsion  had  failed  ; the 
only  justifiable  indication  is  cicatricial  stenosis.  The  operation  has 
few  advocates,  and  will  have  to  give  way  to  more  exact  and  reliable 
operative  methods. 

For  atonic  forms  of  dilatation  that  resist  all  medical  treatment, 
Heinrich  Bircher,  of  Aarau,  Switzerland,  has  devised  a new  opera- 
tion, called  g astro plication.  This  surgeon  attempted  to  improve 
the  motility  of  the  stomach  by  a reduction  of  its  size  through 
making  a fold  or  plait  in  the  gastric  wall.  The  greater  curvature 
is  raised  to  a much  higher  level  by  this  operation.  Bircher  ob- 
tained good  results  in  three  cases,  one  of  which,  however,  died  three 
months  after  the  operation.  A certain  amount  of  muscular  tonicity 
must  still  be  left  in  order  to  make  this  operation  even  a partial 
success  (“American  Jour.  Med.  Sciences,”  1892,  vol.  cm,  p.  333). 


GASTROPEXY — GASTRO- ANASTOMOSIS. 


365 


The  operation  has  not  as  yet  been  repeated  in  a sufficiently  large 
number  of  cases  to  permit  of  a correct  judgment  of  its  real  value. 

Weir  (“  New  York  Med.  Jour.,”  July  9,  1892),  unaware  until  two 
days  before  the  operation  that  Bircher  had  preceded  him,  did  a 
similar  operation,  but  united  the  two  layers  of  the  gastric  wall  by 
four  successive  rows  of  interrupted  silk  sutures,  the  final  one  unit- 
ing the  greater  curvature  to  the  lesser.  Keen  (Joe.  cit)  considers 
the  technic  of  Weir  a decided  improvement  over  Birchers’.* 

Gastropexy  is  the  name  of  an  operation  for  the  relief  of  gastro- 
ptosis,  by  suturing  the  stomach  to  the  anterior  abdominal  wall. 
The  stomach  is  not  opened  during  the  operation.  Duret  (“  Revue 
de  Chir.,”  1896,  xvi,  421)  reports  a successful  case.  Davis  modi- 
fied the  technic  somewhat  and  reported  two  successful  cases 
(“Western  Med.  Rev.,”  Oct.,  1897). 

Treves  described  a case  of  hepatoptosis,  gastroptosis,  and  gen- 
eral enteroptosis  brought  about  by  adhesions  of  the  omentum  to 
old  calcareous,  tuberculous  glands  in  the  mesentery  of  the  ileum 
and  lying  in  the  right  iliac  fossa.  The  glands  were  removed  and 
the  liver  sewed  firmly  to  fibrous  tissues  around  the  ensiform  cartil- 
age. The  adhesions  of  the  omentum  which  had  drawn  the  organs 
down  were  loosened,  which,  together  with  the  hepatopexy,  restored 
the  stomach  and  colon  to  their  places.  The  patient  recovered  en- 
tirely after  having  suffered  for  six  years. 

Gastroplasty,  gastro-anastomosis,  and  gastro-gastrostomy 
are  operations  for  the  relief  of  hour-glass  stomach.  Fifteen  opera- 
tions of  this  kind  have  been  done  (W.  W.  Keen,  loc.  cit.).  In  two 
of  them  radical  relief  could  not  be  given  by  the  operation.  Of  the 
remaining  thirteen  cases,  twelve  were  successful. 

Gastro-anastomosis  is  an  operation  first  performed  by  Wolfler 
for  hour-glass  stomach,  by  which  one  portion  of  the  organ  is  anas- 
tomosed with  the  other  at  the  greater  curvature.  Gastro-anasto- 
mosis remedies  the  separation  of  the  organ  into  two  distinct  cavities 
separated  by  a narrow  isthmus.  Von  Hacker  reports  and  pictures 
cases  of  hour-glass  stomachs  complicated  with  cicatricial  pyloric 


* Professor  Randolph  Winslow,  of  the  University  of  Maryland,  executed  a gastro- 
plication  upon  a well-known  physician  of  Baltimore  upon  my  advice.  The  patient  was 
over  sixty  years  of  age,  made  a perfect  recovery,  and  was  well  at  date  of  revision,  four 
months  after  operation.  There  had  been  motor  insufficiency  for  five  years  and  loss  of 
secretion  due  to  constant  drain  upon  the  secretory  apparatus.  The  secretion  of  HC1  was 

found  to  be  equal  to  20°  — NaOH  four  months  after  operation. 

10 


366  SURGICAL  TREATMENT  OF  ORGANIC  GASTRIC  DISEASES. 

stenosis,  for  which  he  recommends  a double  operation — either  a 
pylorectomy,  or  a pyloroplastic  operation  with  gastro-anastomosis, 
or,  best,  a gastro-enterostomy  and  gastro-anastomosis  (von  Hacker, 
“ Magenoperationen,”  etc.,  Wien,  1895). 

The  Fundamental  Factors  Influencing  the  Rate  of  Mor- 
tality in  Gastric  Operations.— These  are  partly  under  the  control 
of  the  surgeon  and  partly  not.  Those  over  which  we  may  exer- 
cise control  are  (I)  defects  in  the  technic,  (II)  selection  of  the  kind 
of  operation,  (III)  duration  of  the  operation. 

The  factors  that  escape  control  are  (I)  age  of  the  fundamental 
disease,  (II)  nature  and  extent  of  this  disease,  (III)  age  of  the 
patient. 

A.  Factors  Under  the  Control  of  the  Surgeon. 

I.  Faults  in  the  technic , as  a rule,  lead  to  peritonitis,  of  which  one 
must  distinguish  two  kinds  : ( a ) The  septic,  produced  by  infection 
during  the  operation;  and  (b)  perforation  peritonitis,  due  to  a 
technical  defect  in  placing  the  sutures.  Perforation  peritonitis  as 
a result  of  insufficiency  of  the  sutures  is  much  more  common  in 
pylorectomy  than  in  gastro-enterostomy,  because  the  lines  of  suture 
are  much  longer.  However,  peritonitis  may  be  caused  by  errors 
in  diet  or  by  spontaneous  perforations  in  other  parts  of  the  stom- 
ach, independently  of  the  technic.  In  165  fatal  cases  with  autop- 
sies, the  cause  of  death  was  peritonitis  in  one-fourth  of  the  cases; 
only  three  fatal  cases  were  due  to  spontaneous  peritonitis. 

II.  The  selection  of  the  proper  operation  for  any  particular  case  is 
facilitated  by  an  exact  definition  of  the  indications. 

The  indications  for  pylorectomy  are  : (1)  the  operable  carcinoma 
or  sarcoma;  (2)  the  peptic  stenosing  ulcer  or  cicatrix;  (3)  perfora- 
tion from  pyloric  ulcer. 

The  contraindications  are  : 

(1)  ( a ) Firm  adhesions,  especially  posteriorly  on  account  of  dan- 
ger of  injuring  the  hepatic  artery  and  vein ; ( b ) adhesions  with  the 
pancreas,  ( c ) with  the  liver,  (d)  with  the  meso-  and  transverse  colon. 

(2)  Infiltration  of  lymphatic  glands  ( a ) of  the  lesser  omentum, 
( b ) posterior  surface  of  the  stomach,  (c)  of  the  porta  hepatis. 

(3)  Icterus  from  metastases  or  compression  by  the  tumor. 

(4)  Great  exhaustion  of  the  patient. 

Severe  gastric  hemorrhage  can  be  treated  in  most  cases  by  inter- 
nal medication.  Gastric  ulcers  that  have  given  rise  to  repeated 
grave  hemorrhages  have  been  successfully  excised  by  Czerny 
(“  Archiv  f.  klin.  Chir.,”  1884),  Cordua  (quoted  in  Debove  and  Re- 


INDICATIONS  FOR  PYLORECTOMY  AND  GASTRO-ENTEROSTOMY.  367 

mond,  “Traite  de  Mai.  de  PEstomac  ”),  and  Mikulicz  (“  Deutsche 
med.  Wochenschr.,”  1892). 

Dunin  asserts  that  ulcers  in  the  pyloric  region  causing  serious 
hemorrhages  would  heal  rapidly  if  the  pyloric  passage  were  put  at 
rest  by  a gastro-enterostomy  (Mintz,  loc.  cit). 

Kuster  cured  persistent  hematemesis  from  pyloric  ulcer  on  the 
posterior  wall  by  opening  the  anterior  wall,  producing  scabbing  in- 
crustation with  the  thermocautery,  and  making  a wide  gastro-enter- 
ostomy. During  the  operation  a cherry-stone  was  extracted  from 
the  depth  of  the  ulcer.  Mikulicz  did  a pyloroplastic  operation  for 
uncontrollable  hemorrhage.  The  gastro-enterostomy,  ^fter  cica- 
trizing the  ulcers  with  the  thermocautery,  is  generally  a prophy- 
lactic measure  to  forestall  a prospective  pyloric  stenosis.  A pyloro- 
plastic operation  may  accomplish  the  same  object. 

For  perforation  of  gastric  ulcer  many  operations  have  been  exe- 
cuted. Pariser  has  recently  reported  forty-three  such  operations, 
with  thirty-three  deaths  and  ten  recoveries.  Only  in  four  cases  was 
the  perforation  in  the  pylorus  (Pariser,  “ Deutsche  med.  Wochen- 
schr.,” 1895).  N.  Senn  suggested  gastric  distention  with  hydrogen, 
in  order  to  rapidly  find  out  the  seat  of  the  perforation. 

Indications  for  gastro-enterostomy  : 

(1)  Pyloric  carcinoma  with  extensive  adhesions  and  glandular 
metastases.  Frequently  it  is  not  decided  to  do  a gastro-enteros- 
tomy until  the  abdomen  is  opened;  a resection  has  often  been 
planned,  but  had  to  be  replaced  by  a gastro-enterostomy.  If  the 
posterior  wall  alone  is  free  from  infiltration,  von  Hacker’s  method  is 
indicated  ; in  the  reverse  case,  the  methods  of  Wolfler  or  Billroth- 
Brenner. 

(2)  Stenosing  ulcer  ( a ),  both  when  the  pylorus  is  still  isolated 
and  free,  and  ( b ) when  it  is  adherent  to  its  surroundings.  With 
this  indication  pylorectomy  is  unjustifiable,  but  partial  resection 
and  pyloroplastic  surgery  may  yet  compete  with  gastro-enteros- 
tomy. When,  however,  a cicatricial  pyloric  stenosis  extends  into 
the  duodenum,  nothing  but  a gastro-enterostomy  should  be  done. 

(3)  Stenoses  in  the  duodenum  outside  of  the  pylorus.  Four 
operations,  with  three  recoveries,  have  so  far  been  executed  for  this 
indication. 

(4)  Stenoses  by  neoplasms  of  neighboring  organs — the  gall- 
bladder, periportal  lymphatic  glands,  and  pancreas.  Novarro  per- 
formed a gastro-enterostomy  for  pyloric  stenosis  caused  by  echino- 
coccus cyst  of  the  liver  (“  Deutsche  med.  Wochenschr.,”  1891,  No. 


368  SURGICAL  TREATMENT  OF  ORGANIC  GASTRIC  DISEASES. 

4,  S.  152).  Stansfield  did  the  same  operation,  with  good  result,  for 
tumor  of  the  pancreas  (“  Brit.  Med.  Jour.,”  1890,  pp.  294  and  1300), 
making  use  of  Senn’s  bone-plates. 

(5)  Purely  functional  dilatation  due  to  atony  of  the  musculature 
without  pyloric  stricture.  Four  gastro-enterostomies  for  this  indi- 
cation are  on  record.  Gastroplication  (resection  or  reduplication 
of  a fold  of  the  stomach-wall)  is  preferable  for  this  purpose. 

III.  The  Duration  of  Gastric  Operations . — It  is  evident  that  the 
sooner  an  operation  is  completed,  the  less  the  danger  of  shock  and 
sepsis.  With  the  view  of  shortening  the  time  of  operation,  Rydy- 
gier  and  Lauenstein  advised  the  employment  of  continued  sutures, 
which  they  claim  abbreviate  the  time  by  one  hour.  The  most 
celebrated  time-  and  labor-saving  devices  in  gastro-intestinal  sur- 
gery are  by  our  countrymen,  Murphy  and  Senn.  The  advocates 
of  Senn’s  bone-plates  have  claimed  that  the  mortality  under  the 
older  suture  methods  was  from  42.8  per  cent,  to  47  per  cent.  (Her- 
bert Page  and  von  Hacker),  and  in  forty-one  operations  by  the 
Senn  method  the  mortality  was  only  24.5  per  cent. 

The  decalcified  bone-plates  of  Senn  are  not  always  digested.  In 
one  of  the  inventor’s  own  cases  they  were  vomited  undigested  forty 
hours  after  the  operation.  Haberkant  asserts  that  the  advantage 
of  the  saving  of  time  is  counterbalanced  by  less  safety.  For  surgi- 
cal opinions  on  the  Murphy  button  and  Senn  plates  we  must  refer 
to  journals  and  text-bpoks  on  abdominal  surgery.  But  so  much 
is  clear  : shortening  of  the  time  of  operations  by  these  contrivances 
is  a great  gain. 

B.  Factors  that  Escape  Control. 

I.  Age  of  the  Underlying  Disease. — This  can  not  be  determined 
statistically,  for  both  ulcer  and  carcinoma  may  remain  latent  for 
months,  and  it  is  impossible  to  ascertain  the  age  of  these  conditions 
at  the  autopsy.  We  have  observed  a large  carcinoma  in  a white 
woman  who  died  at  Bay  View  Hospital.  The  neoplasm  occupied 
the  posterior  gastric  wall  ; during  life  there  had  been  no  gastric 
symptoms  whatever.  Osier’s  case  of  very  rapid  course  in  gastric 
carcinoma — two  weeks  from  the  onset  of  severe  dyspeptic  symp- 
toms— made  it  plain  at  the  autopsy  that  the  growth  had  been  of 
considerable  duration,  but  had  for  a long  time  not  undermined  the 
patient’s  health  (“Univ.  Medical  Magazine,”  January,  1895).  The 
anamnesis  given  by  patients  regarding  the  period  since  when  they 
have  suffered  from  dyspepsia  is  frequently  unreliable. 

II.  Nature  and  Extent  of  the  Fundamental  Gastric  Disease. — Con- 


EFFECT  OF  AGE  ON  THE  OPERATIVE  RESULTS.  369 

cerning  this  point  the  statistics  show  that  the  mortality  in  pylo- 
rectomy,  as  well  as  in  gastro-enterostomy,  is  greater  for  carcinoma 
than  for  ulcer.  Under  the  head  of  contraindications  to  these 
operations  we  have  dwelt  upon  the  dangerous  influences  of  the 
extent  of  the  disease. 

III.  Effect  of  the  Age  of  the  Patient. — In  the  cases  as  they  are  pre- 
sented for  operation  there  are  so  many  other  governing  factors 
that  the  matter  of  age  does  not  appear,  from  statistics,  to  exert 
much  influence  on  the  result  of  these  operations,  provided  the 
other  conditions  previously  mentioned  are  favorable.  A difference 
becomes  noticeable  when  the  age  is  over  sixty  years.  Among  176 
resections,  the  percentage  of  mortality  of  those  under  fifty  years 
was  50.4  per  cent.,  and  those  over  fifty  years,  52.9  per  cent.  With 
gastro-enterostomy  the  rate  was  42.4  per  cent,  for  those  under 
fifty  years,  and  57.7  per  cent,  for  those  over  fifty.  These  statistics, 
therefore,  do  not  confirm  a marked  influence  of  age  on  the  rate  of 
mortality. 

A critical  consideration  of  these  factors,  in  connection  with  other 
elements  before  mentioned,  justifies  the  hope  that  diagnosis  and 
gastric  surgery  have  not  reached  the  highest  development  as  yet, 
and  we  may  expect  a further  lowering  of  the  rate  of  mortality. 

An  artificial  communication  between  the  stomach  and  intestines, 
as  is  performed  in  gastro-enterostomy,  may  become  much  smaller 
by  cicatricial  contraction.  Kocher  has  reported  two  such  observa- 
tions. In  one  case  Czerny  made  an  opening  three  cm.  in  diameter  ; 
at  the  autopsy,  five  months  later,  it  had  contracted  down  to 
eight  mm. 

Heinsheimer  has  made  careful  analytical  observations  on  the 
metabolism  in  two  cases  of  gastro-enterostomy  (“  Mittheilungen  a. 
d.  Grenzgebieten  d.  Medizin  u.  Chirurg,”  Bd.  1,  S.  350).  In  this 
piece  of  work,  which  was  done  under  von  Noorden,  Rachford’s  ob- 
servation that  fats  require  a very  thorough  and  intense  mixture 
with  the  secretions  of  the  pancreas  and  liver  for  their  digestion 
(“  Centralbl.  f.  Phys.,”  1896,  Heft  4)  was  confirmed.  The  further 
away  the  gastro-intestinal  communication  is  laid  from  the  duodenal 
orifices  of  these  glands,  the  more  defective  the  fat  digestion  and 
resorption.  It  is  therefore  suggested  that  in  gastro-enterostomies 
a jejunal  loop,  as  near  as  possible  to  the  duodenum,  be  anastomosed 
with  the  stomach. 

For  benign  stenoses  of  the  pylorus,  pylorectomy  is  more  and 
more  deserted  in  favor  of  gastro-enterostomy,  which  gives  the 


370  SURGICAL  TREATMENT  OF  ORGANIC  GASTRIC  DISEASES. 

same  functional  results  without  the  dangers  (Ernst  Siegel,  “ Mit- 
theil.  a.  d.  Grenzgebieten  d.  Medizin  u.  Chir.”  Bd.  i,  S.  347). 


DURATION  OF  LIFE  AFTER  RESECTION  IN  51  CASES  OF  CARCINOMA 
OF  PYLORUS. — {Haberkant. ) 


Death. 

Number  of 
Cases. 

Causes  of  Death. 

Living  at  Date 
of  this  Report. 

Number  of 
Cases. 

After  I yz  months, 

Return  of  cancer. 

After  2 months, 

I 

“2  “ 

3 

One  of  metastasis  in  the 

“ 3 “ 

I 

liver. 

. “ 3/2  “ 

] 

2K 

1 

Acute  lung  disease,  no  re- 

“  4 “ 

r 

turn  and  no  metastasis. 

“ 6 “ 

I 

“ 4 

2 

Return. 

“ 7/2  “ 

I 

“ 5 

2 

One  of  lobular  pneumonia. 

“ 8 “ 

I 

one  of  chronic  pyemia. 

“ 9 “ 

I 

“6  “ 

2 

One  of  return,  one  of 

“ I year, 

2 

cicatricial  stenosis. 

“ 1 year  and 

“ 6^  - 

1 

Return. 

2 months, 

I 

“ 7 

2 

“ i)4  years, 

I 

“ 8 

1 

Return. 

“ 2 “ 

2 

“ 10  “ 

1 

Return. 

“ 2 years  and 

“ 11 X “ 

1 

Rectal  and  pelvic  carci- 

2  months, 

2 

noma. 

“ 2)4  years, 

I 

“ 1 year,  . . 

3 

Two  return. 

‘ ‘ a 1 m 0 s t 3 

“ 13  months, 

2 

Return. 

years, 

I 

“ iy  years, 

1 

Return. 

“ 3 >2  years, 

I 

“ 2K  “ 

1 

‘ ‘ 5 years  and 

“ 3 

1 

Cicatricial  stenosis. 

4 months, 

I 

Kocher. 

“ SJ4  “ 

i 

Not  stated  (Billroth). 

Over  8 years, 

I 

Ratimmow. 

Total,  . . 

26 

Total,  . . 

21 

RECOVERIES  AND  DEATHS:  PERCENTAGE  OF  MORTALITY  IN  379 
CASES  OF  RESECTION  OF  PYLORUS .—(Haberkant.) 


Year 

of 

Oper- 

ation. 

Name  of 
Operator. 

Number  Operated  Upon.  | 

Result 

Carci- 

noma. 

Ulcer 

and 

Cica- 

tricial 

Steno- 

sis. 

Sar- 

coma 

and 

Myoma. 

NoIndi- 

CATION 

Stated. 

Remarks. 

Recovered. 

'U 

5 

Recovered. 

T3 

<U 

5 

Recovered.! 

T3 

<U 

5 

Recovered. 

T3 

5 

Recovered. 

T3 

<v 

Q 

1885 

Rydygier,  . 

5 

3 

2 

I 

2 

2 

1885 

Gussenbauer, 

6 

2 

4 

4 

2 

1889 

Augerer,  . . 

6 

I 

5 

I 

5 

1890 

Billroth, 

4i 

19 

22 

12 

16 

6 

6 

I 

Of  these,  thirty-six 

Sar- 

were total  resec- 

coma 

tions;  three  partial, 

two  atypical  pylo- 

rectomies. 

OPERATIVE  STATISTICS. 


37 


Recoveries  and  Deaths:  Percentage  of  Mortality  in  379  Cases  of 
Resection  of  Pylorus. — ( Haberkant . ) — ( Continued. ) 


£ 

0 

Ulcer 

& 

AND 

Sar- 

NoIndi- 

a 

Result. 

Carci- 

ClCA- 

coma 

CATION 

Yf.ar 

H 

Ste  NO- 

Myoma. 

Stated. 

of 

Name  of 

SIS. 

Remarks. 

Opera- 

Operator. 

w 

TION. 

O 

•d 

*d 

*d 

<U 

•d 

<v 

•d 

V 

Ed 

V 

”d 

■d 

s 

■d 

V 

-d 

<y 

•d 

S3 

0 

5 

0 

s 

0 

5 

c 

5 

0 

5 

& 

at 

cd 

a! 

at 

at 

I89O 

Lauenstein,  . 

12 

4 

8 

4 

8 

189O 

Novarro,  . . 
Tillmans, 

3 

2 

1 

I 

I 

1 

I89I 

A 

4 

4 

1892 

v.  Heinecke, 

14 

5 

9 

4 

9 

I 

I892 

Schonborn,  . 

5 

2 

3 

2 

3 

>893 

Roux,  . . . 

5 

3 

2 

3 

2 

One  atypical,  the 

rest  typical,  total 

resections. 

1893 

Doyen,  . . 

7 

6 

1 

2 

1 

4 

All  atypical  pylorec- 

tomies. 

1893 

Lobker,  . . 

13 

7 

6 

5 

5 

2 

1 

1893 

Schede,  . . 

13 

7 

6 

6 

5 

1 

1 

1893 

von  Kleef,  . 

4 

3 

1 

3 

1894 

Kraske,  . . 

4 

1 

3 

1 

3 

I894 

Czerny,  . . 

20 

13 

7 

8 

5 

3 

2 

2 

Three  partial  resec- 

tions, the  rest  typ- 

Sar- 

ical, total  pylorec- 

coma 

tomies. 

1894 

Kocher,  = . 

9 

7 

2 

7 

2 

In  all  nine  cases 

Kocher  used  his 
method  with  fol- 

lowing gastroduo- 
denostomy. 

Kronlein, 

8 

5 

3 

5 

3 

I894 

Kappeler,  . 

14 

9 

5 

8 

5 

1 

Total  mortality,  35  7 

per  cent.  For  car- 
cinoma alone,  38. 1 
per  Cent. 

£ 

00 

Mikulicz, 
Other  cases, 

20 

i5 

5 

13 

5 

2 

exclusive  of 
above,  . . 

166 

79 

87 

60 

76 

8 

6 

2 

9 

5 

Of  these,  147  were 
total  resections  ; 
17  atypical,  and  2 

1 Angi- 

oma fi- 
brosu'm . 

partial  pylorecto- 

1 Lym- 
phosar- 

mies. 

coma. 

Total,  . . . 

379  191 

i I 

*88  130 

i45 

32 

’20 

5 

24 

23 

RESULTS  WITH  GASTRO-ENTEROSTOMY  FROM  1885  TO  1893. 


Year  of  Publica- 
tion. 

Author. 

Number  of  Opera- 
tions. 

Result. 

Total  Mortality. 
Per  Cent. 

Carcinoma. 

Ulcer  and 
Cicatricial 
Stenosis. 

Recovered. 

Died. 

Recovered. 

Died. 

Mortality. 
Per  cent. 

Recovered. 

Died. 

Mortality. 
Per  cent. 

1885 

Kramer,  .... 

20 

8 

12 

5 

II 

68.7 

3 

I 

1886 

Saltzmann,  . . . 

23 

0 

12 

66.6 

1887 

Rockwitz,  . . . 

29 

16 

13 

44.8 

11 

12 

5 

I 

1890 

Novarro,  .... 

55 

24 

43- 6 

1890 

Meliler,  .... 

55-1 

58.8 

38.5 

1891 

Page,  

36 

15 

41.6 

1892 

Hadra,  .... 

76 

33 

43 

56 

1893 

Zeller, 

152 

86 

66 

43  4 

39i 

24 

64 

141 

144 

8 

2 

RESULTS  OF  VARIOUS  OPERATORS  WITH  GASTRO-ENTEROSTOMY.— 


( Haber kant .) 


Year  of  Publica- 
tion. 

Operator. 

Number  of  Cases  Oper- 
ated Upon. 

Carci- 

noma. 

Ulcer 

and 

Cica- 

tricial 

Sten- 

osis. 

Dilata- 
tion 
of  the 
Stom- 
ach. 

Sar- 

coma. 

No  Indi- 
cation 
Stated. 

Remarks. 

Recovered.! 

-d 

5 

Recovered. 

5 

Recovered. 

-6 

5 

Recovered. 

ro 

IU 

s 

Recovered 

T3 

5 

1887 

Liicke,  . . 

8 

5 

I 

2 

1890 

Billroth,  . . 

28 

14 

14 

1890 

Novarro, . . 

IO 

5 

3 

2 

1891 

Lauenstein,. 

17 

10 

3 

2 

2 

1891 

Hahn,  . . . 

II 

5 

6 

1891 

Bowreman  - 

Jesset,  . . 

5 

3 

2 

1891 

Senn,  . . . 

13 

4 

9 

Calculated  according 

to  Czerny. 

1891 

Remedi,  . . 

6 

3 

3 

1893 

Roux,  . . . 

14 

7 

7 

1893 

Doyen,  . . 

10 

6 

4 

Two  carcinomata, 

eight  cicatrices. 

1893 

von  Kleef,  . 

19 

I 

. 

■3 

5 

1893 

Cordivilla,  . 

6 

2 

4 

Operated  in  one  year 

by  von  Hacker’s 

method. 

1893 

v.  Heinecke, 

6 

4 

2 

1893 

Lobker,  . . 

7 

4 

3 

All  according  to  von 

Hacker’s  method. 

1894 

Czerny,  . . 

23 

12 

7 

2 

1 

I 

1894 

Kraske,  . . 

10 

7 

3 

Other  cases, 

exclusive  of 

above,  . . 

195 

66 

59 

20 

9 

2 

1 

1 

; 21 

16 

Total,  . . 

388 

136 

105  35 

12 

3 

1 

■ 

1 

52 

42 

3 72 


OPERATIVE  STATISTICS. 


373 


DURATION  OF  LIFE  AFTER  GASTRO-ENTEROSTOM Y. 


Death. 

Number 

OF 

Cases. 

Living  and  at  the  Time  of 
Report  in  Good  Health. 

Number 

of 

Cases. 

After  I month, 

8 

After  2 months,  ... 

j 

“ I months, 

i 

“3  “ 

2 

“2  “ 

5 

“ 4 “ • ••• 

I 

“2^  “ 

2 

“ 5 “ • • • 

2 

“3  “ 

4 

“6  “ 

2 

“ 3lA  “ 

2 

“7  “ 

2 

“4  “ ...  . 

5 

“ S/z  “ 

I 

“6  “ 

3 

“9  “ 

2 

“ 7'A  “ ... 

i 

“ 10  “ 

I 

“ IO  “ 

i 

“ 1 year  and  11  months,  . 

I 

“ I year,  

3 

“ 2 years,  

I (Hahn). 

“ i year  and  2 months,  . . 

i 

“ years, 

3 

“ I year  and  7 months,  . . 

i 

“ I “ “ 8 “ 

i 

“ I “ “ IO  “ 

i 

Total, 

42 

Total, 

16 

EFFECT  OF  AGE  ON  THE  RESULT  OF  VARIOUS  GASTRIC  OPERA- 
TIONS. — ( Haberkant. ) 


Age. 

Total  Typical 
Resection  of 
Pylorus. 

Gastro-enteros- 

TOMY. 

Atypical  Resec- 
tion of  Pylorus. 

Pyloroplastic 

Operation. 

Number  of 
Operations. 

Recovered. 

Died. 

Number  of 
Operations. 

Recovered. 

Died. 

Number  of 
Operations. 

Recovered. 

Died. 

Number  of 
Operations. 

Recovered. 

Died. 

20  years. 

2 

2 

I 

I 

2 

2 

22-30'  “ 

9 

6 

3 

21 

14 

7 

3 

I 

2 

5 

2 

3 

31-40  “ 

44 

21 

23 

47 

26 

21 

2 

2 

IO 

7 

3 

41-50  “ 

70 

33 

37 

37 

21 

16 

3 

2 

I 

5 

4 

1 

51-60  “ 

37 

20 

17 

33 

l6 

17 

1 

I 

3 

3 

61-70  “ 

13 

4 

9 

11 

2 

9 

Over  70  “ 

1 

1 

1 

1 

1 

1 

uo 

(73) 

374  INFLUENCE  OF  GASTRIC  DISEASES  UPON  OTHER  ORGANS. 


CHAPTER  VIII. 

INFLUENCE  OF  GASTRIC  DISEASES  UPON  OTHER 
ORGANS  AND  ON  METABOLISM. 

Diseases  of  the  stomach  may,  as  is  well  known,  affect  general 
nutrition,  the  action  of  the  heart,  lungs,  and  the  nervous  system. 

In  all  digestive  diseases  with  apparent  malnutrition  the  physi- 
cian should  ascertain  the  amount  and  the  kind  of  food  ingested, 
the  state  of  the  stool,  and  sleep.  The  cause  of  insufficient  inges- 
tion of  food  is  anorexia  in  the  majority  of  cases  ; in  others  the 
patients  have  a good  appetite,  but  avoid  food  because  it  gives  them 
pain,  as  in  the  case  of  gastric  ulcer;  others,  again,  will  not  eat 
because  they  vomit  the  food  soon  after  ingestion.  Loss  of  weight 
is  of  more  serious  significance  in  chronic  than  in  acute  stomach 
diseases.  Instead  of  taking  in  thirty  to  forty  calories  per  kilogram 
of  body  weight,  von  Noorden  found  in  chronic  types,  after  careful 
observation,  that  they  ingested  only  twenty-one  calories  of  their 
own  accord  (v.  Noorden,  “ Ueber  Stoffwechsel  d.  Magenkranken,” 
etc.,  “ Berliner  Klinik,”  Heft  55).  In  cases  in  which  the  HC1  secre- 
tion was  so  diminished  that  only  a fraction  of  the  proteids  could  be 
peptonized  in  the  stomach  and  the  largest  portion  passed  into  the 
intestines  unchanged,  von  Noorden  found  that  resorption  of  the 
main  food-substances  was  sufficient.  With  a good  gastric  peris- 
talsis, preventing  delay  and  fermentation  in  the  stomach,  the  intes- 
tine is  capable  of  supplanting  the  deficient  gastric  digestion.  In 
animals,  total  exclusion  of  the  stomach  from  the  digestive  act 
need  not  injure  general  nutrition,  provided  the  food  is  supplied  in 
a proper  form. 

It  is  very  probable  that  in  certain  forms  of  gastritis,  in  ectasias 
and  carcinoma,  poisonous  substances  are  formed  which  are  re- 
sorbed and  injure  the  metabolism  of  the  tissues.  Friedenwald  has 
recently  found  this  to  be  the  case  in  atony  of  the  intestines  and 
stomach  (“  Med.  News,.”  Dec.  23,  1893). 

Resorbable  and  combustible  gases  are  developed  in  gastrectasias 
with  stagnating  ingesta  and  have  been  described  by  many  observers 
(see  Albu,  “ Die  Autointoxicationen  des  Intestinaltractus,”  p.  19). . 
Putrefaction  of  albuminous  substances  may  occur  in  the  stomach. 
Some  cases  show  the  formation  of  sulphuretted  hydrogen  even 


INFLUENCE  OF  GASTRIC  DISEASES  ON  THE  HEART.  375 

with  co-existent  high  acidity.  Naturally,  stagnation  must  be 
present  to  make  albuminous  decomposition  possible.  Muller  has 
described  a series  of  carcinoma  cases  in  which  more  nitrogen  was  ex- 
creted than  ingested  in  the  food  (“  Zeitschr.  f.  klin.  Med.,”  Bd.  xvi), 
which  strengthens  the  conception  of  carcinomatous  auto-intoxica- 
tion, causing  an  increased  albuminous  breakdown  in  the  tissues. 

In  all  cases  of  subnormal  nutrition  all  etiological  factors  must 
be  sought  out,  and  an  individualized,  highly  nutritious,  concen- 
trated, unirritating  diet  adapted  to  the  patient  after  improving  the 
appetite.* 

Influence  of  Gastric  Diseases  on  the  Heart. — It  is  natural  to 
expect  increased  rapidity  of  the  heart’s  action  in  all  gastric  diseases 
associated  with  fever,  such  as  the  various  forms  of  acute  gastritis, 
in  perigastritis,  and  other  complications  (peritonitis).  But  tachy- 
cardia has  frequently  been  observed  by  us  associated  with  hyper- 
acidity, gastrosuccorrhea,  and  pneumatosis.  In  one  case  of  the 
latter  disease  the  tachycardia  was  so  persistent  as  to  require  special 
treatment  by  local  ice-bag,  aconite,  and  bromid  of  strontium.  In 
all  of  these  cases  fever  was  absent,  and  we  have  no  experimental 
basis  to  explain  the  phenomenon. 

Bradycardia  is  seen  much  more  frequently,  and  the  fact  that  it 
is  aggravated  and  improves  or  disappears  as  the  gastric  trouble 
becomes  worse  or  better,  shows  that  it  is  not  an  accidental  accom- 
paniment, but  is  in  some  causal  relation  with  the  fundamental 
disease — i.  e .,  dilatation  or  ulcer.  In  animals,  slowing  of  the  pulse 
can  be  effected  by  distention  or  rough  manipulation  of  the 
stomach.  Stimulation  of  sensory  nerves  causes  slowing  of  the 
heart-beat,  and  this  may  partly  be  offered  as  an  explanation  of 
bradycardia  in  dilatation  and  ulcer,  though  it  is  far  from  satis- 
factory. It  is  difficult  to  prove  that  irregular  heart’s  action  or 
arrhythmia  is  dependent  upon  gastric  diseases,  even  when  it  actually 
is  associated  with  the  latter.  Arrhythmia  is  so  frequent  that  it  may 
accidentally  be  present  in  an  individual  independently  of  any  gas- 
tric disease. 

Patients  with  weak  hearts,  valvular  disease,  failure  of  compensa- 
tion, should  be  carefully  dieted,  and,  if  in  extreme  dyspnea,  should 
not  be  allowed  anything  but  milk  until  this  symptom  is  relieved. 


*The  literature  on  the  correlation  of  digestive  diseases  and  those  of  other  organs,  and 
vice  versa,  will  be  found  in  Dr.  Hans  Herz’s  “ Storungen  des  Verdauungsapparates  als 
Ursache  u.  Folge  anderer  Erlcrankungen,”  Berlin,  1898. 


376  INFLUENCE  OF  GASTRIC  DISEASES  UPON  OTHER  ORGANS. 

Arrhythmia  and  compensatory  defects  are  more  pronounced  after 
full  meals.  The  relation  is  not  perfectly  clear  ; but  we  have  ob- 
served a number  of  deaths  in  patients  suffering  from  organic  cardiac 
disease,  following  shortly  after  a full  meal  that  was  apparently  en- 
joyed. These  deaths  may  be  attributed  to  a number  of  causes — 
viz. : (1)  Impediment  offered  to  excursions  of  the  diaphragm  by  the 
full  stomach ; (2)  pressure  on  the  weak  heart,  and  irritation  of  the 
pneumogastric  nerve,  due  to  distention  of  the  stomach  by  gases; 
(3)  absorption  of  toxins  from  improperly  digested  food ; (4)  increased 
intracardiac  pressure  occurring  naturally  during  gastric  digestion. 
When  the  heart  is  dilated  or  hypertrophied,  very  small  meals  only 
should  be  permitted. 

Palpitation  of  the  heart  occurs  in  many  persons,  particularly  after 
heavy  meals  ; the  pulse  becomes  faster,  fuller ; the  tension  greater — 
all  this  with  intact  hearts,  but  particularly  observable  in  the  course 
of  chronic  gastric  diseases,  dilatations,  abdominal  plethora,  and 
constipation. 

Respiration. — It  is  undoubted  that  breathing  is  influenced  by 
gastric  troubles,  although  sufficient  attention  has  not  been  given 
to  this  matter.  We  have  noticed  in  a number  of  cases  that  the 
respiratory  expansion  is  lessened  by  gastric  diseases  impeding  the 
excursions  of  the  diaphragm.  This  we  have  produced  experimentally 
in  healthy  individuals  by  inflating  our  stomach-shaped  intragastric 
rubber  bag  within  their  stomach  while  they  were  under  narcosis. 

It  appears,  therefore,  that  undue  or  excessive  gastric  distention 
diminishes  the  amount  of  inspired  air,  independently  of  conscious- 
ness. In  gastric  fermentations  toxic  substances  are  produced, 
which,  when  injected  into  the  circulation,  caused  dyspneic  respira- 
tion of  a paroxysmal  character  (Bouchard  and  Bouveret).  It  is 
probable,  therefore,  that  gastric  diseases  may  affect  respiration 
either  directly  or  mechanically,  through  interference  with  the 
descent  of  the  diaphragm  or  by  the  absorption  of  toxins  and  action 
on  the  respiratory  center.  With  the  intimate,  mutual  correlation 
of  the  physiology  of  the  circulatory  and  respiratory  function,  it  is 
evident  that  a pathological  disturbance  of  one  will  inevitably  affect 
the  other. 

The  Influence  of  Gastric  Diseases  on  the  Nervous  System. 

— Nervous  patients  affected  with  a disease  of  the  stomach  fre- 
quently exhibit  neuroses  of  sensation  : hyperesthesia,  intercostal 
neuralgias,  and  hemicrania.  That  there  is  some  etiological  con- 
nection between  the  stomach  and  these  conditions  is.  made  very 


From  THE  MEDICAL  RECORD, 

New  York, 

44  The  reproach  that  the  English  language  can  boast 
of  no  treatise  on  anatomy  deserving  to  be  ranked  with 
the  masterly  works  of  Henle,  Luschka,  Hyrtl,  and 
others,  is  fast  losing  its  force.  During  the  past  few 
years  several  works  of  great  merit  have  appeared, 
and  among  these  Morris'  4 Anatomy'  seems  destined 
to  take  the  first  place  in  disputing  the  palm  in  ana- 
tomical fields  with  the  German  classics.  The  nomen- 
clature, arrangement,  and  entire  general  character 
resemble  strongly  those  of  the  above-mentioned  hand- 
books, while  in  the  beauty  and  profuseness  of  its 
illustrations  it  surpasses  them.  This  edition  offers  but 
few  changes ; a chapter  on  the  skin  has  been  added, 
and  a useful  list  of  vestigial  and  abnormal  structures 
has  been  compiled.  Sections  especially  worthy  of 
praise  are  those  on  surgical  and  topographical  anat- 
omy, and  the  chapter  on  the  nervous  system  is  pre- 
sented with  great  clearness  and  fullness.  The  ever- 
growing popularity  of  the  book  with  teachers  and 
students  is  an  index  of  its  value,  and  it  may  safely 
be  recommended  to  all  interested." 


From  THE  PHILADELPHIA 
MEDICAL  JOURNAL. 


Of  all  the  text-books  of  moderate  size  on  human 
anatomy  in  the  English  language,  Morris  is  undoubt- 
edly the  most  up-to-date  and  accurate.  The  changes 
from  the  first  edition  are  not  marked;  perhaps  the 
most  noticeable  feature  is  that  there  are  twenty  less 
cuts  than  in  the  first  edition.  Those  which  have  been 
omitted,  however,  will  not  be  greatly  missed.  The 
saving  of  space  by  the  omission  of  a discussion  of 
histology  is  a decided  advantage,  giving  room  for 
much  matter  of  importance  in  these  days  when 
every  student  is  obliged  to  own  a special  treatise  on 
histology.  To  enumerate  the  numerous  differences 
which  are  noticeable  in  the  descriptions  given  by  this 
book  from  those  in  many  of  the  older  anatomies 
would  require  too  much  space.  The  changes,  how- 
ever, almost  without  exception,  tend  toward  an  im- 
proved nomenclature  and  greater  accuracy.  This  is 
particularly  noticeable  in  the  parts  devoted  to  descrip- 
tions of  the  abdominal  viscera  and  the  joints.  ♦ . . 
For  the  student,  the  surgeon,  or  for  the  general  prac- 
titioner who  desires  to  review  His  anatomy,  Morris 
is  decidedly  the  book  to  buy/r 


MORRIS'  ANATOMY*  Second 
Edition.  790  Illustrations,  of 
which  over  200  are  in  Colors. 

Human  Anatomy.  A Complete  Systematic  Treatise 
by  Various  Authors,  Including  Special  Sections  on 
Surgical  and  Topographical  Anatomy,  the  Skin,  and 
Vestigial  and  Abnormal  Structures.  Edited  by  Henry 
Morris,  M.A.  and  M.B.  (Lond.),  F.R.C.S.,  Senior 
Surgeon  to  Middlesex  Hospital ; Examiner  In  Surgery, 
University  of  London;  Member  of  the  Council,  and 
Chairman  of  the  Court  of  Examiners,  Royal  College 
of  Surgeons,  etc.  Second  Edition.  Rewritten  in  Parts 
and  thoroughly  revised  throughout.  With  790  Illus- 
trations, the  greater  part  of  which  are  Original,  over  200 
being  printed  In  Colors.  Royal  Octavo.  1274  pages. 

Cloth,  $6.00 ; Leather,  $7.00 ; Half  Russia,  $8.00 

Morris'  “Anatomy  **  was  published  at  a time  when  methods  of 
teaching , the  art  of  engraving,  and  distinct  advance  in  anatomical 
illustration  made  desirable  a new  and  modem  text-book*  The  rapid 
sale  of  the  first  edition,  its  immediate  adoption  as  a text-book  by  a 
large  number  of  medical  schools,  and  its  purchase  by  physicians 
and  surgeons  proved  its  value  and  made  it  from  the  day  of  publi- 
cation a standard  authority. 

In  making  this  new  edition  the  editors  and  publishers  have 
used  every  endeavor  to  enhance  its  value.  The  text  has  been 
thoroughly  revised  and  in  many  parts  rewritten;  the  editor  has 
devoted  himself  to  the  task  of  making  it  a harmonious  whole; 
many  new  illustrations  have  replaced  those  used  in  the  first  edition, 
and  a large  number  have  been  printed  in  colors,  while  the  typo- 
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The  illustrations,  in  number,  correctness,  and  excellence  of 
execution,  are  equaled  by  no  similar  treatise;  about  $1000  having 
been  expended  on  new  and  improved  blocks  for  this  edition  alone. 

P.  BLAKISTON’S  SON  & CO.,  PUBLISHERS, 
5012  WALNUT  STREET,  PHILADELPHIA. 


GASTRIC  VERTIGO. 


377 


probable  by  the  fact  that  very  frequently  they  only  occur  after  full 
meals  (dinner),  or,  if  they  existed  before,  they  are  aggravated  by 
copious  eating,  and  become  ameliorated  or  disappear  as  digestion 
is  completed.  The  pains  often  return  toward  night  and  on  going 
to  bed,  causing  insomnia.  Patients  that  are  experienced  in  the 
use  of  the  stomach-tube  are  able  to  arrest  these  pains  at  times  by 
lavage.  Occasionally,  the  colon  is  the  cause  of  the  pain  irradia- 
tion ; this  is  especially  to  be  looked  for  in  membranous  colitis  or 
compression  of  the  colon  from  tight  lacing,  or  in  the  various  forms 
of  enteroptosis. 

Gastric  vertigo  is  a form  of  dizziness  or  partial  unconsciousness 
without  pain,  but  frequently  with  nausea  and  vomiting,  occurring 
in  gastric  sufferers.  Trousseau,  who  gave  a classical  description 
of  this  affection,  argued  that  one  of  its  peculiarities  was  that  con- 
sciousness remained  clear  during  the  attack  (Trousseau,  “ Clin, 
del’  Hotel  Dieu,”  Paris,  tome  in,  1868).  Leube  and  Trousseau 
were  of  the  opinion  that  it  occurred  most  frequently  with  chronic 
gastritis.  Boas  and  Herz  consider  that  myasthenia  is  the  most 
frequent  substratum. 

We  have  observed  transient  loss  of  consciousness  which  at  times 
developed  from  typical  stomach  vertigo.  This  affection  occurs,  in 
our  experience,  in  neuropathic  patients  with  hyperacidity,  particu- 
larly when  the  stomach  is  empty,  and  is  associated  more  often 
with  this  gastric  neurosis  than  others. 

It  is  a more  frequent  complication  of  hyperchylia  than  is  gener- 
ally known,  since  many  patients  will  not  speak  of  their  transient 
attacks  unless  especially  questioned.  Emesis  often  checks  the 
attack,  and  Trousseau  mentions  that  a cup  of  bouillon  or  a cake 
soaked  in  wine  may  check  the  vertigo. 

Treatment  of  the  fundamental  gastric  disease  removes  the 
vertigo,  as  a rule,  but  in  explanation  of  the  way  in  which  the  ver- 
tigo is  caused,  its  nervous  mechanism,  etc.,  we  have  nothing  but 
hypotheses. 

Symptoms. — The  symptoms  accompanying  gastric  vertigo  are 
nausea,  eructation,  pyrosis,  vomiting,  sensitiveness  in  the  epigastric 
region,  pain  in  the  stomach,  and  a feeling  of  pressure,  fullness,  and 
distention.  In  the  majority  of  cases  constipation  exists,  and  the 
abdomen  is  frequently  distended  with  gases.  In  some  few  cases  a 
dilatation  was  found  to  be  present.  Vertigo  has  been  observed  to 
occur  almost  at  any  stage  of  digestion — before,  during,  and  after 
meals.  Sometimes  the  attacks  of  giddiness  are  announced  by  a 

25 


37§  INFLUENCE  OF  GASTRIC  DISEASES  ON  THE  NERVOUS  SYSTEM. 

sensation  of  great  hunger  or  bulimia.  Leube  mentions  that  gastric 
vertigo  may  occur  in  some  persons  after  the  ingestion  of  certain 
foods.  It  may  occur  either  at  intervals  of  several  days  or  several 
times  in  the  same  day.  It  is  generally  a chronic  and  permanent 
trouble,  but  in  its  lighter  forms  it  has  no  serious  influence  on  the 
condition  of  the  patient.  The  treatment  of  gastric  vertigo  necessi- 
tates the  treatment  of  the  underlying  condition  of  the  stomach. 

Leube  has  described  an  intestinal  vertigo  associated  with  intes- 
tinal diseases  of  various  kinds,  but  generally  not  of  a serious  char- 
acter. The  most  frequent  causes  are  constipation  and  intestinal 
parasites,  mainly  lumbricoid  and  tape-worms.  These  attacks  of 
gastric  vertigo  are  as  yet  not  satisfactorily  explained.  Leube  has 
in  some  cases  been  able  to  produce  the  attack  by  pressure  on  the 
stomach  or  intestines  (Leube,  “ Ueber  den  Magenschwindel  ” ; 
Ziemssen’s  “ Handb.  d.  spec.  Path.  u.  Ther.,”  vol.  n,  p.  66).  Mayer 
and  Pribram  claim  to  have  observed  excitation  of  the  vasomotor 
center  after  irritation  of  the  stomach,  particularly  of  the  serous  coat 
(Mayer  and  Pribram,  “ Ueber  reflect.  Bezieh.  d.  Magens  z.  d.  In- 
nervationscentren  f.  d.  Kreislaufsorg.,”  “Sitzungsber.  d.  Wien.  Akad. 
d.  Wiss.,”  1872).  A second  theory  in  explanation  of  stomach  vertigo 
presumes  that  it  is  caused  by  cerebral  anemia,  or  hyperemia, 
which  is  not  described  as  a reflex  act,  but  as  a direct  detrimental 
influence  on  the  circulation  of  the  brain.  This  hypothesis  exag- 
gerates the  degrees  of  circulatory  variation  that  can  possibly  occur 
in  such  light  forms  of  digestive  disturbance  in  which  vertigo  is 
observed.  A third  theory  explains  gastric  vertigo  on  the  basis  of 
auto-intoxication.  It  is  presumed  that  products  of  abnormal  diges- 
tion, which  collect  when  the  motor  function  of  the  stomach  and 
intestines  is  disturbed,  are  absorbed  into  the  circulation,  and  act 
directly  upon  the  brain.  There  is  an  abundance  of  experimental 
evidence,  as  well  as  clinical  experience,  which  proves  that  such  an 
effect  of  toxic  chemical  substances  is  possible.  Such  toxic  irrita- 
tion may  be  indirect,  and  is  intermediated  through  the  vasomotor 
center.  Brieger  has  isolated  a substance  from  dilated  stomachs 
which  he  has  termed  peptotoxin,  which  has  an  extremely  poisonous 
effect  when  injected  into  the  circulation  of  animals.  In  case  of  the 
presence  of  intestinal  parasites,  the  toxic  metabolic  products  of  the 
helminthiasis  are  added  to  those  of  disturbed  digestive  function. 

Rosenbach  has  demonstrated  that  there  is  a regulatory  apparatus 
for  the  body  movements  and  for  equilibrium  in  the  epigastric  re- 
gion. This  center  distinctly  enters  into  function  when  tests  are 


TETANY  OF  GASTRIC  ORIGIN. 


379 


made  with  eyes  closed.  This  observation,  if  confirmed,  would  per- 
mit of  new  insight  into  the  pathology  of  gastric  vertigo.  For,  if 
this  abdominal  regulatory  apparatus  receives  abnormal  impulses, 
it  is  plausible  that  they  may  be  conducted  to  the  cerebrum  by  way 
of  the  sympathetic  system. 

Tetany. — The  term  signifies  characteristic  convulsive  attacks 
which  occur  in  the  course  of  gastric  diseases,  particularly  in  dila- 
tations associated  with  hypersecretion.  The  term  “ tetany  ” was 
first  used  in  1852  by  Corvisart.  The  spasms  are  prevailingly  tonic 
contractions,  alternating  with  less  severe  twitchings  in  the  flexor 
muscles  of  the  arms,  calves,  and  generally  also  of  the  abdominal 
muscles.  The  facial,  cervical,  and  maxillary  muscles  are  occasion- 
ally attacked  by  the  tetany,  the  eyes  may  be  turned  upward,  and 
even  emprosthotonos  of  short  duration  has  been  reported.  The 
convulsions  may  be  painful  and  consciousness  may  be  clear  or 
completely  obscured.  In  one  case  of  Kussmaul’s  the  power  of 
speech  was  lost ; in  another  the  patient  spoke  disconnectedly 
and  his  pupils  did  not  react  to  light.  In  a third  the  symptoms 
referring  to  the  cerebrum  were  absent,  but  a fourth  case  of  Kuss- 
maul’s  was  of  an  epileptic  form  and  character.  Bouveret  and 
Devic  (“  Rech.  clin.  et  experim.  sur  la  tetanie  d’origine  gastrique,” 
“ Revue  de  Medec.,”  1892,  12,  p.  48)  have  collected  twenty  three 
cases  of  these  tetanic  attacks,  and  Albu  (“  Autointoxicationen  des 
Intestinaltractus,”  Berlin,  1895)  states  that  not  more  than  thirty-six 
cases  of  this  complication  of  gastric  diseases  have  been  reported. 
Kussmaul  gave  the  first  classical  description  of  these  attacks  in  his 
famous  publication  on  the  treatment  of  gastric  dilatations  by  a new 
method  by  means  of  the  stomach-pump  (“  Deutsches  Archiv  f. 
klin.  Med.,”  Bd.  vi). 

Clinically,  it  is  not  correct  to  designate  all  tonic  muscular  con- 
vulsions of  gastric  origin  as  tetany.  In  true  gastric  tetany  there 
is  an  increased  mechanical  excitability  of  the  muscles,  and  an  in- 
creased mechanical  and  electrical  irritability  of  the  motor  and  sen- 
sory nerves,  which  precede  the  attack  and  may  persist  long  after  it. 
Cases  have  been  reported  by  Fleiner  and  Kussmaul  which  strongly 
resembled  typical  tetanus.  Cases  are  reported  in  which  the  clinical 
picture  varied  between  tetany,  tetanus,  and  epileptiform  convul- 
sions. In  most  of  the  cases  Trousseau’s  phenomenon — i.  e.,  the 
production  of  spasms  by  pressure  on  the  nerve-trunks — was  present. 
Among  twenty-seven  cases  that  were  collected  by  Riegel,  sixteen 
proved  fatal.  According  to  this,  tetany  is  a very  grave  complica- 


380 


TETANY  CAUSED  BY  AUTO-INTOXICATION. 


tion  of  gastric  diseases.  The  gastric  diseases  with  which  tetany  is 
associated  are  extensive  dilatations,  due  mostly  to  stenosis  of  the 
pylorus  or  duodenum,  by  ulcer  or  cicatrix.  In  several  cases  the 
stenosis  was  due  to  a carcinoma  that  had  developed  from  a cica- 
trix. Bouveret  and  Devic  attribute  great  importance  to  hyper- 
secretion for  the  production  of  tetany.  This  complication  has, 
however,  been  observed  in  other  dilatations  in  which  there  was  no 
hypersecretion.  Thus  far  three  hypotheses  have  been  put  forward 
attempting  to  explain  the  origin  of  tetany:  (i)  That  of  Kussmaul, 
according  to  which  it  is  caused  by  desiccation  of  the  organism  in. 
consequence  of  copious  loss  of  water.  (2)  The  explanation  accord- 
ing to  which  tetany  is  caused  by  a reflex  irritation  of  the  central 
and  peripheral  nervous  systems,  and  that  the  irritation  issued  from 
the  central  branches  of  the  gastro-intestinal  tract.  (3)  That  of 
auto-intoxication. 

Kussmaul’s  theory  rested  upon  the  apparent  analogy  between 
tetany  and  the  cramps  in  the  legs  occurring  with  Asiatic  cholera, 
which  are  believed  to  be  due  to  condensation  and  thickening  of 
the  blood  resulting  from  loss  of  water.  We  know,  however,  that 
these  cramps  occur  also  in  cholera  sicca.  The  loss  of  water, 
Kussmaul  thought,  was  brought  about  by  the  exhaustive  vomiting 
which  usually  precedes  the  attack  of  tetany,  but  cases  have  been 
reported  in  which  tetany  occurred  without  a preliminary  attack  of 
vomiting.  In  cholera  nostras  (the  acute  gastro-enteritis  of  chil- 
dren), where  the  loss  of  water  is  very  great,  tetany  occurs  very 
rarely. 

Blazicek  described  a case  of  gastric  tetany  in  which  the  percent- 
age of  water  in  the  blood  was  not  reduced. 

The  second  theory,  that  of  the  reflex  origin,  has  been  proposed 
by  Germain  See.  The  arguments  of  Bouveret  and  Devic,  and  of 
Ewald  (“  Berlin,  klin.  Wochenschr.,”  1894,  No.  2),  emphasize  the 
fact  that  the  reflex  phenomena  are  based  upon  a preliminary 
chronic  intoxication,  which  increases  the  irritability  of  the  muscles 
and  nerves.  Tetany,  according  to  these  authors,  is,  therefore,  not 
a reflex  phenomena,  any  more  than  are  the  convulsions  of  a strych- 
ninized  frog,  which  result  from  the  slightest  cutaneous  irritation. 

Most  modern  authors  (Gerhardt,  Bouveret  and  Devic,  Albu, 
Ewald,  Heim,  Loeb,  Schlesinger,  and  Baginsky)  favor  an  explana- 
tion of  tetany  on  the  basis  of  gastro-intestinal  auto-intoxication. 
It  is  not  a bacterial  intoxication  caused  by  metabolic  products  of 
pathogenic  bacteria  introduced  with  the  food  which  these  authors 


DYSPEPTIC  ASTHMA. 


3« 


have  reference  to,  but  to  poisons  formed  in  the  stagnating,  ferment- 
ing contents  of  the  dilated  stomach.  Kulneff  has  extracted  toxic 
products  from  the  gastric  contents  in  carcinoma  and  dilatation, 
which,  according  to  their  chemical  structure,  were  classed  as  dia- 
mins.  These  toxins  were  extracted  by  Brieger’s  method  (extrac- 
tion with  alcohol  and  precipitation  with  mercuric  chlorid).  Bouveret 
and  Devic  extracted  substances  from  the  stomachs  of  three  cases 
of  tetany  with  hyperchlorhydria  that  produced  spasms  when  in- 
jected into  animals.  Evvald  and  Jacobson  have  isolated  alkaloidal 
bodies  from  the  urine  of  tetany  patients,  and  Albu  isolated  the 
double  platinic  and  gold  salt  of  an  alkaloidal  substance  from  the 
urine  of  a woman  afflicted  with  tetany.  This  substance  was  absent 
from  the  urine  when  the  patient  was  free  from  the  attacks.  Tetany 
occurs,  in  the  majority  of  cases,  only  when  abnormal  fermentations 
and  putrefactions  occur  in  the  stagnated  contents  of  the  stomach 
and  intestines.  This  intoxication  theory  explains  the  nephritis 
which  Loeb  has  observed  in  connection  with  tetany.  The  author 
has  reported  three  cases  of  nephritis  which  probably  owe  their 
origin  to  auto-intoxication  (Hemmeter,  “ Maryland  Med.  Jour.,” 
July  24  and  31,  and  Aug.  7,  1897).  The  subject  is  not  sufficiently 
investigated  to  permit  of  definite  conclusions  regarding  the  causa- 
tion. 

Asthma  Dyspepticum. — In  1876  Henoch  described  a clinical 
phenomenon  in  children,  in  which  attacks  very  similar  to  asthma 
were  associated  with  digestive  disturbances  (Henoch,  “ Berlin, 
klin.  Wochenschr.,”  1876,  No.  18),  and  in  1882  Silbermann  de- 
scribed similar  cases,  also  occurring  in  children  (“  Berlin,  klin. 
Wochenschr.,”  1882,  No.  23).  The  attacks  of  asthma  dyspepticum 
are  characterized  by  a very  abrupt,  acute  onset,  after  a very  evident 
error  in  diet  or  after  constipation  or  febrile  gastritis.  There  is  a 
pronounced  dyspnea,  with  cyanosis,  very  small,  compressible,  and 
hurried  pulse,  cold  extremities,  collapse,  and,  generally,  no  symp- 
toms of  severe  gastric  disturbance.  The  symptoms  disappear  as 
suddenly  as  they  begin,  after  an  emetic  has  taken  effect  or  spon- 
taneous vomiting  has  occurred.  Strumpell  (“  Specielle  Pathologie 
u.  Therapie  ”)  doubts  the  existence  of  asthma  dyspepticum,  and 
Riegel  also  (“  Die  Erkrankungen  des  Magens,”  Wien,  1896,  S. 
192).  The  literature  on  this  subject  is  very  limited,  and  many  of 
the  cases  reported  do  not  impress  us  as  strictly  belonging  to  the 
clinical  picture  of  asthma  dyspepticum.  O.  Rosenbach  (“  Deutsche 
medizin.  Wochenschr.,”  1879,  No.  42)  describes  a number  of  cases 


382  INFLUENCE  OF  GASTRIC  DISEASES  UPON  OTHER  ORGANS. 

which,  although  he  separates  them  from  dyspeptic  asthma,  very 
much  resemble  this  clinical  picture.  The  patient  complained  of 
oppression,  want  of  air,  difficulty  in  breathing,  and  a sensation  of 
fear.  The  scarcity  of  reports  on  this  complication  is  explained  by 
the  fact  that  the  physician  very  rarely  has  an  opportunity  for  ob- 
serving these  cases  during  the  attack ; as  a rule,  they  cease  spon- 
taneously within  a few  hours,  and  are  frequently  interrupted  by 
the  patients  by  mechanical  manipulations  to  facilitate  vomiting. 

It  is  well  known  that  conditions  of  more  or  less  anxious  oppres- 
sion in  breathing  are  observed  occasionally  in  normal  individuals, 
but  more  frequently  in  those  afflicted  with  gastro-intestinal  dis- 
eases. The  attacks  occur  in  connection  with  the  larger  meals,  the 
patients  having  a feeling  as  if  they  could  not  breathe  properly. 
The  respiratory  oppression  and  distress  cease  spontaneously  during 
the  course  of  digestion,  or  are  relieved  by  eructation  of  gases.  If 
these  abnormal  sensations  are  augmented,  and  when  they  occur 
at  short  intervals  and  after  moderate  ingestion  of  food,  the  condi- 
tion becomes  pathological.  A fear  of  smothering,  with  cyanosis, 
cool  extremities,  greatly  hurried  pulse,  and  dyspnea,  occurring  in 
the  sequence  of  gastro-intestinal  disturbances,  represent  a clinical 
picture  which  we  are  justified  in  designating  as  asthma  dyspepticum. 
Oppler  (“  Allg.  med.  Centralztg.,”  1896,  No.  71)  and  Lauterbach 
(“  Wien.  med.  Presse,”  1894,  No.  48)  have  each  described  one  case 
of  asthma  dyspepticum  as  a sequence  to  gastric  atony.  The  case 
of  Oppler  recovered  under  lavage,  diet,  massage,  electricity,  and 
the  use  of  strychnin  and  belladonna.  The  cardinal  symptom  of 
the  phenomenon  is  the  paroxysmal  dyspnea.  It  occurs  most  fre- 
quently among  women,  and  especially  among  the  neurasthenic  and 
hysterical.  Potain  (Association  pour  PAvancement  des  Sciences, 
Montpellier,  1879)  and  Barie  (“Revue  de  Medecine,”  1883,  tome 
in,  p.  1)  have  together  reported  thirty-two  cases  in  France,  a 
number  of  which  gave  indications  that  they  were  genuine  asthma 
dyspepticum.  Boas  (“  Archiv  f.  Verdauungskrankheiten,”  Bd.  11, 
S.  444)  gives  a very  interesting  report  of  eleven  cases — ten  males 
and  one  female. 

Instead  of  going  into  details  concerning  the  symptomatology, 
we  will  describe  a case  which  has  been  observed  by  the  author 
repeatedly  during  attacks  : 

The  lady  in  question  lived  in  the  immediate  neighborhood  of  the  writer. 
Mrs.  S.,  aged  twenty-six,  has  suffered  for  years  with  symptoms  of  atony. 
Mother  living  and  healthy  ; father  died  with  cancer  of  the  stomach.  She  has 


DYSPEPTIC  ASTHMA. 


3«3 


been  married  four  years,  but  has  no  children  ; heart  and  lungs  normal.  The 
dyspeptic  symptoms  are  those  of  atony  and  nervous  dyspepsia  with  hyper- 
acidity. There  are  no  signs  of  enteroptosis  ; right  kidney  is  firmly  attached  in 
its  normal  position  ; no  history  of  uterine  trouble  ; constipation.  Results  of 
analysis  of  test-meal:  Total  acidity,  90;  free  HC1,  50;  combined  HC1,  22;  ery- 
throdextrin  present  in  excess  ; lactic  acid  absent.  Examination  of  the  urine 
for  toxic  products  gave  the  following  results  when  it  was  first  examined  ; 
this  was  shortly  after  an  attack,  and  was  also  followed  by  an  attack  on  the  next 
day:  Preformed  sulphates,  3.970  gm.;  combined  sulphates,  0.35  gm., — ratio, 
II. I ; urea,  51.028  gm. ; indigo  blue,  very  strong  reaction.  December  14,  1896. — 
On  this  date  the  patient  was  very  melancholy,  and  suffered  much  from  intes- 
tinal flatulence.  The  writer  was  called  just  as  an  attack  was  beginning,  and 
found  the  patient  on  the  sofa,  with  the  servants  rubbing  her  hands  and  feet, 
which  had  a bluish  tint  and  were  quite  cold  to  the  touch.  She  had  thrown 
open  the  windows  on  a cold  night  to  get  air,  and  was  gasping  for  breath  ; the 
pulse  was  148.  The  patient  was  in  mortal  fear  of  smothering.  There  were 
marked  cardiac  oppression  and  a very  peculiar  wheezing  sound  with  each 
breath,  and  tenderness  to  pressure  in  the  epigastric  region  ; accentuation  of  the 
second  cardiac  sound.  A stomach-tube  was  passed,  and  about  500  gm.  of 
highly  acid  liquid  drawn  off,  composed  mostly  of  melted  ice-cream  and  straw- 
berries. An  enema  was  given  containing  warm  claret  and  camphor,  and  hot 
bottjes  were  placed  to  the  feet.  The  patient  broke  out  in  a perspiration  within 
thirty  minutes  after  the  enema,  and  had  quite  recovered  two  hours  after  the 
attack.  This  same  patient  has  since  that  time,  which  was  a year  ago,  been 
seen  in  two  other  attacks  very  similar  to  this  one,  both  of  them  yielding  to  the 
same  treatment.  Formerly,  she  had  one  attack  every  month,  not  in  any  con- 
nection with  the  menstrual  period,  however.  Addition  at  time  of  revision, 
September,  1899. — With  strict  observance  of  diet  and  the  use  of  alkalies  this 
patient  has  not  had  an  attack  during  the  last  fourteen  months. 

There  are  no  satisfactory  explanations  of  asthma  dyspepticum 
up  to  the  present  date.  Potain  ( loc . cit.)  believes  in  a reflex  irrita- 
tion from  the  gastro-intestinal  tract,  which  causes  contraction  of 
the  small  pulmonary  vessels.  In  the  resistance  to  the  pulmonary 
circulation  which  is  thus  brought  about  the  respiratory  gaseous 
exchanges  are  interfered  with,  and  Potain,  as  well  as  Barie,  claim 
to  have  found  dilatation  of  the  right  ventricle,  with  accentuation 
of  the  second  pulmonary  sound  during  the  attack.  A.  Frankel 
(article  on  “ Asthma  ” in  Eulenburg’s  “ Real-Encyclopadie,”  3. 
Aufl.)  considers  asthma  dyspepticum  a reflex  disturbance  of  car- 
diac asthma,  caused  especially  by  a weakness  of  the  left  ventricle, 
which  then  secondarily  causes  a passive  congestion  in  the  pul- 
monary circulation.  This  explanation  concedes  the  trouble  to  be 
essentially  cardiac  asthma.  There  is  a very  intimate  connection 
between  disturbed  digestion  and  cardiac  action,  which  we  have 
already  dwelt  upon,  and  the  conception  of  Frankel  is  not  without 


384  INFLUENCE  OF  GASTRIC  DISEASES  UPON  OTHER  ORGANS. 

foundation  in  those  cases  in  which  the  heart’s  action  is  not  per- 
fectly sound.  Boas  has  reported  cases  in  which  the  attacks  were 
brought  on  by  a disturbed  gastric  digestion,  with  bronchitis  and 
emphysema. 

Abnormal  gastro-intestinal  meteorism  may  force  up  the  dia- 
phragm mechanically,  and  if  there  is  any  debility  about  the  pul- 
monary capillaries,  passive  congestion  can  not  fail  to  occur.  With 
the  evacuation  or  escape  of  the  gas  the  attack  will  cease  entirely. 
Senator  (“  Berlin,  klin.  Wochenschr.,”  1883,  No.  22),  G.  Lewin,  and 
Albu  (Joe.  cit.)  claim  that  dyspeptic  asthma  is  caused  by  the  absorp- 
tion of  toxic  substances  from  the  digestive  tract.  The  theory  of 
auto-intoxication  has  been  criticized  by  Boas,  since  asthma  dys- 
pepticum  is  not  met  with  in  any  gastro-intestinal  diseases  associated 
with  extensive  putrefaction  and  fermentation ; whereas  in  those 
slight  forms  of  gastric  disease  in  which  this  asthma  really  does 
occur,  there  is  very  little  formation  of  toxic  products. 

Prognosis  is  favorable.  Boas,  Lauterbach,  and  Oppler  have 
reported  cures.  One  of  the  author’s  cases  has  not  had  an  attack 
for  two  and  a half  years  following  treatment. 

Treatment  is  mainly  a prophylactic  and  dietetic  one.  The  stom- 
ach should  be  sparingly  treated,  the  bowels  kept  open,  and  all  food 
causing  flatulence  must  be  scrupulously  avoided.  The  underlying 
neurasthenia  and  pulmonary  or  heart  affections  should  receive  thera- 
peutic attention.  In  atony  with  hyperacidity,  strychnin  sulphate, 

of  a grain,  with  extract  of  belladonna,  -^-of  a grain  three  times 
daily,  and  electricity  can  be  recommended.  During  the  attack  itself 
speedy  evacuation  of  the  stomach  by  the  tube  and  of  the  bowel  by 
warm-water  irrigation  are  the  most  effective  means  of  treatment. 

The  patients  will  usually  not  object  to  the  tube  in  these  attacks, 
because  their  suffering  and  want  of  air  is  so  great  that  they  are 
willing  to  undergo  anything  to  be  relieved  ; but  when  it  can  not 
be  used  on  account  of  heart  or  lung  trouble,  emetics  should  not 
be  used  either,  because  they  are  more  depressing  upon  the  heart 
than  the  use  of  the  tube.  When  the  heart  is  sound  and  emesis  is 
absolutely  indicated,  we  recommend  the  following : 

R . Pulvis  ipecac., 1.5  gr.  xxiij 

Antimon.  et  potass,  tartrate,  . . 0.05  gr.  f.  M. 

SlG. — Make  two  powders,  to  be  taken  one-half  hour  apart. 

Prompt  emesis  may  be  effected  by  the  use  of  apomorphin, 
hypodermically,  in  doses  of  TTT  of  a grain ; but  in  most  cases 


INFLUENCE  OF  NERVOUS  DISEASES  UPON  THE  STOMACH.  385 

the  vomiting  unfortunately  continues  for  some  time  after  the 
stomach  is  evacuated  ; it  is,  therefore,  not  recommended  for  this 
purpose. 

The  Influence  of  Nervous  Diseases  Upon  the  Stomach. — 

This  subject  will  be  considered  in  connection  with  the  various 
nervous  disorders  of  digestion.  It  is  a well-known  fact  that 
emotional  excitement  may  cause  an  alteration  in  the  gastric  secre- 
tions, and  that  intense  nervous  depression  may  produce  gastric 
distress,  fullness,  pressure,  eructation,  nausea,  constipation  or 
diarrhea,  meteorism,  and  tenesmus.  Mental  overexertion  may 
lead  to  nervous  dyspepsia.  Anatomical  alterations  in  the  central 
nervous  system  may  be  accompanied  by  motor,  secretory,  and 
resorptive  disturbances.  In  this  connection  we  refer  again  to  the 
gastric  disturbances  occurring  with  tabes,  and  to  the  fact  that  Koch 
and  Ewald  caused  gastric  hemorrhages  by  cutting  the  spinal  cord 
(“  Klinik  d.  Verdauungskrankheiten,”  loc.  cit.).  Brown-Sequard  and 
Schiff,  as  well  as  Ebstein  (“  Archiv  f.  exper.  Pathol.,”  Bd.  n,  S.  183), 
produced  gastric  hemorrhage  after  experimental  injuries  to  the 
anterior  corpora  quadrigemina.  We  have  personally  observed 
submucous  hemorrhages  and  small  areas  of  necrosis  in  the 
stomach  eight  days  after  section  of  one  or  both  vagi  in  cats,  dogs, 
rabbits,  and  guinea-pigs.* 

Malaria. — It  is  a very  well-known  fact,  and  generally  accepted 
by  the  physicians  of  the  Southern  and  Eastern  States,  that  malaria 
very  often  complicates  gastric  diseases,  and  may  even  be  an  under- 
lying cause.  It  is  very  probable  that  a malarial  state  of  the  blood 
may  be  instrumental  in  causing  gastric  ulcer,  which  in  this  case 
has  been  asserted  by  London  to  be  due  to  pigment  emboli.  In  a 
case  of  pernicious  malarial  fever  that  died  at  Bay  View  Hospital 
there  was  found  an  abundant  deposit  of  pigment  between  the  pep- 
tic. ducts,  and  also  within  and  between  the  cells  of  the  ducts.  At 
our  clinic  it  is  a standing  rule  to  examine  all  persistent  cases  of 
stomach  trouble  for  the  presence  of  the  malarial  parasite  in  the 
blood.  For  the  characteristics  of  this  organism,  and  the  methods 
of  examination,  we  refer  to  the  article  by  W.  H.  Welch  and  William 
S.  Thayer,  in  the  “ Loomis-Thompson  System  of  Medicine,”  and 
also  to  the  able  monographs  of  W.  S.  Thayer  on  this  subject 
(“  Lectures  on  the  Malarial  Fevers,”  London,  Kimpton,  1898),  also 


* If  both  vagi  are  intersected,  the  right  one  must  be  reached  beneath  the  origin  of  the 
recurrent  laryngeal  nerve  to  preserve  the  sensibility  of  the  respiratory  passages. 


386  INFLUENCE  OF  ANEMIA  AND  CHLOROSIS  ON  THE  STOMACH. 

Thayer  and  Hewetson  (“  The  Malarial  Fevers  of  Baltimore,”  Johns 
Hopkins  Press,  1895).  In  counties  of  the  eastern  shore  of  Vir- 
ginia malarial  gastralgia  is  frequent.  Malaria  does  not,  as  a rule, 
affect  the  secretion  or  motility,  except  in  the  various  forms  of  per- 
nicious malarial  fever.*  In  gastric  troubles  showing  any  period- 
icity, or  microscopic  or  clinical  evidence  of  malaria,  quinin  should 
be  promptly  administered,  and  if  not  effective  within  twelve  hours, 
the  hydrobromate  of  quinin  should  be  injected  hypodermically. 

Dr.  Hans  Herz,  in  his  recent  work  (“  Disturbances  of  Digestion 
as  a Cause  and  Consequence  of  other  Diseases  ”),  does  not  mention 
malaria  as  a cause  of  disease  of  the  stomach. 

Anemia  and  Chlorosis. — The  relation  between  pernicious  ane- 
mia and  atrophy  of  the  stomach  has  been  considered,  and  the  claim 
of  Austin  Flint  to  the  priority  of  this  clinical  association  has  been 
emphasized  in  the  chapter  on  Achylia  Gastrica.  Anemia  and  chloro- 
sis are  influential  etiological  factors  in  the  causation  of  gastric  dis- 
eases, if  they  are  primary  conditions.  This  relation  of  the  two  states 
is  very  difficult  to  establish  and  probably  very  rare.  Hayem  (“  Des 
Alterations  du  chimisme  Stomacal  dans  la  Chlorose,”  “ Bulletin 
Med.,”  1891,  No.  87)  asserts  that  the  alterations  in  the  stomach  and 
intestines  are  the  primary  cause.  Ewald  and  Rosenheim  maintain 
that  the  digestive  disturbances  may  be  the  results  and  not  causes 
of  the  anemia.  There  are,  undoubtedly,  cases  in  which  the  anemia 
is  the  cause,  and  others  in  which  it  is  the  result.  In  some  in- 
stances the  treatment  will  throw  light  on  this  causative  relation. 
If  the  secretory  and  motor  functions  of  the  stomach  become  normal 
with  the  cure  of  undoubted  anemia,  the  gastric  disturbance  was  the 
result  of  the  state  of  the  blood;  but  if  the  secretory  and  motor  dis- 
turbances are  marked,  and  perhaps  of  long  standing,  and  examina- 
tions show  only  a slight  deviation  from  the  normal  state  of  the 
blood,  the  digestive  disturbance  is  the  primary  one.  Often  it  is 
possible,  when  patients  remain  under  observation  for  a long  time, 
to  observe  the  progressive  anemia  developing  as  a sequence  to 
gastro-intestinal  atrophy. 

The  effect  of  syphilis  on  gastric  digestion  has  been  considered 
in  a separate  chapter. 


* A very  reliable  and  accurate  Southern  colleague  informed  us  of  a case  of  periodical 
hematemesis,  which  he  had  observed  near  Savannah,  occurring  every  third  day,  which 
was  cured  by  quinin.  A form  of  the  algid,  pernicious  malarial  fever  is  called  by  some 
Southern  doctors  “gastric  malarial  fever.” 


EFFECT  OF  PULMONARY  DISEASES  ON  THE  STOMACH.  387 

Respiratory  Organs — Mouth,  Nose,  Pharynx,  and  Larynx. 

— Numerous  inflammations  of  these  parts  may  cause  invasion  of  the 
stomach,  by  direct  infection — i.  e.,  swallowing  of  infectious  material. 
Abnormalities  in  the  formation  of  the  gums,  cleft  palate,  deviations 
of  the  septum,  retracted  gums,  or  chronically  enlarged  tonsils  may, 
by  causing  one  of  the  many  forms  of  stomatitis,  or,  compelling 
mouth-breathing,  bring  on  gastric  disturbance.  Stenoses  of  the 
nasal  passages  in  gastric  sufferers  imperatively  demand  correction  ; 
in  short,  all  conditions  leading  to  mouth-breathing  may  induce 
dyspepsia.  If  this  is  the  case  with  simple  catarrhal  changes,  it  is 
of  course  much  more  serious  with  carcinoma,  syphilis,  tuberculosis, 
or  other  destructive  processes  (noma)  about  the  mouth,  nose,  throat, 
larynx,  and  antrum  of  Highmore. 

In  persistent  gastric  hyperacidities  we  have  frequently  observed 
what  may  be  termed  a reflex  pharyngitis  and  posterior  nasal 
catarrh,  which  were  permanently  cured  by  treatment  of  the  hyper- 
acidity after  direct  throat  and  nose  treatment  had  failed.  The 
amount  of  mucus  in  the  pharynx  became  largest  when  the  gastric 
acidity  was  highest;  at  this  period  the  hawking  and  spitting  were 
incessant ; they  became  less  as  the  acidity  was  reduced  either  by 
normal  evacuation  of  the  stomach  or  the  use  of  alkalies.  The 
latter  were  in  some  cases  poured  in  through  the  stomach-tube, 
when  their  beneficial  action  on  the  pharyngeal  mucous  flow  was 
also  very  evident. 

Pulmonary  Diseases. — The  most  prominent  among  these  is 
pulmonary  tuberculosis.  W.  Fenwick  found  gastritis  to  be  present 
in  nearly  all  the  cases  of  pulmonary  tuberculosis,  chronic  bron- 
chitis, emphysema,  and  acute  pneumonia.  He  asserts  that  in  dis- 
eases of  the  brain  no  gastric  involvement  was  observed  by  him 
(“Virchow’s  Archiv,”  1889,  Bd.  cxviii,  S.  187);  he  found  gastritis 
in  eleven  cases  out  of  fifteen  of  phthisis.  Marfan  (“  Troubles  et 
Lesions  Gastriques  dans  la  Phthisie  Pulmonaire,”  Paris,  1887) 
found  but  five  cases  in  sixty-one  of  tuberculosis  in  which  the  gas- 
tric symptoms  preceded  the  pulmonary.  It  is  very  difficult  to 
decide,  when  a dyspeptic  is  at  the  same  time  affected  with  pul- 
monary tuberculosis,  which  trouble  is  primary.  As  a rule,  dis- 
eases limited  to  the  stomach  can  not  so  weaken  the  general  state 
of  health  as  to  predispose  to  pulmonary  tuberculosis.  Rapid 
exhaustion  from  localized  gastric  diseases  occurs  only  in  carci- 
noma, which  is  in  itself  rapidly  fatal  before  lung  trouble  is  devel- 
oped to  any  great  extent;  but  when  the  gastric  disease  is  associated 


388  INFLUENCE  OF  OTHER  DISEASES  ON  THE  STOMACH. 

with  intestinal  disturbances,  so  that  the  digestion  is  very  much 
interfered  with,  general  nutrition  may  be  so  impoverished  that 
tuberculosis  can  be  more  readily  acquired.  Hutchinson  (“The 
Morbid  States  of  the  Stomach  and  Duodenum,”  London,  1878) 
publishes  an  analysis  of  a large  number  of  cases,  and  states  that 
the  digestive  disturbances  precede  the  tubercular  infection  in  about 
one-third  of  the  cases.  It  is  in  these  cases  of  suspected  pulmonary 
disease,  associated  with  digestive  troubles,  that  the  ability  of  a 
good  auscultator  will  tell.  Gastro-enterologists  should  not  fail  to 
avail  themselves  of  their  experience  in  auscultation  and  percussion. 
Whenever  sputum  can  be  obtained,  it  should  be  examined  for 
tubercle  bacilli.  The  state  of  the  gastric  secretion  and  the  motor 
function  in  tuberculosis  have  been  studied  by  Edinger  ( loc . cit .), 
Rosenthal  {loc.  cit. ),  Shetty  (loc.  cit.),  O.  Brieger  (loc.  cit.),  Immer- 
mann  (loc.  cit.),  Hildebrandt  (loc.  cit.),  and  Einhorn  (loc.  cit).  The 
state  of  the  secretory  and  motor  functions  in  pulmonary  phthisis 
varies,  in  our  experience,  with  the  stage  of  the  pulmonary  disease. 
In  the  incipient  stages  of  phthisis,  secretion  and  motility  may  be 
normal  for  a long  time ; they  will  become  more  and  more  deranged 
as  the  pulmonary  trouble  progresses,  so  that  in  the  final  stages  of 
pulmonary  caseation,  breakdown,  and  formation  of  cavities,  all  gas- 
tric function  may  be  extinguished.  Brieger  (loc.  cit.)  states  that  in 
the  initial  stages  the  cases  of  normal  and  disturbed  secretion  are 
about  equally  divided.  In  moderately  severe  cases  secretion  was 
normal  only  in  one-third,  or  33  per  cent. ; in  the  remainder  secre- 
tion was  variable,  but  generally  depressed.  In  6.6  per  cent,  there 
was  no  secretion  whatever.  In  advanced  cases  of  phthisis  secre- 
tion was  normal  only  in  16  per  cent,  of  the  cases.  It  was  more  or 
less  defective  in  the  rest  of  the  cases,  and  in  9.6  per  cent,  there  was 
complete  arrest  of  secretion^  Immermann  (loc.  cit)  found  the 
gastric  peristalsis  normal  in  fifty-three  put  of  fifty-four  tests, 
whereas  Klemperer  (loc.  cit.)  claims  to  have  found  marked  inhibi- 
tion of  the  peristalsis  by  his  method.  The  amount  of  gastric 
secretion  and  the  state  of  the  peristalsis  are  not  satisfactory  expon- 
ents of  the  digestive  powers  of  phthisical  patients.  The  only 
correct  way  to  find  out  whether  such  patients  have  digestive  power 
sufficient  to  maintain  the  nitrogen  equilibrium  is  by  quantitative 
experiments  on  metabolism.  By  giving  weighed  amounts  of  certain 
foods  after  the  nitrogen  balance  has  been  established,  and  deter- 
mining the  quantity  that  is  digested  and  the  quantity  that  is 
excreted  undigested,  together  with  careful  determination  of  the 


EFFECT  OF  PULMONARY  DISEASES  ON  THE  STOMACH.  389 

amount  of  nitrogen  in  the  urine,  we  have  been  able  to  discover 
that  tuberculous  patients  (first  stage  of  pulmonary  tuberculosis), 
with  absolute  achylia  gastrica,  may,  with  care  as  to  diet,  still 
be  able  to  maintain  their  nitrogen  equilibrium,  provided  the 
gastric  peristalsis  was  preserved.  In  future  the  exact  state  of 
the  pulmonary  disease,  its  duration  and  extent,  together  with 
a statement  of  the  condition  of  all  the  remaining  organs,  would 
be  desirable,  if  the  correlation  existing  between  gastric  and  pul- 
monary troubles  is  to  be  put  upon  a basis  of  approximate 
exactness.  Although  the  treatment  of  the  tuberculosis  is  the 
main  object,  it  will  be  impossible  to  maintain  nitrogen  equilibrium 
with  a defective  digestive  apparatus  ; it  is,  therefore,  essential  that 
the  functions  of  the  stomach  should  be  improved  as  far  as  possible. 
In  this  way  a system  of  forced  alimentation,  such  as  has  been  very 
successfully  employed  by  Debove  (loc.  cit.),  Dettweiler,  Lieber- 
meister,  Leyden,  Riihle,  and  Peiper,  may  become  possible.  In 
each  individual  case  the  diet  and  the  medicine  should  be  ordered 
according  to  the  state  of  the  gastric  functions  found  from  test- 
meals.  We  have  had  three  patients  affected  with  pulmonary  tuber- 
culosis and  gastritis  at  the  Maryland  General  Hospital  during  the 
winter  of  1896  and  1897,  who  gained  considerably  in  weight  by 
treatment  of  the  existing  gastritis.  One  patient  with  pulmonary 
tuberculosis  and  a tubercular  rectal  fistula  gained  fourteen  pounds 
in  two  months  under  daily  lavage  and  administration  of  HC1  and 
strychnin,  together  with  nutritious  diet.  * 

Diseases  of  the  Heart. — We  have  already  spoken  of  the  effect 
of  gastric  disturbances  in  producing  tachycardia,  bradycardia,  and 
arrhythmia.  The  diseases  of  the  stomach  which  are  caused  by 
valvular  affections  of  the  heart  are  brought  about  by  the  venous 
stasis  and  passive  congestion.  Under  the  head  of  chronic  gastritis 
we  have  spoken  of  the  efficacy  of  digitalis  when  valvular  disease  is 
in  clear  etiological  association  with  the  gastric  affection.  Concerning 
the  state  of  the  secretion  in  heart  diseases,  there  is  no  agreement  in 
the  observations  thus  far  reported.  In  twenty  patients  with  heart 
disease  Adler  and  Stern  (“  Berl.  klin.  Wochenschr.,”  1889,  No.  49) 
found  free  HC1  always  present  in  sixteen,  variable  in  two,  and 
always  absent  in  two  cases.  Huff  er  states  that  in  ten  cases  of  mostly 
valvular  lesions  suppression  of  the  secretion  of  HC1  and  absence  of 


*The  tuberculous  fistula  was  treated  by  Dr.  Samuel  T.  Earle,  and  healed  up  com- 
pletely before  the  patient  left  the  hospital. 


i 


390 


INFLUENCE  OF  OTHER  DISEASES  ON  THE  STOMACH. 


albumin  digestion  were  found  nine  times  and  hyperacidity  in  a single 
case.  Most  of  his  patients  are  stated  to  have  been  in  the  stage  of 
perfect  cardiac  compensation.  These  observations  of  Hufler  are 
not  intelligible  in  the  light  of  the  pathological  physiology  of  cardiac 
diseases ; for  perfect  compensation  means  that  the  arterial  and 
venous  pressure  in  all  the  organs  is  normal ; under  this  state  we 
can  not  conceive  of  any  passive  congestion  in  the  stomach.  Ger- 
main See  held  that  the  initial  “ Gastricismus  ” was  the  earliest  sign 
of  a valvular  trouble  ; that  evidence  of  passive  congestion  may 
be  present  when  there  is  as  yet  no  murmur  or  accentuated  sound. 
By  perfect  compensation  we  mean  the  natural  compensation  of  the 
heart-muscle,  not  the  transient  improved  tonus  effected  by  a drug 
(digitalis).  In  our  experience  gastric  secretion  was  normal  in 
eight  cases  of  mitral  regurgitation,  two  cases  of  aortic  regurgita- 
tion, and  two  cases  of  mitral  insufficiency,  with  perfect  compensa- 
tion. As  soon  as  compensation  becomes  defective,  the  gastric 
symptoms  make  their  appearance,  and  secretion  is  found  altered. 

Diseases  of  the  Liver. — The  close  anatomical  and  physio- 
logical relationship  between  the  liver  and  the  stomach  explains 
the  sympathetic  manner  in  which  diseases  of  one  organ  fre- 
quently reflect  upon  the  other.  Excepting  in  the  diseases  of  the 
biliary  passages  and  gall-bladder,  it  is  impossible  to  say  which 
organ  is  primarily  affected.  During  the  passage  of  gall-stones 
gastric  secretion  is  suppressed ; this  suppression  is  due  to  a reflex 
influence  caused  by  the  intense  pain.  We  have  analyzed  the 
vomited  matter  which  was  brought  up  during  attacks  of  biliary 
colic:  In  three  cases  it  was  neutral,  very  faintly  acid  (=  6°, 

decinormal  NaOH) ; in  one  case  it  showed  presence  of  combined 
HCl — no  free  HC1;  in  two  cases  it  was  alkaline  (=  8°-io°, 
H2S04).  The  alkalinity  of  this  vomit  was  not  due  to  the 
presence  of  bile  or  pancreatic  juice,  because  they  were  found  to 
be  absent.  Cases  of  cirrhosis  of  the  liver,  and  even  of  cancer 
of  the  liver,  may  run  a latent  course  for  a long  time,  the  symp- 
toms being  those  of  chronic  gastritis.  We  have  made  1 1 8 
analyses  of  gastric  contents  in  cases  of  catarrhal  jaundice  (“  Bulletin 
of  the  Maryland  University  Hospital,”  vol.  in,  No.  2,  p.  30).  In 
twenty  cases  of  icterus  (catarrhal)  free  and  combined  HCl  were 
absent  in  twelve ; free  HCl  absent  but  combined  HCl  present  in 
four;  free  and  combined  HCl  present  in  six.  It  would,  of  course, 
be  important  to  know  whether  those  cases  in  which  free  HCl  was 
absent  during  the  icterus  had  chronic  gastritis  before  the  jaundice. 


EFFECTS  OF  DIABETES  AND  RENAL  DISEASES.  39 1 

In  six  of  these  eight  cases  free  HC1  was  found  two  months  after  the 
recovery  from  the  attack  at  that  time  there  were  no  evidences  of 
gastritis. 

Gout  and  Rheumatism. — Burney  Yeo  claims  that  dyspepsia  is 
a frequent  and  prominent  manifestation  of  gout(“  Brit.  Med.  Jour./' 
Jan.  7 and  14,  1888).  This  specific  gouty  disorder  of  the  stomach 
is  claimed  to  exist  in  states  of  uric  acid  diathesis  by  a number  of 
contributors  to  British  medical  journals.  Ewald  states  that  he  has 
not  met  with  a single  case  of  true  gout  with  coincident  gastric  dis- 
turbances, but  that  he  has  seen  numerous  such  examples  in  chronic 
articular  rheumatism,  in  which  the  dyspepsia  was  so  marked  that 
the  pains  in  the  joints  were  comparatively  insignificant.  Anomalies 
of  secretion  in  gout  have  been  repeatedly  observed  by  us.  The 
most  frequent  secretory  trouble  is  hyperacidity. 

Alexander  Haig  recognizes  gout  of  the  intestines  and  cecum 
(“Uric  Acid  as  Causation  in  Disease,”  pp.  330  and  623),  also 
gastro-intestinal  irritation,  as  a cause  of  uricacidemia  (loc.  cit.,  p.  49). 
Without  entering  into  the  literature  of  the  relation  of  uric  acid, 
gout,  and  rheumatism  to  gastro-intestinal  diseases,  we  wish  to  say 
that  the  nature  of  these  diseases  is  still  too  obscure  to  permit  of 
any  exact  scientific  determinations  of  the  relation  in  question. 
Gout  and  uric  acid  diathesis  occur  in  the  same  constitutions,  sug- 
gesting that  the  conditions  are  identical.  The  author  has  had 
occasion  to  study  numerous  cases  of  gastralgia  that  yielded  to 
nothing  but  salicylate  of  soda  and  colchicum,  also  many  cases  of 
enteritis  that  were  improved  by  diet  free  from  uric  acid  (milk);  still, 
these  observations  do  not  convince  him  of  the  correctness  of  the 
terms  “ gout  of  the  stomach  or  intestines  ” which  Haig  uses. 

Diabetes  Mellitus. — Although  there  is  no  constancy  in  the 
character  of  the  secondary  gastric  symptoms  accompanying 
diabetes,  there  are  few  cases  of  this  disease  in  which  the  stomach 
is  not  involved.  Diabetes  affects  the  stomach  in  two  ways  prin- 
cipally: either  by  arresting  its  functions  through  auto-intoxication 
or  by  production  of  gastritis.  The  presence  of  great  thirst, 
polyuria,  polyphagia,  ocular  disturbances,  pruritus,  emaciation, 
usually  means  coexistent  gastric  involvement.  Rosenstein  and 
Gans  have  examined  the  gastric  functions  in  diabetes  (Rosenstein, 
“ Berl.  klin.  Wochenschr.,”  1890,  No.  13).  Their  results  show  that 
the  disturbances,  although  present,  show  no  constancy  in  type. 
The  polyphagia  and  polydipsia  of  diabetes  have  been  known  to 
cause  gastrectasia.  Our  personal  observation  on  diabetic  patients 


392  INFLUENCE  OF  OTHER  DISEASES  ON  THE  STOMACH. 

indicates  that,  as  a rule,  peristalsis  and  secretion  are  normal.  Our 
material  in  this  line  has  been  limited.  Eight  normal  tests  of  both 
functions  were  found  in  twelve  cases  studied.  In  the  abnormal 
cases,  hyper-,  sub-,  and  anacidity  were  found  in  different  patients, 
and  in  the  same  patient  at  different  times  (heterochylia).  There  is 
no  sugar  present  in  the  gastric  secretion  (Kiilz).  The  disease  has 
been  known  to  begin  with  severe  gastric  symptoms  from  the  onset, 
and  Teschemacher  advises  that  the  urine  be  examined  for  sugar  in 
all  cases  where  severe  acute  gastritis  repeatedly  occurs  without  a 
traceable  cause. 

Diseases  of  the  Kidney. — The  stomach  is  always  more  or  less 
affected  in  renal  diseases,  and  the  symptoms  of  disturbed  gastric 
digestion  very  often  appear  long  before  albumin  is  present  in  the 
urine.  In  the  “ Maryland  Medical  Journal,”  July  24  and  31,  and 
August  7,  1897,  I have  reported  three  cases  of  nephritis  which 
were  probably  due  to  chronic  auto-intoxication  from  the  gastro- 
intestinal tract.  In  this  connection  I wish  to  emphasize  the 
gastric  diseases  which  are  caused  by  preexisting  affections  of  the 
kidneys.  Naturally,  it  is  unavoidable  that  a certain  amount  of 
auto-intoxication  will  accompany  the  association  of  renal  with  gas- 
tric disease,  no  matter  which  is  the  primary  affection.  Albu  (Joe. 
cit. ) and  Biernacki  (“  Berk  klin.  Wochenschr.,”  1891,  No.  25  and 
No.  26)  emphasize  the  influence  of  retained  metabolic  products  in 
producing  gastric  disturbances.  These  retained  products  of  metab- 
olism injure  the  stomach  in  two  ways : (1)  By  acting  as  toxins 
through  the  vascular  channels  directly  upon  the  parenchyma  of 
the  gastric  walls,  and  (2)  by  irritation  of  the  surface  of  the  stomach, 
since  they  are  very  frequently  excreted  in  this  manner.  Fenwick 
(loc.  cit)  states  that  the  gastric  mucosa  is  capable  of  secreting  urea 
like  the  intestinal  mucosa,  and  that  the  excretion  of  this  product 
causes  an  acute  catarrh  of  the  gastric  glands.  I have  analyzed  the 
vomit  of  two  patients  afflicted  with  chronic  interstitial  nephritis, 
and  repeatedly  found  urea  or  ammonia  in  it.  If  the  total  nitrogen 
excreted  in  the  urine  is  approximately  normal,  the  vomit  does  not 
contain  urea,  in  my  experience.  This  would  indicate  that  the 
gastro-intestinal  canal  is  not  called  upon  to  vicariously  secrete 
urea,  until  the  kidneys  can  no  longer  do  so.  A variety  of  gastric 
diseases  have  been  found  to  exist  in  connection  with  chronic  Bright’s 
disease.  We  shall  see  in  the  clinical  part  that  acute  and  chronic 
gastritis,  fatty  degeneration  of  the  glandular  epithelium,  and, 
according  to  Ewald,  amyloid  degeneration  may  occur.  Edema  of 


RELATION  OF  RENAL  AND  GASTRIC  DISEASES. 


393 


the  gastric  walls  is  a very  rare  complication.  The  effects  of  floating 
kidney  in  producing  stenosis  of  the  duodenum  have  been  con- 
sidered in  the  chapter  on  Enteroptosis.  Allan  A.  Jones  (“  Gastric 
Conditions  in  Renal  Disease,”  “ New  York  Med.  Jour.,”  Jan.  19, 
1895)  has  frequently  found  suppression  of  gastric  secretion  in 
patients  with  kidney  diseases.  Einhorn  reports  a case  of  achylia 
gastrica  due  to  renal  calculus,  which  had  existed  for  a long  time. 
After  removal  of  the  stone  by  operation,  the  gastric  symptoms  at 
once  disappeared.  According  to  Biernacki,  the  secretory  function 
is  arrested  in  renal  affections. 

Renal  Disturbances  in  Connection  with  Digestive  Diseases. 

— During  disturbed  digestion  a number  of  toxic  substances  formed 
in  the  gastro-intestinal  canal  reach  the  kidneys  through  vascular 
channels,  and  are  there  excreted.  Substances  very  closely  related 
to  serum-albumin  find  their  way  out  through  the  kidneys  : for  in- 
stance, albumoses,  egg-albumen,  and  hemoglobin.  Under  this 
increased  work  the  kidneys  may  become  diseased.  In  experi- 
mental injections  of  egg-albumen  it  has  been  observed  that  more 
albumen  is  excreted  than  was  injected.  If  the  disturbance  persists 
for  a long  time,  albuminuria,  excretion  of  epithelia',  and  leukocytes 
become  more  permanent. 

There  are  abnormal  conditions  of  the  blood  in  which  the  excre- 
tion of  the  urine  may  become  totally  suppressed : for  instance,  the 
blood  disintegration  after  grave  icterus  and  extensive  burns. 

There  are  two  kinds  of  renal  albuminuria:  (1)  Those  due  to 
pathological  changes  in  the  parenchyma  or  innervation  or  vascular 
supply  of  the  kidney,  and  (2)  the  hematogenous  variety,  in  which 
a primarily  healthy  kidney  serves  as  a purifying  organ  to  excrete 
useless  albuminous  substances.  Both  varieties  may  occur  com- 
bined, for  the  same  cause  may  alter  blood  and  kidney  simultaneously 
(scarlatina,  typhoid  fever),  an<J  continued  excretory  overburdening, 
by  elimination  of  albumin,  may  secondarily  lead  to  inflammatory 
changes  in  the  kidney  ; this  probably  occurs  where  intermittent 
albuminuria  gradually  passes  over  into  interstitial  nephritis.  Ac- 
cording to  Senator,  albumin  very  often  occurs  in  the  urine  after 
excessively  albuminous  meals,  the  so-called  physiological  albumi- 
nuria. It  is  conceivable  that  the  albuminous  food  has  been  too 
abundant  or  has  not  undergone  a normal  or  sufficient  proteolysis, 
and  really  enters  the  circulation  as  a foreign  substance ; for  there 
are  very  great  varieties  of  albumins  and  our  imperfect  chemical 
methods  do  not  permit  us  to  distinguish  between  them.  So-called 
26 


394  GASTRIC  DISEASES  AND  THOSE  OF  OTHER  ORGANS. 

“dyspeptic  albuminuria”  occurs  occasionally  in  a transient  way, in 
connection  with  chronic  gastric  diseases,  particularly  dilatations, 
without  being  followed  by  inflammatory  changes  in  the  kidney. 
Muller  found  albuminuria  in  72  per  cent,  of  gastric  cancers ; in 
cancers  of  other  organs  of  the  body  he  found  it  in  only  35  per 
cent.  The  author  has  discovered  albuminuria  in  75  per  cent,  of 
his  gastric  cancer  cases  ; so  it  would  appear  that  cancers  of  the 
stomach  must  be  assigned  a special  influence  in  the  production 
of  this  abnormality.  V.  Noorden  discovered  albuminuria  after 
severe  gastralgias  with  gastric  ulcer  and  also  after  gastric  hemor- 
rhage. In  explanation  of  these  phenomena  we  have  nothing  but 
theories,  prominent  among  which  are  the  auto-intoxication  and  the 
reflex  theory.  Anemia  and  cachexia  may  be  brought  on  by  all 
long-standing  gastro-intestinal  diseases,  and,  when  once  estab- 
lished, lead  to  nephritis.  Albuminuria  has  been  assigned  to  rapid 
fall  of  arterial  pressure  during  severe  diarrheas.  Toxic  and 
bacterial  albuminuria  has  been  described  as  due  to  toxins  and 
bacteria  originated  in  the  intestines.  When  the  intestines  and 
stomach  are  inflamed,  the  process  of  proteolysis  is  defective,  and 
albuminous  bodies  enter  the  circulation  imperfectly  prepared,  and 
must  be  excreted  again,  damaging  the  renal  structures  secondarily. 
Toxins,  in  passing  from  the  intestines  into  the  blood,  are  supposed 
to  alter  the  structure  of  the  blood  albumin-molecule,  which  then 
passes  out  through  the  kidney — one  form  of  hematogenous  albu- 
minuria. 

Digestive  Disturbances  in  Connection  with  Renal  Diseases. 

— Both  in  acute  and  chronic  nephritis  digestive  symptoms  may  be 
entirely  absent.  In  some  cases  digestive  disturbances  are  pro- 
nounced before  the  albuminuria  can  be  detected.  Sudden  severe 
nausea  and  vomiting,  particularly  when  occurring  with  headache, 
in  absence  of  evident  cause,  is  suggestive  of  nephritis.  Vomiting 
is  the  most  frequent  motor  disturbance  of  the  stomach,  in  associa- 
tion with  kidney  disease,  and  three  kinds  are  recognizable:  (1)  A 
copious  watery  vomit,  containing  sparingly  of  mucus,  the  total 
acidity  of  which,  in  our  experience,  is  6°  to  8°  (^NaOH), contain- 
ing no  free  nor  combined  HC1.  The  specific  gravity  is  1002  ; it  gen- 
erally occurs  in  the  morning,  before  breakfast.  (2)  Hematemesis; 
it  is  rare  that  large  amounts  of  blood  are  vomited.  (3)  Vomit 
containing  constituents  of  the  urine,  particularly  urea. 

We  have  discovered  urea  as  such  in  the  vomit  of  chronic  nephri- 
tis (to  test  this  we  took  only  such  cases  as  showed  a deficient 


THE  KIDNEYS  AND  DIGESTIVE  DISEASES.  395 

excretion  of  urea),  but  more  frequently  carbonate  or  chloride  of 
ammonia.  The  vomit  becomes  alkaline,  and  has  a penetrating, 
ammoniacal  odor. 

The  secretory  gastric  function  varies ; there  may  be  normal, 
hyper-,  sub-,  or  anacidity.  We  know  that  many  gastric  symptoms 
are  traceable  to  cachectic  conditions — anemia  and  hydremia;  there- 
fore, all  concomitant  defects  of  digestion  can  not  logically  be 
assigned  to  the  nephritis  when  these  states  are  coexistent.  Both 
organs  may  be  diseased  from  the  same  cause. 

Retention  of  nitrogenous  constituents  of  the  urine  (urea,  uric 
acid,  etc.)  does  not  occur  in  all  cases  of  nephritis;  but  when  this 
elimination  is  subnormal,  a vicarious  excretion  of  these  products 
through  the  gastro-intestinal  mucosa  may  occur  and  has  been  ob- 
served by  the  author.  Uric  acid  has  been  found  in  such  small 
traces  that  it  may  be  regarded  as  the  uric  acid  contained  in  the  food 
before  it  was  eaten.  But  urea  occurs  in  quantities  much  in  excess 
of  what  could  be  in  the  food,  and  in  morning  vomit  before  food 
was  taken.  It  is  self-evident  that  the  passage  of  urea  which  is 
decomposable  into  ammonium  carbonate  through  the  gastric 
mucosa  must  severely  injure  the  secretory  cells,  and  even  cause 
gastritis.  A certain  class  of  nephritis  cases  exhibit  vomiting  that 
can  be  called  nervous  or  uremic  ; the  causes  of  irritation  of  the  cen- 
tral nervous  organs  and  those  of  the  uremia  in  these  cases  are 
closely  related,  perhaps  identical. 

There  are  a large  number  of  digestive  disturbances  in  associa- 
tion with  albuminuria,  or  rather  with  nephritis,  which  can  not  be 
attributed  to  anemia,  cachectic,  nervous,  or  uremic  conditions,  nor 
even  to  lessened  excretion  of  water  or  nitrogen.  The  author  does 
not  look  upon  urea  as  the  essential  and  only  dangerous  substance 
that  is  retained,  nor  upon  albumin  as  the  only  essential  material 
that  is  lost  in  nephritis.  There  are  toxins,  or  rather  bodies,  the 
result  of  retrogressive  metamorphosis,  which  are  retained  at  a time 
when  the  total  nitrogen  eliminated  is  still  normal ; these  poisonous 
materials  seek  a way  out  through  the  gastro-intestinal  canal,  and 
may  bring  about  catarrhal,  inflammatory,  and  ulcerative  conditions 
in  the  intestines.  J.  Fischer  and  Grawitz  have  recently  described 
uremic  intestinal  ulcers,  and  Marchiafava  describes  hemorrhagic 
gastric  erosions  leading  to  hematemesis  due  to  the  same  condi- 
tion. The  so-called  cyclic  albuminuria  is  a very  vague  conception: 
digestive  disturbances  are  said  to  occur  in  connection  with  it. 
But  it  is  not  easy  to  define  exactly  what  cyclic  albuminuria  is. 


396  GASTRIC  DISEASES  AND  THOSE  OF  OTHER  ORGANS. 

Perhaps  latent  nephritis  breaking  out  and  remaining  quiescent 
alternately ; perhaps  hematogenous  or  nervous  albuminuria.  Finally, 
there  is  a form  of  albuminuria  in  which  the  urine  shows  high  specific 
gravity,  little  albumin,  excessive  excretion  of  uric  acid  and  urates 
at  times,  but  rarely  oxalates,  and  numerous  cylinders  or  hyaline 
casts.  This  condition  Da  Costa  looks  upon  as  a disease  of  meta- 
bolism in  which  both  albuminuria  and  digestive  disturbances  are 
the  expression  of  the  former.  Vomiting  has  been  caused  by 
painful  swelling  of  the  kidney  in  acute  inflammatory  conditions. 
The  relation  of  movable  or  floating  kidney  to  digestive  diseases 
has"  been  considered  in  the  chapter  on  Enteroptosis. 

Relation  of  Digestive  and  Skin  Diseases. — There  can  be  no 
doubt  that  digestive  troubles  have  an  influence  in  the  production 
of  eczema,  urticaria,  erythema,  the  various  forms  of  acne,  and  pem- 
phigus ; but  there  is  only  doubtful  evidence,  vice  versa,  that  skin 
troubles  have  any  effect  upon  the  gastric  function,  excepting  ex- 
tensive cutaneous  burns.  When  the  skin  has  been  destroyed  over 
large  areas,  duodenal  and  sometimes  gastric  ulcers  were  observed 
to  develop.  The  homeopaths  assume  a great  many  digestive  trou- 
bles to  be  caused  by  so-called  “ systemic  ” itch,  and  Pedioux 
(“  L’Union  Med.,”  1866,  p.  235)  considered  dyspepsia  an  expression 
of  a herpetic  state  of  the  system.  These  inferences  are  too  absurd 
to  be  considered  seriously. 

The  relation  of  skin  and  digestive  diseases  may  be  considered 
from  three  aspects:  (l)  Skin  diseases  of  which  the  causes  appar- 
ently emanate  from  the  gastro-intestinal  tract;  (2)  digestive  dis- 
eases the  causes  of  which  apparently  emanate  from  the  cutaneous 
surface;  (3)  conditions  of  abnormality  simultaneously  occurring 
in  both  skin  and  digestive  tract,  due  apparently  to  some  common 
cause.  The  track  through  which  irritations  may  reach  the  skin 
from  the  digestive  canal  is  either  through  the  nerves  or  by  way  of 
the  blood-vessels.  If  the  disturbance  can  be  plainly  assigned  to  a 
nervous  influence,  we  speak  of  it  as  a “ reflex  ”;  if  it  is  traceable  to 
a blood-vascular  influence,  it  is  most  often  attributed  to  “ auto- 
intoxication.” A distinct  line  of  separation  between  the  two  can  not 
be  drawn,  as  it  is  not  even  certain  whether  we  are  correct  in  assum- 
ing this  classification.  In  some  patients  urticaria  may  develop  in 
a very  few  minutes  after  the  ingestion  of  food ; in  some  others  that 
manifest  an  idiosyncrasy  against  certain  kinds  of  food-substances, 
the  urticaria  has  been  known  to  develop  immediately  after  touch- 
ing that  substance  to  the  mucosa  of  the  mouth.  Now,  the  appear- 


SKIN  AND  ALIMENTARY  CANAL. 


397 


ance  of  this  phenomenon  is  entirely  too  rapid  to  be  assignable  to  the 
blood  or  vascular  intermediation — it  must  be  a reflex.  This 
nervous  reaction,  no  doubt,  takes  place  in  many  forms  of  urticaria 
and  erythemas,  in  the  cutaneous  eruptions  that  follow  nervous 
colics,  dentition,  and  those  that  occur  in  association  with  intestinal 
parasites. 

In  cases  of  acne,  however,  that  develop  in  the  course  of  chronic 
digestive  disturbances  and  in  the  pruritus  of  icterus  and  diabetes, 
it  is  more  probable  that  the  course  of  events  has  been  abnormal 
putrefactions  and  fermentations  in  the  intestinal  canal,  effecting  a 
pathological  condition  of  the  blood.  Singer  has  given  this  view 
somewhat  of  an  experimental  basis  by  demonstrating  the  increase 
of  ethereal  sulphates  in  the  urine  of  such  patients.  Albu  attributes 
the  cutaneous  efflorescences  after  ingestion  of  certain  foods  (straw- 
berries, lobsters),  and  even  the  urticaria  after  copaiba  or  turpentine, 
not  to  these  substances  themselves,  but  to  the  results  of  a gastro- 
intestinal catarrh  set  up  by  them. 

Digestive  diseases  in  etiological  relation  with  preexisting  skin 
diseases  are  chiefly  those  consequent  upon  exposure  of  the  skin 
to  extremes  of  temperature,  the  gastric  and  intestinal  catarrhs 
due  to  cold  or  taking  cold,  and  the  (gastric)  duodenal  ulcers  fol- 
lowing burns. 

Pathological  conditions  in  which  both  the  skin  and  the  digestive 
tract  are  simultaneously  affected  are  represented  by  the  febrile 
exanthemata — infectious  diseases  involving  both  the  skin  and  the 
alimentary  passage  (scarlatina,  measles,  typhoid,  variola,  etc.). 

Among  the  typical  eruptions  that  befall  both  tissues  are  the 
erythema  exudativum  multiforme,  erythema  bullosum  (Werman), 
and  erythema  nodosum  (Pospelow).  The  acute  and  subacute 
phlyctenular  eruptions  (herpes  zoster)  may  occur  in  the  mouth  as 
well  as  on  the  epidermis.  Also  pemphigus  and  lichen  ruber  and 
planus.  The  unfortunate  sufferers  of  pemphigus  in  the  mouth 
surface  are  easily  mistaken  for  syphilitics  on  account  of  the  simi- 
larity in  the  eruptions.  The  phlyctenular  pemphigus  can,  however, 
be  distinguished  by  its  superficial  location  (subepidermal,  intra- 
epithelial), the  acute  course,  absence  of  lymph-gland  involvement 
and  scar-formation,  and  the  characteristic  phlyctenular  eruption  of 
the  epidermis  as  soon  as  this  makes  its  appearance.  Diseases  of 
the  mouth  of  these  types  are,  as  a rule,  not  recognized  except 
when  a typical  skin  eruption  precedes  or  follows  it.  (See  Schech, 
“ Krankheiten  d.  Mundhohle”;  Kraus,  “ Krankheiten  d.  Mund- 


398  GASTRIC  DISEASES  AND  THOSE  OF  OTHER  ORGANS. 

hohle”  ; in  Nothnagel’s  “ Specielle  Pathol,  u.  Therap.  ”;  also  J. 
Mikulicz  and  W.  Kiimmel,  “ Die  Krankheiten  des  Mundes.” 

* Very  curious  reciprocal  relations  have  been  observed  between 
skin  and  digestive  tract : for  instance,  the  improvement  or  disap- 
pearance of  a number  of  skin  diseases  after  severe  diarrheas  and 
loss  of  blood  from  hemorrhoids.  The  dermal  disease  sometimes 
returns  when  the  digestive  trouble  is  cured.  Scabies  has  been 
cured  by  an  intervening  diarrhea  in  this  way.  The  explanation  is 
hypothetical,  but  there  is  no  doubt  that  diarrheas  have  a strong 
derivative  influence  on  the  circulation  in  the  skin.  Kobner  ob- 
served a case  of  pemphigus  vegetans  with  diarrheas  ; as  long  as  the 
bowels  were  loose,  new  vegetations  did  not  appear,  and  the  old  ones 
showed  tendency  to  healing,  but  when  the  diarrhea  ceased,  the 
skin  pemphigus  became  aggravated.  There  are  even  cases  on 
record  where  long-standing  digestive  diseases  disappeared  with  the 
sudden  eruption  of  a cutaneous  affection.  Urticaria  and  derma- 
titis have  been  reported  to  act  in  this  manner.  S.  Fenwick 
observed  sudden  cessation  of  severe  gastralgia  with  hyperacidity 
on  the  appearance  of  an  eczema.  He  believes  to  have  noticed  this 
association  of  hyperacidity,  gastralgia,  and  cutaneous  eczema  fre- 
quently. The  term  “ eczema  of  the  stomach  ” which  Fenwick  uses, 
in  this  connection,  seems  not  well  founded.  These  relations 
between  skin  and  digestive  tract  are  not  sufficiently  supported  by 
pathological  evidences  to  permit  of  exact  deductions.  Such  cases 
are  exceedingly  rare  in  our  experience.  Fenwick  supposes  that 
the  epidermis  and  lining  epithelium  of  digestive  tract  may  sub- 
stitute for  one  another  in  the  excretion  of  toxins,  and  therefore 
symptoms  may  disappear  on  one  membrane  when  the  other  takes 
up  the  excretory  work. 

The  striking  way  in  which  certain  exceptional  forms  of  enteritis 
and  colitis  are  cured  by  arsenic,  after  other  treatment  has  failed,  is 
suggestive  of  the  existence  of  an  eruption  on  the  intestinal  mucosa, 
or  at  least  of  an  abnormal  condition  analogous  to  certain  of  the 
skin  diseases  referred  to.  The  functions  of  the  skin  are  imper- 
fectly understood,  and  until  we  know  them  better,  the  above  rela- 
tions must  remain  unintelligible.  The  skin  is  a protective,  secretory 
and  excretory,  heat-regulating,  and  sensory  organ.  But  in  addi- 
tion to  all  these  functions  it  seems  to  be  a receptive  apparatus, 
transformer  and  transmitter  of  forms  of  energy  of  the  most  delicate 
and  subtle  kind  (“  Therapeutic  Value  of  the  Solar  Rays,”  by 
Albert  Adams,  “ Phila.  Monthly  Med.  Jour.,”  March,  1899,  p.  75). 


LITERATURE. 


399 


LITERATURE 

ON  THE  CORRELATION  OF  DISEASES  OF  THE  STOMACH  TO  THOSE  OF 
OTHER  ORGANS. 

1.  Adler  und  Stern,  “ Ueber  die  Magenverdauung  bei  Herzfehlern,’’ 
“ Munch,  med.  Wochenschr.,”  1889,  No.  33. 

2.  Bernstein,  Iwan,  “ Die  Dyspepsie  der  Phthisiker,”  Inaug.  Dissert.,  Dor- 
pat,  1889. 

3.  Biernacki,  “ Ueber  das  Verhalten  des  Magens  bei  Nierenentziindung,” 
“ Berl.  klin.  Wochenschr.,”  1891,  Nos.  25,  26. 

4.  Brieger,  O.,  “ Ueber  die  Functionen  des  Magens  bei  Phthisis  pulmonum,” 
“ Deutsche  med.  Wochenschr.,”  1888,  No.  14. 

5.  Buzelygan  und  Gluczinsky,  “ Ueber  das  Verhalten  des  Magensaftes  bei 
den  verschiedenen  Formen  der  Anamie  und  besonders  der  Chlorose,”  “Inter- 
nal klin.  Rundschau,”  1891,  No.  34. 

6.  Colleville,  “ Progr.  med.,”  1883’  No.  20. 

7.  Destureaux,  “ De  la  Dilatation  du  Coer  Droit  de  l’Origine  Gastrique,” 
“ These  de  Paris,”  1879. 

8.  Edinger,  “Deutsches  Archiv  f.  klin.  Med.,”  1891. 

9.  Einhorn,  Max,  “ N.  Y.  Med.  Record,”  May  4,  1889  ; also  “ Berlin,  klin. 
Wochenschr.,”  1889,  No.  48. 

10.  Ewald,  “ Neunter  Congress  fiir  innere  Medizin  zu  Wien,”  1890. 

11.  Fenwick,  W.,  “Ueber  den  Zusammenhang  einiger  krankhafter  Zu- 
stande  des  Magens  mit  anderen  Organerkrankungen,”  “Virchow’s  Archiv,’’ 

1889,  Bd.  cxviii,  S.  187. 

12.  Fenwick,  Samuel,  “Atrophy  of  the  Stomach,”  London,  1880,  p.  49. 

13.  Fenwick,  loc.  cit. 

14.  Gans,  Edgar,  “ Neunter  Congress  fiir  innere  Medizin,”  Wiesbaden, 

1890. 

15.  Glax,  “ Ueber  die  Neurosen  des  Magens,”  Wien,  1887,  S.  206. 

16.  Grusdew,  “ Wratsch,”  1889,  Nos.  15,  16;  “ Centralblatt  fiir  klin.  Med.,” 
1890,  S.  92,  Fr. 

17.  Hayem,  “ Des  Alterations  du  chimisme  Stomacal  dans  la  Chlorose,” 
“Bulletin  medec.,”  1891,  No.  87. 

18.  Henry  and  Osier,  “ Atrophy  of  the  Stomach,  with  Clinical  Features  of 
Progressive  Pernicious  Anemia,”  “ American  Jour,  of  Medical  Sciences,” 
April,  1886. 

19.  Herz,  Hans,  “ Storungen  d.  Verdauungsapparates  als  Ursache  u.  Folge 
anderer  Erkrankungen  ” (Berlin,  1898),  Exhaustive  Literature,  Pp.  525  to  543. 

20.  Hildebrand,  H.,  “ Deutsch.  med.  Wochenschr.,”  1889,  No.  15. 

21.  Huchard,  “ Maladies  du  Coeur.” 

22.  Hiifler,  “ Ueber  die  Functionen  des  Magens  bei  Herzfehlern,”  “ Miinch. 
med.  Wochenschr.,”  1889,  No.  33. 

23.  Hutchinson,  “ The  Morbid  States  of  the  Stomach  and  Duodenum,” 
London,  1878. 

24.  Illoway,  “Cardiac  Disturb,  from  Gastric  Irritat.,”  “N.  Y.  Med.  Jour.,” 
April,  1897. 

25.  Immermann,  “ Verhandlungen  des  Congresses  fiir  innere  Medizin,” 
Wiesbaden,  1889. 


400 


THE  BLOOD  AND  URINE  IN  STOMACH  DISEASES. 


26.  Jones,  Hadfield,  “Diseases  of  the  Stomach.” 

27.  Jones,  Allen  A.,  “ N.  Y.  Med.  Jour.,”  January  19,  1895. 

28.  Klemperer,  “ Ueber  die  Dyspepsie  der  Phthisiker,”  “ Berlin,  klin. 
Wochenschr.,”  1889,  No.  11. 

29.  Leube,  “ Beitrage  zur  Diagnostik  der  Magenkrankheiten,”  “Deutsches 
Archiv  fur  klin.  Med.,”  Bd.  xxxm. 

30.  Marfan,  B.,  “Troubles  et  Lesions  Gastriques  dans  la  Phthisie  Pulmo- 
naire,”  Paris,  1887. 

31.  Pick,  “ Therapie  der  Chlorose,”  “Wiener  med.  Wochenschr.,”  1891, 
No.  50. 

32.  Pidoux,  “ Rapport  de  l’herpetisme  et  des  dyspepsies,”  “ L’Union  med.,” 
1886,  No.  1. 

33.  Potain,  “ Congres  de  l’Association  Franqaise,”  Paris,  1878. 

34.  Rosenstein,  “ Ueber  das  Verhalten  des  Magensaftes  und  Magens  bei 
Diabetes  mellitus,”  “ Neunter  Congress  fur  innere  Medizin,”  Wien,  1890. 

35.  Rosenthal,  C.,  “ Ueber  das  Labferment,”  “ Berliner  klin.  Wochen- 
schr.,” 1888,  No.  45. 

36.  Schetty,  loc.  cit .,  “ Deutsches  Archiv  f.  klin.  Med.,”  Bd.  xliv,  S.  219. 

37.  See,  G.,  “ Du  Diagnostic,  etc.,  des  Malad.  du.  Coeur.” 

38.  Werner,  G.,  “ Gastrische  Krisen  als  Initialsymptom  einer  Tabes  dor- 
salis,” “ Inaug.  Dissert.,”  Berlin,  1889. 

39.  Yeo,  Burney,  “ On  the  Treatment  of  the  Gouty  Constitution,”  “ British 
Med.  Journal,”  January  7 and  14,  1888. 


CHAPTER  IX. 

THE  BLOOD  AND  URINE  IN  STOMACH  DISEASES* 

In  general  we  may  say  that,  while  we  are  unable  to  make,  in 
any  given  case,  the  diagnosis  of  stomach  disease  from  an  examina- 
tion of  the  blood  alone,  it  will,  in  many  instances,  render  great 
assistance  in  connection  with  other  symptoms. 

The  presence  of  an  oligocythemia  is  found,  in  cases  of  long- 
continued  stomach  disturbances,  serious  enough  in  character  to 
interfere  with  the  nutrition  of  the  body.  For  example,  in  chronic 
gastritis  there  is  always  a moderate  degree  of  oligocythemia,  the 
decrease  in  the  number  of  red  corpuscles  running  nearly  parallel 
with  the  disturbance  of  nutrition. 

In  the  severe  forms  of  atrophic  gastritis  the  decrease  is  some- 
times enormous  ; so  much  so  that  many  of  these  cases  are  consid- 

* For  the  articles  on  “ The  Condition  of  the  Blood  and  Urine  in  Stomach  Diseases  ” 
and  on  “ The  Stomach  Gases  ” the  author  is  indebted  to  Dr.  E.  L.  Whitney. 


LEUKOCYTOSIS  IN  GASTRIC  DISEASES. 


401 


ered  as  cases  of  primary  pernicious  anemia,  the  true  cause  not 
being  discovered  until  the  postmortem  examination  is  made. 

In  cancer  of  the  stomach  the  oligocythemia  is  usually  marked, 
in  cases  of  well-developed  cachexia  the  number  of  red  corpuscles 
often  being  found  to  be  between  one  and  two  million,  in  some  in- 
stances falling  below  one  million. 

In  ulcer  of  the  stomach  quite  variable  conditions  may  be  found. 
In  cases  of  chronic  ulcer  of  the  stomach  with  slight  hemorrhages, 
the  blood  changes  may  be  those  of  a simple  secondary  anemia,  or 
the  blood  may  approach  the  normal  in  its  proportions.  In  acute 
or  subacute  ulcer  of  the  stomach  the  blood  may  show  a normal 
number  of  corpuscles,  unless  there  has  been  a recent  hemorrhage 
of  considerable  severity.  In  case  of  hemorrhage,  the  decrease  in 
the  number  of  red  corpuscles  is  in  proportion  to  the  amount  of 
blood  lost. 

In  simple  or  benign  dilatation  of  the  stomach  the  anemia  is  pro- 
portional to  the  disturbance  of  nutrition  which  it  produces. 

Leukocytosis. — Considerable  may  be  learned  from  a study  of 
the  occurrence  and  degree  of  leukocytosis  in  stomach  diseases. 

Under  normal  conditions  a moderate  degree  of  leukocytosis 
(10,000  to  15,000)  develops  after  meals,  depending  upon  the  absorp- 
tion of  proteid  materials  from  the  gastro-intestinal  tract.  This  does 
not  take  place  in  the  majority  of  cases  of  cancer  of  the  stomach, 
but  does  occur  in  ulcer  of  the  stomach — a fact  of  considerable 
diagnostic  importance. 

There  is  usually  present  in  cancer  of  the  stomach,  as  in  malig- 
nant disease  in  other  situations,  a constant  increase  in  the  number 
of  white  corpuscles,  varying  from  10,000  to  50,000,  the  normal 
number  being  taken  as  about  7000  leukocytes. 

In  the  acute  inflammatory  diseases  of  the  stomach,  such  as  any 
of  the  forms  of  acute  gastritis,  there  is  present  leukocytosis  of  vary- 
ing intensity.  This  is  an  important  fact  to  remember  in  making  a 
diagnosis  between  acute  gastritis  and  typhoid  fever  in  its  early 
stages, — acute  gastritis  being  accompanied  by  a moderate  leukocy- 
tosis, typhoid  fever  showing  a normal  or  decreased  number  of 
leukocytes. 

After  severe  hemorrhage  from  a gastric  ulcer,  gastric  cancer,  or 
from  varices  in  the  esophagus  or  stomach,  as  from  any  loss  of  blood, 
the  so-called  “ posthemorrhagic  leukocytosis  ” occurs — a fact 
which  should  be  taken  into  account  in  forming  any  conclusions 
from  leukocytosis  in  the  course  of  gastric  diseases.  This  leukocy- 


402 


THE  BLOOD  AND  URINE  IN  STOMACH  DISEASES. 


tosis,  as  a rule,  disappears  in  about  three  or  four  days,  and  can  thus 
be  excluded  by  frequently  repeating  the  examination. 

Red  Corpuscles. — In  cancer  of  the  stomach  in  its  later  stages, 
the  red  corpuscles  frequently  show  the  changes  in  form  known 
as  poikilocytosis,  in  an  exquisite  manner.  In  cases  of  severe 
anemia  of  any  kind,  poikilocytosis*  may  occur,  but  in  pernicious 
anemia  and  cancer  this  change  is  most  pronounced. 

Hemoglobin. — In  the  various  anemic  states  depending  upon 
diseases  of  the  stomach  the  hemoglobin  is  decreased. 

In  ulcer  of  the  stomach  it  is  a common  observation  to  find  a 
normal  or  only  slightly  decreased  number  of  red  corpuscles  with  a 
considerable  decrease  in  the  amount  of  hemoglobin,  the  so-called 
“ chlorotic  blood.”  After  hemorrhages,  especially  when  severe, 
the  number  of  red  corpuscles  may  in  a short  time  decrease  consid- 
erably. 

In  cancer  of  the  stomach  in  its  early  stages  the  blood  may  pre- 
sent a similar  picture;  but  in  the  later  stages  the  number  of  cor- 
puscles is  decreased  extremely,  the  hemoglobin  not  being  dimin- 
ished proportionally. 

In  other  diseases  of  the  stomach  the  alterations  are  usually  those 
of  secondary  anemia,  the  red  corpuscles  and  hemoglobin  being 
reduced  in  a corresponding  ratio. 

Stained  specimens  of  blood  from  patients  suffering  from  the 
cancerous  cachexia  in  a severe  form  will  usually  show  the  presence 
of  a considerable  number  of  normal-sized  nucleated  red  corpuscles, 
as  well  as  megaloblasts,  the  latter  being  much  in  the  minority,  a 
point  which  may  be  of  importance  in  the  diagnosis  of  severe  can- 
cerous cachexia  from  primary  pernicious  anemia. 

After  severe  hemorrhages  from  gastric  ulcer,  fairly  numerous 
normoblasts  may  be  found,  in  addition  to  a decrease  in  the  number 
of  red  corpuscles,  and  in  the  amount  of  hemoglobin.  These 
changes  may  be  of  importance  in  the  diagnosis  of  true  gastric 
hemorrhage  from  the  attempts  at  deception  made  by  malingerers 
and  hysterical  patients. 

In  chronic  atrophic  gastritis  the  blood*  may  show  the  exact 
picture  of  a primary  pernicious  anemia — viz.,  marked  oligocy- 
themia, increase  in  color  index,  decrease  in  specific  gravity,  pres- 
ence of  nucleated  red  corpuscles,  normoblasts,  microblasts,  and 
megaloblasts,  with  a decrease  in  the  number  of  white  corpuscles. 
In  by  far  the  larger  number  of  cases,  however,  the  blood  changes 
are  simply  those  of  a severe  secondary  anemia. 


STATE  OF  THE  BLOOD  IN  GASTRIC  DISEASES.  4O3 

Alkalinity  of  the  Blood. — The  researches  of  Loewy  concern- 
ing the  alkalinity  of  the  blood  in  health  and  disease,  by  the 
method  which  he  has  devised,  have  shown  the  sources  of  error 
in  the  methods  formerly  in  use,  and  rendered  a revision  of  our 
opinions  necessary.  The  method  is  one  which  will  probably 
supersede  all  others  for  the  clinical  laboratory,  on  account  of 
simplicity  of  execution  and  accuracy.  At  present  there  are  not 
enough  observations  recorded  to  permit  us  to  speak  of  its  applica- 
tion in  diagnosis.  In  the  observations  made  with  reference  to 
digestion  it  has  been  shown  that  a rich  secretion  of  HC1  by  the 
stomach  increases  the  alkalinity  of  the  blood,  and  vice  versa. 
Whether  this  fact  can  be  of  utility  in  the  study  of  gastric  diseases 
must  remain  at  present  undecided. 

In  addition  to  the  examination  of  the  blood  for  the  preceding 
constituents,  it  may  be  of  importance  in  cases  of  continued  fever 
with  marked  gastric  symptoms,  in  which  the  diagnosis  lies  between 
some  severe  inflammatory  disease  of  the  stomach  and  typhoid  fever, 
to  make  a trial  of  the  Widal  test  for  typhoid. 

This  test  is  of  no  value  in  the  early  days  of  the  disease,  the 
reaction  seldom  appearing  before  the  seventh  day,  and  rarely  on 
the  fifth  or  sixth  day. 

The  results  of  our  knowledge  of  the  blood  changes  in  the  vari- 
ous stomach  diseases  may  be  summed  up  as  follows  : 

Acute  Gastritis . — Usually  a slight  degree  of  leukocytosis,  in- 
creasing with  the  intensity  of  the  inflammation. 

Chronic  Gastritis. — A decrease  in  the  number  of  red  corpuscles 
and  hemoglobin,  the  leukocytes  showing  normal  numbers,  as  a 
rule. 

Chronic  Atrophic  Gastritis. — The  blood  may  show  the  same 
changes  as  in  the  simple  chronic  gastritis,  or  may  show  the  blood 
changes  of  pernicious  anemia:  poikilocytosis,  marked  decrease  of 
red  corpuscles,  a marked  decrease  in  hemoglobin,  the  decrease 
being  less  in  proportion  than  that  of  the  red  corpuscles,  a 
decrease  in  the  number  of  leukocytes,  and  the  presence  of  a 
large  number  of  nucleated  red  corpuscles,  normoblasts,  megalo- 
blasts,  and  microblasts. 

Gastric  Ulcer. — In  the  old  chronic  forms  of  ulceration  the  blood 
usually  shows  the  changes  of  a secondary  anemia,  as  in  chronic 
gastritis. 

In  ulcers  of  recent  origin  the  blood  may  show  no  variations 
from  the  normal,  or  it  may  show  the  characteristic  changes  of 


404 


THE  BLOOD  AND  URINE  IN  STOMACH  DISEASES. 


chlorosis — viz.,  nearly  a normal  number  of  red  corpuscles  with 
a considerable  decrease  in  the  percentage  of  hemoglobin. 

After  hemorrhages,  the  changes  are  those  common  to  loss  of 
blood  from  any  part  of  the  body — a decrease  in  the  red  corpuscles 
and  hemoglobin,  an  increase  of  the  leukocytes  for  a few  days,  and 
the  presence  of  normoblasts  in  the  blood. 

In  ulcer  digestion  leukocytosis  occurs,  a point  of  some  value  in 
the  differential  diagnosis  between  ulcer  and  cancer. 

Cancer  of  the  Stomach. — In  the  early  stages  the  changes  may  be 
simply  those  of  secondary  anemia.  In  the  later  stages,  when  the 
cachexia  becomes  apparent,  the  blood  changes  are  rather  character- 
istic. There  is  a marked  decrease  in  the  number  of  red  corpuscles 
and  in  the  amount  of  hemoglobin,  the  former  being  often  between 
one  and  two  million,  the  latter  from  twenty  to  thirty  per  cent. 
There  are  often  a number  of  nucleated  red  corpuscles,  both  normo- 
blasts and  megaloblasts.  The*  red  corpuscles  may  show  variations 
in  size,  averaging  smaller  than  normal,  often  with  an  exquisite 
poikilocytosis.  A leukocytosis  is  usually  present,  varying  greatly 
in  its  intensity.  There  is,  with  rare  exceptions,  no  digestion  leuko- 
cytosis. T.  P.  Henry  inclines  to  the  opinion  that  the  reduction  of 
red  corpuscles  in  gastric  carcinoma  is  not  proportionate  to  the 
cachexia,  while  in  pernicious  anemia  the  cachexia  does  not  keep 
step  with  the  oliogocythemia.  The  number  of  red  corpuscles  is 
rarely  below  2,000,000  in  cancer,  while  in  pernicious  anemia  it  is 
often  below  this,  and  he  believes  this  to  be  a diagnostic  differentia- 
tion (“Arch.  f.  Verdauungskrank.,”  Bd.  iv,  Heft  1). 

In  dilatation  of  the  stomach  from  benign  causes,  the  changes  are 
simply  those  of  secondary  anemia,  the  alterations  being  propor- 
tional to  the  disturbances  of  nutrition. 


THE  GASES  OF  THE  STOMACH. 

Under  normal  conditions  the  stomach  contains  a mixture  of 
gases,  derived  in  part  from  air  swallowed  with  the  food,  in  part  from 
chemical  and  fermentative  processes  in  the  stomach,  and  possibly 
from  a small  amount  of  C02  eliminated  from  the  blood  flowing 
through  the  gastric  mucosa.  The  contents  of  a normal  stomach, 
removed  at  the  height  of  digestion,  and  placed  in  a fermentation 
tube  at  the  body  temperature,  exhibit  for  several  days  only  slight 
gas  formation,  this  occurring  only  when  the  free  HC1  has  been 
nearly  or  completely  neutralized  by  the  food  products.  After  this, 


TESTS  FOR  GASES  OF  THE  STOMACH.  405 

fermentation  and  putrefaction  proceed  as  usual  in  fluids  rich  in 
proteid  and  carbohydrate  material. 

Under  pathological  conditions,  such  as  marked  dilatations  with 
stenosis,  especially  when  due  to  malignant  disease,  the  case  is 
altered.  The  food,  which  usually  contains  a variable  number  of 
bacteria,  is  not  properly  sterilized  in  the  stomach  on  account  of  the 
partial  deficiency  or  absence  of  HC1,  and  it  remains  for  a long  time 
in  the  stomach  ; in  addition,  it  is  not  subjected  to  a normal  peris- 
talsis. The  requisite  conditions  for  an  abundant  bacterial  growth 
are  thus  present — viz.,  an  animal  fluid  (containing  both  carbohy- 
drates and  animal  proteids),  heat,  and  moisture. 

Various  gases  have  been  found  in  the  stomach  in  such  condi- 
tions, among  which  may  be  named  acetylene,  hydrogen,  carbon 
dioxid,  nitrogen,  oxygen,  marsh  gas  (CH4),  and  sulphuretted 
hydrogen. 

The  question  of  the  special  variety  of  gas  is  not  of  so  much  im- 
portance as  that  of  the  formation  of  any  gas.  Accurate  gas  analyses 
have,  up  to  the  present  time,  yielded  little  of  diagnostic  value, 
and  from  their  difficulty  will  seldom  be  attempted  by  the  general 
practitioner. 

The  presence  of  combustible  gases  in  dilated  stomachs  was 
first  demonstrated  by  G.  Hoppe-Seyler  (“  Verhandl.  d.  Congr.  f. 
innere  Medizin,”  1892,  S.  392)  and  F.  Kuhn  (“  Zeitschr.  f.  klin.  Med.,” 
Bd.  xxi,  S.  572).  These  investigators  demonstrated  that  hydrogen, 
marsh  gas,  etc.,  could  be  formed  notwithstanding  the  presence  of 
a considerable  amount  of  free  H'Cl.  The  influence  of  various 
antiseptic  agents  on  the  process  of  gas  formation  in  the  stomach 
has  been  carefully  investigated  by  F.  Kuhn,  whose  results  con- 
stitute an  important  practical  contribution  to  the  therapy  of 
gastrectasia. 

To  test  for  the  presence  and  amount  of  gas  formation,  the  freshly 
drawn  stomach  contents  are  well  mixed  and  broken  up  into  a finely 
divided  state,  poured  into  a fermentation  tube  (that  devised  by 
Einhorn  for  the  estimation  of  sugar  in  urine,  or  the  ureometer  of 
Doremus  may  be  used),  and  the  tube  (loosely  stoppered  with  cotton) 
placed  in  a warm  oven  at  the  temperature  of  the  body.  If  none 
of  these  is  at  hand,  a fair  substitute  may  be  improvised  by  filling  a 
large  test-tube  with  the  stomach  contents  and  inverting  over  a small 
beaker  partially  filled  with  the  same  material,  allowing  the  lower 
end  of  the  test-tube  to  dip  into  the  stomach  contents  in  the  beaker, 
to  retain  the  fluid  in  the  tube  by  atmospheric  pressure. 


406  the  blood  and  urine  in  stomach  diseases. 

If  evolution  of  gas  takes  place  within  a few  hours,  the  presump- 
tion is  that  we  have  to  deal  with  a case  of  stenosis  of  the  pylorus  ; 
and  if,  at  the  same  time,  we  find  a marked  formation  of  lactic  acid 
and  an  absence  of  HC1,  we  may  assume  that  it  is  a case  of  malig- 
nant stenosis  of  the  pylorus  with  a high  degree  of  dilatation. 

In  non-malignant  stenosis  we  find,  as  a rule,  that  the  gas  forma- 
tion goes  on  rather  less  rapidly  and  is  not  associated  with  an 
excess  of  lactic  acid  as  in  malignant  stenosis. 

In  dilatation  unaccompanied  by  stenosis,  and  even  in  the  pres- 
ence of  small  quantities  of  free  HC1,  we  find  that  gas  is  formed  ; 
often,  however,  only  after  the  tube  has  been  allowed  to  stand  for 
several  days. 

The  gas  may  be  submitted  to  various  tests  to  determine  its 
character. 

A few  c.c.  of  a strong  solution  of  caustic  soda  are  placed  in  the 
lower  part  of  the  fermentation  tube  and  allowed  to  stand  for  some 
time.  If  the  gas  is  composed  partly  or  wholly  of  C02,  it  will  be 
absorbed  by  the  alkali,  and  its  volume  percentage  may  be  read  off 
directly  by  the  decrease  in  volume  of  the  gas. 

A small  amount  of  theg  as  is  allowed  to  bubble  out,  and  a piece 
of  filter-paper,  previously  dipped  in  a solution  of  lead  acetate,  is 
held  in  the  gas  as  it  escapes.  If  any  sulphuretted  hydrogen  is 
present,  the  paper  will  turn  black,  due  to  the  formation  of  lead 
sulphid. 

A portion  of  the  gas  may  be  tested  for  inflammability  by  allow- 
ing it  to  flow  out  as  before,  and  attempting  ignition  by  holding  a 
lighted  match  to  it  as  it  escapes.  If  it  take  fire  or  give  a slight 
explosion,  the  probabilities  are  that  hydrogen,  marsh  gas,  or  acety- 
lene are  present. 

URINARY  CHANGES  IN  STOMACH  DISEASES. 

While  many  interesting  and  valuable  observations  upon  the  urin- 
ary alterations  in  stomach  diseases  have  been  made,  it  must  be 
stated  that,  up  to  the  present,  little  of  diagnostic  importance  has 
been  determined.  It  is  not  without  interest,  however,  to  take  a 
short  review  of  the  topics  so  far  as  it  concerns  the  subject  of  this 
book. 

The  Amount. — So  long  as  appetite,  digestion,  and  absorption 
from  the  stomach  and  intestinal  tract  are  little  interfered  with,  there 
are  only  trifling  alterations  in  the  quantity  of  urine. 

The  quantity  of  urine  sinks  in  cases  of  vomiting : as,  for  exam- 


TOTAL  ACIDITY  OF  THE  URINE  IN  GASTRIC  DISEASES.  407 

pie,  in  acute  gastritis  and  gastric  ulcer,  the  decrease  in  the  amount 
of  urine  being  in  an  almost  exact  ratio  to  the  amount  of  fluid  lost 
by  vomiting. 

It  is,  however,  in  marked  cases  of  gastric  dilatation  and  pyloric 
stenosis  that  the  greatest  decrease  in  the  amount  of  urine  is  noticed. 
In  well-marked  cases  of  dilatation  the  amount  of  urine  often  sinks 
to  from  300  to  500  c.c.  Under  these  conditions  a continued  low 
quantity  is  an  unfavorable  prognostic  sign,  while  an  increase  indi- 
cates an  improvement  in  the  motor  function. 

The  specific  gravity  has  little  diagnostic  significance,  but,  in 
general,  has  about  the  same  value  as  the  amount  of  urine.  In 
cases  of  dilatation,  in  which  the  element  of  inanition  is  beginning 
to  be  a factor  in  the  clinical  picture,  we  find  that  the  solids  of  the 
urine,  as  indicated  by  the  specific  gravity,  fall ; while  in  cases  in 
which  the  nutrition  is  well  preserved,  the  total  solids  of  the  urine 
approximate  the  normal  value. 

The  Reaction. — Bence  Jones,  in  1819,  first  explained  the  well- 
known  relation  existing  between  the  secretion  of  gastric  juice  and 
the  reaction  of  the  urine.  After  a meal  the  acidity  of  the  urine 
decreases,  often  becoming  neutral  or  amphoteric,  and,  occasionally, 
alkaline  in  from  three  to  five  hours.  Subsequently,  the  acidity  of 
the  urine  increases,  reaching  about  the  average  a short  time  after 
the  food  has  been  propelled  from  the  stomach  into  the  intestines. 
The  range  of  variation  is  greater  following  a full  meal  than  a 
light  repast,  so  that  a greater  fall  in  the  acidity  is  found  after 
dinner  than  after  either  of  the  other  meals. 

This  phenomenon  Bence  Jones  explained  upon  the  ground  of  a 
greater  alkalinity  of  the  blood,  as  a consequence  of  abstraction 
from  it  of  acids  or  acid-forming  substances.  The  presence  of  an 
increased  alkalinity  of  the  blood  leads  to  increased  excretion  of 
alkalies  in  the  urine  and  a diminished  acidity.  An  additional 
factor  may  be  the  presence  of  alkalies  or  of  alkaline  carbonates  in 
the  food,  which  neutralize  the  acidity  of  the  gastric  juice,  and  assist 
also,  after  absorption,  in  increasing  the  alkalinity  of  the  blood. 

From  these  physiological  facts  the  variations  of  the  reaction  in 
disease  are  easily  understood.  In  the  vomiting  of  ulcer,  if  profuse, 
a large  amount  of  acid  is  withdrawn  from  the  system  ; and,  in  some 
cases,  the  urine  may  exhibit  for  some  time  a neutral,  or  even 
alkaline,  reaction.  In  cases  of  hyperacidity  of  the  gastric  juice  in 
which  a larger  quantity  of  acid  than  normal  is  withdrawn  from 
the  blood,  the  curve  of  urinary  acidity  undergoes  greater  varia- 


408  the  blood  and  urine  in  stomach  diseases. 

tion  than  under  normal  conditions.  In  cases  in  which  there  is 
a considerable  diminution,  or  a total  absence  of  the  acid  secre- 
tion of  the  stomach,  this  variation  in  the  reaction  of  the  urine  does 
not  occur,  or  if  any  variation  does  take  place,  it  is  less  marked  than 
under  normal  conditions.  Hence  it  will  be  seen  that  in  cases  of 
atrophic  gastritis,  severe  chronic  gastritis,  and  in  carcinoma  of  the 
stomach,  with  an  absence  of  HC1,  little  or  no  variation  in  the  acidity 
of  the  urine  occurs,  a fact  that  may  be  of  some  importance  in  the 
differential  diagnosis  between  carcinoma  and  ulcer  of  the  stomach, 
especially  when  the  occurrence  of  hematemesis  or  bloody  stools 
contraindicates  the  use  of  the  stomach-tube. 

The  Chlorids. — The  amount  of  chlorin  depends  primarily 
upon  the  amount  of  food,  and,  with  it,  on  the  amount  of  chlorids 
absorbed  from  the  stomach.  The  amount  of  chlorids  present  in 
the  urine  is  also  in  an  inverse  ratio  to  the  amount  of  HC1  secreted 
by  the  stomach. 

In  ulcer  of  the  stomach,  associated  with  considerable  vomiting 
of  a large  amount  of  highly  acid  gastric  juice,  a considerable 
decrease  in  the  amount  of  urinary  chlorids  will  be  found,  as  also  in 
other  cases  of  vomiting  in  which  a large  amount  of  HC1  is  lost. 

In  hyperacidity  without  vomiting,  the  amount  of  urinary  chlorids 
decreases  as  secretion  goes  on,  diminishing  in  well-marked  cases 
to  a very  low  percentage,  increasing  again  as  absorption  from  the 
stomach  and  intestine  goes  on,  finally  reaching  the  highest  part  of 
the  chlorid  curve  five  or  six  hours  (sometimes  later)  after  the  in- 
gestion of  the  meal. 

In  cases  of  anacidity  this  curve  of  urinary  chlorids  does  not 
occur,  no  fall  of  chlorids  occurring  after  the  meal,  a slight  increase 
taking  place  as  the  absorption  of  the  food  goes  on. 

In  severe  cases  of  gastrectasia  with  pyloric  stenosis,  the  amount 
of  chlorids  in  the  urine  sinks  very  considerably,  the  decrease  being 
in  proportion  to  the  severity  of  the  affection.  An  increase  in  the 
amount  of  chlorids  without  a corresponding  change  in  the  diet 
may  be  taken  as  a symptom  of  improvement,  in  this  respect  being 
even  of  more  prognostic  importance  than  the  increase  in  the 
amount  of  urine  which  usually  occurs  at  the  same  time. 

Taken  in  connection  with  the  total  nitrogen  of  the  urine,  the 
amount  of  chlorids  may  be  of  assistance  in  determining  the  ques- 
tion of  a benign*  or  malignant  stenosis  of  the  pylorus. 

If  one  finds,  for  example,  in  the  urine  a small  amount  of  chlorids 
and  a proportionally  small  amount  of  nitrogen,  it  speaks  for  a 


SIGNIFICANCE  OF  PREFORMED  AND  ETHEREAL  SULPHATES.  40Q 

simple  inanition,  a benign  stenosis  ; but  if,  on  the  other  hand,  one 
finds  a small  amount  of  chlorids  and  a relatively  large  amount  of 
nitrogen,  it  speaks  for  the  presence  of  a malignant  stenosis. 

The  Phosphates. — The  investigation  of  the  excretion  of  phos- 
phates in  stomach  diseases  has  yielded  little  in  the  line  of  diagno- 
sis as  yet.  The  deposit  of  basic  phosphates  in  the  freshly  voided 
urine  passed  after  meals  is  quite  frequently  seen  in  cases  of  hyper- 
acidity, though  the  same  change  may  also  occur  in  perfectly 
healthy  individuals.  The  deposit  of  the  basic  earthy  phosphates  in 
these  cases  is  due  to  the  alkaline  tide  spoken  of  in  the  paragraph 
upon  the  reaction  of  the  urine. 

In  hyperacidity,  according  to  Robin,  the  excretion  of  phosphoric 
acid  is  considerably  increased. 

According  to  F.  Muller,  the  excretion  of  phosphates  is  increased 
in  cancer  of  the  stomach,  though  not  in  all  cases. 

Of  more  diagnostic  importance,  however,  is  the  relation  exist- 
ing between  the  excretion  of  nitrogen  and  phosphoric  acid.  Under 
normal  conditions  the  proportion  is  about  as  follows  : 

N : P205  : : 100  : 17  to  20. 

In  malignant  diseases  in  general,  the  proportion  of  P205  rises, 
in  one  case  of  gastric  carcinoma  recorded  by  Chas.  E.  Simon  the 
relation  being  ioo  : 34. 

The  Sulphates. — Of  the  two  forms  in  which  sulphuric  acid 
occurs  in  the  urine,  the  preformed  sulphates  have  only  a passing 
interest  as  being  a measure  of  the  proteid  metabolism  going  on  in 
the  system  ; while  the  ethereal  sulphates  have  a more  direct  bear- 
ing, as  they  seem  to  be  formed  chiefly  by  putrefactive  changes 
within  the  intestine.  As  a normal  secretion  of  HC1  and  a normal 
motility  seem  to  be  the  chief  checks  upon  intestinal  putrefaction, 
it  can  be  readily  seen  that  in  cases  of  sub-  or  anacidity,  especially 
when  associated  with  an  impaired  motility,  the  putrefactive  changes 
in  the  intestine  are  increased  and  lead  to  an  increased  formation 
and  excretion  of  the  ethereal  or  combined  sulphates. 

In  expressing  an  opinion  as  to  the  condition  of  the  stomach 
from  the  amount  and  proportion  of  the  ethereal  sulphates,  care 
must  be  taken  to  exclude  any  intestinal  or  peritoneal  troubles, 
which  would,  by  themselves,  have  a tendency  to  increase  the 
amount  of  putrefaction  in  the  intestine. 

Under  normal  conditions  the  amount  of  the  total  sulphuric  acid 
is  from  two  to  three  gm.,  increasing  under  a meat  diet,  decreasing 
27 


4io 


THE  BLOOD  AND  URINE  IN  STOMACH  DISEASES. 


under  a vegetable  diet;  the  amount  of  ethereal  sulphuric  acid  being 
from  two  to  three  decigrams. 

The  average  normal  ratio  between  the  preformed  and  ethereal 
sulphuric  acid  is  as  ten  is  to  one,  the  proportion  being  stated,  as  a 
rule,  as  follows  : 

A : B : : io  : I 

In  cases  of  nervous  anacidity  with  periods  of  normal  secretion,  it 
may  assist  in  forming  an  opinion  as  to  the  severity  of  the  case 
to  find  a normal  ratio  of  the  sulphates.  In  a case  of  anacidity 
due  to  some  organic  trouble,  the  amount  of  ethereal  sulphates  will, 
as  a rule,  be  increased,  and  the  ratio,  instead  of  being  one  to  ten, 
may  be  increased  to  a marked  degree,  in  some  cases  reaching 
nearly  equal  amounts. 

Inaoxyl-sulphate  of  potassium  has,  for  the  most  part,  the  same 
significance  as  an  excessive  amount  of  ethereal  sulphates  or  an 
increase  in  their  ratio. 

This  chromogen  of  the  urine  is  a product  of  the  putrefactive  bac- 
teria of  the  intestinal  canal.  As  the  result  of  their  action  upon  the 
proteid  bodies  of  the  intestinal  canal,  indol  is  produced,  from  which, 
by  successive  oxidations,  indigo-blue  is  formed.  This,  by  combi- 
nation with  the  elements  of  sulphuric  acid  and  potassium,  forms 
the  substance,  indoxyl-sulphate  of  potassium,  or  indican. 

Quantitative  methods  for  determination  of  the  amount  of  indican 
have  recently  been  published,  but  for  practical  purposes  the  quali- 
tative color  test  is  sufficient : 5 c.c.  urine  are  mixed  with  5 c.c: 
pure  hydrochloric  acid,  then  3 c.c.  of  chloroform  are  added,  and  a 
small  drop  of  a solution  of  calcium  hypochlorite.  Then  the  mix- 
ture is  shaken;  the  indigo  formed  from  the  indican  by  oxidation 
passes,  into  the  chloroform.  If  the  first  drop  of  hypochlorite  of 
calcium  solution  causes  no  blue  coloring  of  the  chloroform,  a 
second  drop  is  added,  and  so  on  until  the  blue  color  is  no  longer 
intensified.  A strong  coloration  of  blue,  particularly  if  no  food 
has  been  taken  for  six  hours,  signifies  a pathological  increase  of 
the  percentage  of  indican. 

Owing  to  the  fact  that  certain  species  of  bacteria  may  be  present 
which  do  not  form  indol,  the  absence  or  presence  of  this  body  in 
normal  amounts  in  the  urine  does  not  prove  the  absence  of  putre- 
factive changes  in  the  intestinal  canal. 

Recent  observations  of  Charles  E.  Simon  (loc.  cit.)  show  that 
indican  is  present  in  excess  in  the  urine,  in  cases  of  marked  sub- 


UREA  AND  NITROGEN  IN  GASTRIC  DISEASES. 


41 


acidity,  anacidity,  gastric  carcinoma,  stenosis  of  the  pylorus  from 
any  cause,  and  also  in  cases  of  gastric  ulcer  with  hyperacidity. 

Careful  study  of  a series  of  cases  of  gastric  diseases  with  relation 
to  the  urine  seems  to  show  that  those  cases  of  gastric  diseases  with 
a marked  increase  in  the  amount  of  indican,  are  those  which  are 
associated  with  a lack  of  motor  power. 

It  must  be  said,  however,  that  the  ratio  of  the  ethereal  to  the 
preformed  sulphates  is  a better  index  to  amount  of  intestinal 
putrefaction. 

Indigo-red,  also  called  urrhodin,  has  essentially  the  same  signifi- 
cance as  indigo-blue  or  indican. 

Urea  and  Nitrogen . — The  nitrogen  eliminated  in  the  urine  may 
come  direct  from  the  food  ingested  or  from  the  nitrogenous  metab- 
olism of  the  body. 

In  general  it  may  be  said  that  those  diseases  which  are  attended 
with  impaired  digestion  of  proteid  foods  are  attended  with  a 
decrease  in  the  amount  of  nitrogen  eliminated  in  the  urine.  In  the 
cachexia  which  results  from  cancer  of  the  stomach,  the  elimination 
of  nitrogen  is  greater  than  is  the  elimination  in  simple  inanition  of 
the  same  degree  of  severity. 

There  is.at  present  no  explanation  of  this  fact,  unless  it  be  due  to 
some  product  of  the  tumor  itself  which  is  eliminated  by  the  urine, 
or  to  the  increased  metabolism  of  the  body  resulting  from  some 
product  of  the  neoplasm.  This  theory  as  to  the  production  of  some 
poisonous  substance  by  the  tumor  itself  is  supported  by  the  fact 
that  even  small  carcinomata,  situated  in  a part  of  the  body  where 
they  in  no  way  influence  the  bodily  functions,  give  rise  occasionally 
to  an  increase  in  the  elimination  of  nitrogen  by  the  urine. 

The  proportions  of  the  various  nitrogenous  bodies  in  the  urine, 
according  to  the  few  published  observations,  depart  considerably 
from  the  normal  in  carcinoma.  In  normal  urine  the  nitrogenous 
matter  is  divided  about  as  follows:  Urea,  96  per  cent.;  uric  acid, 
1.8  per  cent.;  ammonia,  1.2  per  cent.;  and  extractive  matters,  0.6 
per  cent,  to  0.8  per  cent. 

In  cases  of  carcinoma  examined  by  Topfer  the  proportions  were 
as  follows  : Urea  as  low  as  80  per  cent. ; uric  acid,  one  to  five  per 
cent. ; ammonia,  0.2  per  cent,  to  13  percent.,  and  extractive  matters 
13  per  cent,  to  23  per  cent.  Von  Noorden  also  found  the  ammonia 
increased  (10.2  per  cent,  to  13.9  per  cent.). 

It  is  thus  seen  that  in  these  cases  there  is  a relative  decrease  in 
the  amount  of  urea,  with  or  without  a rise  in  the  amount  of  uric 


412 


THE  BLOOD  AND  URINE  IN  STOMACH  DISEASES. 


acid,  and  a considerable  increase  in  the  relative  amounts  of  am 
monia  and  extractives. 

Acetone  and  Diacetic  Acid. — Acetone  and  diacetic  acid  occur 
in  the  urine  in  various  disturbances  of  the  digestive  tract  affecting 
both  the  stomach  and  intestines,  and,  according  to  Lorenz,  their 
occurrence  is  not  infrequent. 

Acetone  occurs  frequently  in  the  digestive  disturbances  of  chil- 
dren, and  is  by  some  authors  considered  as  the  cause  of  the  con- 
vulsions which  so  often  accompany  these  derangements. 

Acetone  is  found  in  the  urine  in  increased  amounts  in  cases  of 
inanition  and  in  cachectic  conditions,  and  to  this  fact  may  be 
assigned  the  occurrence  of  acetone  in  increased  amount  in  cases  of 
cancer  and  of  dilatation  of  the  stomach. 

In  general  it  may  be  said  that  the  increase  in  amount  of  acetone 
and  the  presence  of  diacetic  acid  indicate  an  increase  in  albumin 
disintegration  of  the  tissues.  When  diacetic  acid  is  found,  the 
prognosis  is  always  grave. 

Albumin. — Albumin  is  not  of  infrequent  occurrence  in  cases 
of  gastric  disturbances.  It  may  be  the  result  of  any  severe  stomach 
disease. 

Von  Noorden  found  albumin  with  relative  frequency  after  the 
onset  of  severe  gastric  pains,  such  as  occur  at  intervals  in  ulcer  of 
the  stomach,  and  also  after  profuse  hematemesis.  In  cases  of  can- 
cer of  the  stomach,  especially  in  the  later  stages,  albumin  is  found, 
either  regularly  or  temporarily,  in  a large  proportion  of  cases 
(see  section  on  Relations  of  Renal  to  Gastric  Diseases). 

Peptonuria. — The  question  as  to  the  occurrence  of  peptone  in 
the  urine — as  the  word  peptone  is  now  employed — is  not  definitely 
settled. 

Under  certain  conditions  the  urine  fails  to  react  to  the  ordinary 
tests  for  albumin,  such  as  Heller’s  nitric  acid  test,  Purdy’s  acetic 
acid  and  potassium  ferrocyanid  test,  and  the  boiling  test ; while  it 
certainly  contains  some  form  of  proteid  which  reacts  to  the  biuret 
test. 

The  question  whether  this  is  a secondary  albumose,  pure  pep- 
tone, or  a mixture  of  the  two,  is  of  minor  importance  from  a clinical 
standpoint.  Recent  investigations  show  that,  in  the  course  of 
absorption,  peptones  are  acted  upon  by  the  epithelium  of  the  gastro- 
intestinal tract  and  reconverted  into  the  coagulable  proteids. 

This  theory  renders  the  occurrence  of  peptonuria  in  the  course 
of  gastric  ulcer,  carcinoma  of  the  stomach,  erosions  of.the  mucosa. 


THE  DIAZO  REACTION. 


413 


and  ulceration  of  the  intestine  easy  of  comprehension.  The  occur- 
rence of  these  bodies  in  such  diseases  is  general  in  this  class  of 
cases,  though  many  observers  have  failed  to  demonstrate  them  in 
all  cases. 

Ferments. — Under  normal  conditions  the  urine  contains  a vari- 
able quantity  of  pepsin  and  rennin  ferment.  The  maximum  excre- 
tion of  pepsin  is  found  from  four  to  six  hours  after  meals.  Pepsin 
is  often  found  to  be  decreased  or  entirely  absent  in  the  urine  in 
cases  of  cancer  of  the  stomach,  and  would  probably  be  found,  in 
the  course  of  extended  observations,  to  vary  in  an  exact  ratio  to 
the  amount  of  pepsin  formed  by  the  stomach. 

Rennin  is  found  to  undergo  the  same  variations  as  pepsin,  and 
its  variations  have  the  same  clinical  significance. 

Ehrlich’s  Diazo  Reaction. — The  presence  or  absence  of  this 
color  reaction  of  the  urine  was  formerly  thought  to  be  of  great 
diagnostic  importance  for  the  recognition  and  differentiation  of 
typhoid  fever.  In  the  two  diseases  of  the  stomach  (acute  and 
phlegmonous  gastritis)  with  which,  in  its  earlier  stages,  typhoid 
fever  might  be  confounded,  it  would  be  of  great  value  were  its 
accuracy  undoubted.  Quite  an  extended  experience  with  this  test, 
used  on  all  patients  entering  the  hospital  for  several  months, 
showed  conclusively  that  it  could  not  be  relied  upon  as  a differen- 
tial test,  several  patients  giving  a typical  reaction  whose  history 
before,  during,  and  after  the  examination  excluded  typhoid  abso- 
lutely. On  the  other  hand,  even  in  typhoid  fever  the  reaction 
frequently  is  absent,  so  that  any  absolute  deductions  as  to  the  dis- 
ease from  this  reaction  are  apt  to  be  misleading.  Von  Jaksch 
looks  upon  the  reaction  as  merely  a poor  test  for  acetone. 


PART  THIRD. 


THE  GASTRIC  CLINIC. 


CHAPTER  I. 

ACUTE  GASTRITIS. 

Simple  Acute  Gastritis. — Phlegmonous  or  Purulent  Gastritis. — Sup- 
purative Inflammation  of  the  Gastric  Mucosa. — Abscess  of  the 
Stomach. — Infectious  Gastritis. — Gastritis  Mycotica  or 
Parasitaria. — Gastritis  Diphtherica  and  Crou- 
posa.  — Toxic  Gastritis.  — Gastritis  Venenata. 

Gastritis  is  a collective  or  generic  term  which  comprehends  all 
inflammatory  processes  of  the  stomach  proper,  including  the  so- 
called  catarrh  of  the  superficial  layer  of  columnar  epithelium,  the 
inflammation  of  the  glandular  parenchyma  and  interstitial  connec- 
tive tissue,  the  purulent  infiltration  of  the  submucosa  and  muscu- 
laris,  and  also  the  penetrating  excoriations  of  corrosive  poisons. 

It  is  natural  that  these  manifold  morbid  conditions  should  pre- 
sent considerable  variations  in  etiology  as  well  as  in  the  intensity 
of  the  symptoms.  It  is  almost  impossible  to  draw  a sharp  limit 
separating  the  simple  superficial  catarrhs  from  the  deeper,  pene- 
trating inflammations.  Penzoldt  suggests  the  line  between  mucosa 
and  submucosa. 

We  may  designate  as  simple  gastritis  that  inflammation  of  the 
gastric  mucosa  which  involves  not  only  the  superficial  columnar 
epithelium,  but,  as  a rule,  the  glandular  parenchyma.  This  con- 
dition may  occur  in  an  acute  and  in  a chronic  form,  and  undereach 
classification — the  acute  and  the  chronic  gastritis — one  may  arrange 
two  subdivisions  : (i)  the  primary  and  (2)  the  secondary  gastritis. 

We  therefore  have  (1)  the  acute,  simple,  primary  gastritis,  which 
occurs  as  the  original  disease  ; and  (2)  the  acute  secondary  gastritis 
known  as  the  gastritis  sympathica  acuta,  which  occurs  not  as  the 

414 


CLASSIFICATION  OF  FORMS  OF  GASTRITIS. 


4*5 


original  disease,  but  as  a frequent  accompaniment  of  numerous 
acute  febrile  disorders.  All  the  exanthematous  infectious  diseases — 
measles,  scarlatina,  variola,  typhus  and  typhoid  fevers,  puerperal 
fever,  pyemia,  dysentery,  croup,  and  diphtheria — are  known  to  effect 
pathological  changes  in  the  gastric  mucosa  directly,  or  to  influence 
it  detrimentally  by  reflex  nervous  action  (Hoppe-Seyler,  “Allge- 
meine  Biologie,”  1877,  p.  242). 

There  is  a very  plausible  desire  evident  in  some  recent  works 
on  the  subject  to  avoid  the  name  stomach  or  gastric  catarrh , because 
the  word  catarrh  has  reference  to  a superficial  inflammation,  but  in 
gastritis  we  are  dealing  also  with  parenchymatous  inflammation. 
Penzoldt  uses  the  expression  “ simple  gastritis  ” for  an  inflammation 
reaching  no  deeper  than  the  submucosa  (< gastritis  simplex) ; for  the 
penetrating  results  of  suppurative  or  purulent  inflammation  he  uses 
the  term  “ grave  gastritis  ” [gastritis  gravis).  He  does  not  favor 
the  terms  “ toxic  ” and  “ infective  gastritis,”  for  to  a certain  extent 
all  forms  of  this  disease  are  toxic  and  infective,  and  in  his  book, 
“ Specielle  Therapie  innerer  Krankheiten,”  vol.  iv,  page  320,  he  dis- 
cusses only  (1)  simple  and  grave  acute  gastritis,  (2)  chronic  gastritis, 
and  (3)  purulent  or  suppurative  gastritis.  Fleischer  (“Specielle 
Therap.  u.  Pathol,  d.  Magen-  u.  Darmkr.,”  S.  793)  describes  (1)  sim- 
ple acute,  (2)  secondary  or  sympathetic  acute,  (3)  phlegmonous  or 
purulent,  (4)  toxic,  (5)  diphtheric,  croupous,  mycotic,  parasitic,  (6) 
chronic  gastritis.  Excepting  those  forms  mentioned  by  Fleischer 
under  group  5,  Boas  describes  all  of  these  in  separate  chapters. 

Ewald  mentions  and  describes  all  of  these  forms,  and  subdivides 
the  suppurative  inflammation  (the  gastritis  plilegmonosa  purulenta ) 
into  an  idiopathic  primary  and  a metastatic  secondary  form.  Sidney 
Martin’s  treatise  on  “ The  Organic  and  Functional  Diseases  of  the 
Stomach”  deals  with  the  symptomatology,  pathology,  and  treatment 
of  acute  and  chronic  gastritis  in  one  chapter  (Chap,  vm),  and  then 
goes  on  to  speak  of  toxic  and  infective  gastritis  in  the  next  chapter 
(Chap.  ix).  Albert  Mathieu  (“  Therapeutique  des  Maladies  de  l’es- 
tomac,”  3me  Edition,  Paris,  1898)  briefly  mentions  acute,  chronic, 
and  atrophic  gastritis,  and  the  varying  amount  of  mucus  and  acid 
accompanying  these  diseases ; none  of  the  other  forms  are  re- 
ferred to. 

Rosenheim  (“  Pathol,  u.  Therap.  d.  Krankh.  des  Verdauungs- 
apparates,”  p.  99)  describes  gastritis  as  acute,  simple,  phlegmonous, 
toxic,  diphtheric,  and  chronic.  Einhorn  approaches  the  simple 
classification  of  Penzoldt,  and  divides  acute  gastritis  into  (1)  simple, 


4i  6 


ACUTE  GASTRITIS. 


(2)  phlegmonous,  and  (3)  toxic,  and  then  proceeds  to  the  considera- 
tion of  chronic  gastritis. 

Alois  Pick  describes  (1)  acute,  (2)  infectious,  (3)  phlegmonous, 
(4)  toxic,  (5)  parasitic,  and  (6)  chronic  gastritis  (“  Vorlesungen  fiber 
Magen-  u.  Darmkrankheiten,”  S.  73);  and  Fleiner  (“  Lehrbuch  d. 
Krankheiten  d.  Verdauungsorgane  ”)  gives  an  account  of  (1)  gas- 
tritis catarrhalis  acuta,  for  which  he  also  uses  the  name  gastricismus  ; 

(2)  gastritis  toxica  ; (3)  interstitial  suppurative  gastritis,  stomach  ab- 
scess and  stomach  phlegmone,  or  gastritis  phlegmonosa  or  inter- 
stitialis,  or  submucosa  purulenta,  or  also  linitis  suppurativa;  (4) 
mycotic  gastric  inflammations;  (5)  chronic  gastritis. 

Osier,  in  his  new  “ Principles  and  Practice  of  Medicine,”  pages 
348  and  359,  considers  (1)  acute  simple,  (2)  phlegmonous  or  acute 
suppurative,  (3)  toxic,  (4)  diphtheric  or  membranous,  (5)  mycotic 
or  parasitic,  and  (6)  chronic  gastritis.  Under  the  last  he  gives  a 
special  paragraph  to  the  chronic  forms  with  extreme  connective- 
tissue  proliferation  and  increase  in  thickness  of  the  submucosa  and 
muscularis,  under  the  name  of  sclerotic  gastritis. 

These  references  are  sufficient  to  demonstrate  the  discrepancy 
existing  in  later  works  concerning  the  separate  and  distinct  recog- 
nition of  the  various  forms  of  this  disease,  and  that  a more  uniform 
classification  would  be  desirable. 

In  accordance  with  Penzoldt,  this  treatise  will  describe  only  (1) 
simple  acute  gastritis,  (2)  simple  chronic  gastritis,  and,  separately, 

(3)  the  forms  in  which  the  element  of  pus  formation  is  a factor — the 
suppurative  gastric  inflammations ; and  in  a supplement  the  forms 
due  to  toxic  or  corrosive  agents,  and  the  remaining  very  rare  varie- 
ties, may  be  appropriately  described. 

Nature  and  Concept. — One  should  be  very  careful  not  to  diagnose 
every  temporary,  transient  gastric  disturbance  as  acute  gastritis, 
nor  a prolonged  loss  of  appetite,  with  eructations,  coated  tongue, 
and  no  other  demonstrable  signs  and  symptoms,  as  chronic  gas- 
tritis— this  is,  in  the  majority  of  such  cases,  neither  justifiable  nor 
conducive  to  the  scientific  development  of  diagnosis.  It  is  incon- 
ceivable that  all  the  functional  and  anatomical  changes  which  one 
is  accustomed  to  find  in  acute  inflammations  in  other  tissues  should 
really  be  present  in  every  brief  digestive  disturbance  after  dietetic 
errors,  alcoholic  abuse,  etc. 

We  could  not  designate  a brief  irritation  of  the  nose,  with 
sneezing  and  secretion  of  mucus,  lasting  several  hours,  as  nasal 
catarrh.  By  catarrh  of  the  air-passages  we  understand  a more 


NATURE  AND  CONCEPT  OF  GASTRITIS. 


417 


lasting  affection,  with  a somewhat  typical  course,  and  more  per- 
manent changes,  of  both  a structural  and  functional  nature,  in 
the  mucosa.  Indeed,  Sydney  Martin  very  appropriately  considers 
these  functional,  lighter  forms  of  gastric  disturbance  in  separate 
chapters,  and  classifies  them  under  (1)  gastric  irritation  and  (2)  gas- 
tric insufficiency.  Functional  disorders,  then,  are  irregularities  of 
gastric  motility,  absorption,  and  secretion,  and  also  of  the  innerva- 
tion and  vascular  supply,  in  which  organic  diseases  of  the  stomach 
— ulcer,  gastritis,  neoplasm,  etc. — are  absent.  It  can  not  with  cer- 
tainty be  stated  that  all  histological  changes  are  absent  in  functional 
disorders  ; at  least  not  in  functional  disorders  of  secretion.  We 
have  become  convinced  of  certain  changes  in  the  acid  and  ferment 
cells  that  are  apparently  quite  constant. 

Ever  since  Beaumont’s  pioneer  observations  it  has  been  known 
that  every  severe  inflammatory  irritation  of  the  gastric  mucosa 
produces  an  alteration  in  the  gastric  secretion,  the  quantity  and 
effectiveness  of  which  is  much  reduced;  it  is  known,  furthermore, 
that  the  impairment  of  one  function  of  the  stomach,  as  a rule, 
rapidly  involves  that  of  another.  The  inner  lining  of  the  stomach 
can  not,  in  the  true  anatomical  meaning  of  the  word,  be  called  a 
mucous  membrane,  because  it  is  devoid  of  one  of  the  essential  attri- 
butes of  a mucous  membrane — the  mucous  glands.  The  mucus  of 
a normal  stomach  is  surprisingly  small  in  amount  (see  chapter  on 
Examination  of  Stomach  Contents),  and  owes  its  origin  not  to 
glands,  but  to  mucoid  degeneration  of  the  superficial  columnar 
epithelial  cells. 

As  this  cylindrical  epithelium  continues  down  into  the  alveoli 
of  the  peptic  tubules  without  any  distinct  border  line,  all  irritants 
striking  the  former  must  of  necessity  affect  the  parietal  or  border 
cells  as  well  as  the  chief  cells  of  the  gland-duct.  It  is  characteris- 
tic of  the  pathology  of  gastric  digestion  that  impairment  of  one 
important  function,  or  rather  of  one  of  the  many  physiological  pro- 
cesses of  which  the  digestive  act  is  composed,  soon  creates  sympa- 
thetic disturbance  in  the  remaining  functions,  so  that  the  clinical 
picture  of  an  acute  or  a chronic  gastritis  is  that  of  a combination 
of  disturbances. 

It  is  not  established,  nor  very  essential,  which  function  suffers 
first,  but  probably  in  most  cases  a derangement  of  secretion  or  of 
motility  starts  the  morbid  series,  and  the  remaining  functions  follow 
in  the  affection.  For  example:  If  by  ingestion  of  food  which  is 
already  in  a state  of  fermentation  an  acute  gastritis  has  been  in- 


ACUTE  GASTRITIS. 


duced,  the  reduction  in  the  amount  of  hydrochloric  acid  produces 
a hindrance,  not  only  in  the  normal  chemistry  of  the  stomach,  but  re- 
sorption and  motility  are  also  very  soon  retarded.  This  pronounced 
subacidity  has  in  its  consequence  an  imperfect  digestion  of  the  pro- 
teids,  so  that  very  small  amounts  of  acid  albumin  and  hemialbumose 
are  detectable  in  the  vomit,  and  peptone  is  found  in  traces  only.  A 
further  step,  then,  is  that  these  undigested  proteids  continue  to 
remain  in  the  stomach  longer  than  with  normal  proteolysis.  This 
means  a much  more  prolonged  burdening  of  the  gastric  walls;  the 
stomach  does  not  gain  sufficient  rest  in  which  to  prepare  itself  for 
the  demands  of  the  following  meal;  the  distention  by  the  weight 
of  the  food  lasts  longer. 

On  the  other  hand,  much  more  of  the  carbohydrates  will  in  this 
subacidity  be  converted  into  soluble  starch,  maltose,  and  dextrose, 
than  with  a normal  secretion  of  hydrochloric  acid.  With  the  pro- 
gressing stagnation  and  putrefaction  of  proteids,  these  products  of 
starch  inversion  mean  more  ready  food  for  bacteria,  which  are 
constantly  introduced  with  the  saliva,  and,  finding  in  the  moisture 
and  suitable  temperature  of  the  gastric  contents  congenial  condi- 
tions for  their  development,  the  danger  of  progressive  decomposi- 
tion is  very  great.  The  toxic  products  of  this  carbohydrate  and 
proteid  decomposition  are  irritants  to  the  mucosa,  and  increase  the 
already  existing  inflammation. 

When  this  inflammation  has  reached  a certain  stage,  an  inflam- 
matory edema  of  the  muscular  layer  sets  in,  effectually  destroying 
the  motility,  and  simultaneously  (as  in  most  all  serous  and  mucous 
inflammations)  an  alkaline  transudate  exudes  into  the  mucosa,  neu- 
tralizing the  last  vestige  of  hydrochloric  acid  that  may  yet  be 
secreted.  Lactic,  butyric,  and  acetic  acid  are  evolved  from  the  fer- 
menting carbohydrates,  and,  further  on,  H2C03  and  H. 

When  these  gases  begin  to  expand,  and  the  already  impaired 
motility  can  not  expel  them  by  eructation,  the  stomach  is  still 
further  distended.  The  normal  hydrochloric  acid  not  only  acts  as 
an  antiseptic  and  antifermentative,  but,  as  we  know,  undoubtedly 
brings  about  energetic  peristalsis,  which  effects  a thorough  mixing 
of  the  ingesta,  and,  frequently,  repeated  contact  and  friction  with 
those  portions  of  the  secretory  membrane  whose  glands  produce 
the  hydrochloric  acid  and  ferments.  This  mixing  and  triturating 
peristalsis  is  at  the  same  time  a most  essential  stimulus  to  absorp- 
tion, and  eventually  effects  the  timely  expulsion  of  the  chyme  into 
the  duodenum. 


ETIOLOGY. 


419 


With  impaired  motility,  therefore,  the  food  masses  remain  too 
long  in  one  and  the  same  place.  An  intimate  contact  of  the  in- 
gesta  with  the  membrane,  as  is  produced  by  healthy  peristalsis,  is 
essential  for  normal  stimulation  to  continued  secretion  ; hence,  the 
secretion  of  the  oxyntic  and  ferment  cells,  already  damaged  by  in- 
flammatory infiltration,  soon  ceases  entirely.  Resorption  is  not 
only  impaired  by  absence  of  intimate  contact  with  ingesta,  but  by 
the  fact  that  the  epithelial  surface  is,  in  the  various  forms  of  gas- 
tritis, covered  with  a tough,  glassy  mucus,  epithelial  detritus,  and 
sometimes  pus.  In  addition  to  this,  one  must  not  overlook  the 
element  of  the  effects  of  the  inflammatory  changes  on  the  rate, 
tonicity,  quality,  and  quantity  of  the  circulation  on  all  of  the  gastric 
functions. 

The  damaging  effects  of  inflammation  might  be  partly  made  up 
again  by  a healthy  peristalsis,  but,  as  this  is  not  present,  resorption 
and  secretion  are  inhibited.  The  suspension  of  the  resorption  must 
be  looked  upon  as  an  act  of  self-protection,  as  there  are  nothing 
but  poisons  to  absorb  in  these  conditions.  There  is,  fortunately, 
no  excessive  formation  of  peptone,  as  this  is  prevented  by  the 
subacidity.  We  say  “ fortunately,”  because  it  would  simply  be  food 
for  bacteria.  So  it  is  evident  that,  in  an  acute  gastritis,  there  are 
numerous  concurrent  deleterious  elements  and  changes  which 
are  essentially  similar  to  those  of  most  light  and  severe  gastric  in- 
flammations. 

The  clinical  picture  is  a very  manifold  one,  as  in  the  individual 
cases  one  may  observe  first  one  and  then  another  function  that  is 
most  seriously  damaged.  It  is  natural  to  observe  exceptions  from 
the  rule:  thus,  in  prolonged  anacidity  we  may  find  cases  in  which 
the  motility  is  unimpaired,  which,  of  course,  favors  intestinal  diges- 
tion by  timely  evacuation  of  the  chyme,  so  that  even  the  symptoms 
of  dyspepsia  may  be  lacking. 

Etiology. — In  the  majority  of  cases  acute  simple  gastritis  is 
caused  by  errors  in  diet.  Irritation  may  be  caused  by  quantity  as 
well  as  by  quality  of  the  food.  Decomposed  articles  of  liquid  or  solid 
nature  will  set  up  inflammation  through  the  bacteria  and  toxins 
they  contain.  These  germs  must  not  be  thought  to  invade  the 
mucosa  proper  in  all  cases;  they  exert  effects  by  their  chemical 
products.  Ewald  ( loc . cit.)  says  he  has  never  found  bacteria  in  the 
gastric  tissues  in  these  cases.  Spoiled  or  decomposed  meat,  fish, 
or  vegetables,  cheese,  wine,  cider,  or  beer  that  has  not  completed 


420 


ACUTE  GASTRITIS. 


its  fermentation,  infected  milk,  and  impure  pond  water  have  been 
known  to  produce  severe  acute  gastritis. 

Excessive  indulgence  in  perfectly  healthy  food  can  provoke  the 
trouble,  not  only  by  the  mechanical  distention  and  irritation  which 
are  caused  thereby,  but  by  the  inability  of  the  motive  power  to 
move  the  ingesta  about  and  to  expel  them  into  the  duodenum,  and 
also  by  the  deficiency  in  thq  secretion  of  gastric  juice,  which  may 
be  able  to  digest  a normal  but  not  an  excessive  amount  of  food. 
The  amount  that  can  be  digested  under  normal  conditions  without 
causing  acute  gastritis  will  naturally  vary  considerably  in  different 
individuals. 

Chemical  Causes. — Among  these  may  be  mentioned  quinin  salts 
in  large  doses ; all  metallic  salts,  particularly  those  of  copper,  anti- 
mony, arsenic,  lead,  gold,  mercury,  and  silver ; acids  and  alkalies, 
unless  properly  diluted. 

We  have  observed  an  acute  gastritis  follow  the  use  of  two  gm. 
of  sodium  salicylate  three  times  daily,  and  feel  convinced  that  iodid 
of  potassium,  if  not  given  properly  mixed  with  food  (right  after 
meals),  may  lead  up  to  gastritis.  The  various  drugs  used  inter- 
nally for  gonorrhea — cubebs,  copaiba,  and  the  oil  of  sandalwood — 
may,  in  susceptible  individuals,  bring  about,  after  long  use,  a condi- 
tion of  the  gastric  mucosa  in  which  acute  gastritis  is  readily  set  up. 

Psychic  Causes. — It  is  said  that  grief,  sorrow,  terror,  anger,  and 
even  excessive  joy  (?),  have  been  observed  to  produce  gastritis. 
Sexual  excesses,  particularly  in  neurasthenics,  are  on  record  as 
causes. 

Thermic  Causes. — Large  quantities  of  very  cold  or  very  hot  liquids, 
particularly  the  former,  can  produce  the  disease  when  taken  in 
rapidly  when  the  body  is  in  an  overheated  state. 

Mechanical  Causes. — It  is  possible  that  pieces  of  fish-bone,  egg 
shells  or  oyster  shells,  or  fruit  seeds,  if  accidentally  ingested,  may,  by 
mechanically  scratching  or  bruising  the  mucosa,  cause  a gastritis. 
We  had  occasion  to  observe  a singular  case  of  this  disease  in  a 
professional  base-ball  player,  caused  by  a blow  from  a base-ball 
pitched  with  great  speed.  The  bruise  extended  from  the  xiphoid 
cartilage  to  the  left  hypochondriac  region.  The  player  was  knocked 
senseless,  and,  after  partial  recovery,  vomited  a meal,  which  he  had 
taken  two  hours  before,  mixed  with  blood  and  much  mucus;  later 
on  he  vomited  some  milk  that  was  given  him,  and  on  being  tested, 
this  vomit  was  alkaline. 

The  pain  was  so  severe  that  morphin  had  to  be  injected  hypo- 


ETIOLOGY  OF  GASTRITIS. 


421 


dermically,  and  food  was  kept  out  of  his  stomach  altogether  for 
three  days,  during  which  period  he  was  fed  by  Boas’  nutrient 
enema.  The  attack  lasted  two  weeks,  and  the  patient  made  a 
perfect  recovery,  free  HC1  reappearing  at  the  end  of  the  first  week. 

Predisposition. — Manassein  has  shown  that  fever  produced  experi- 
mentally in  dogs  which  he  had  made  anemic  by  depriving  them  of 
much  blood,  caused  considerable  suppression  of  the  secretion  of 
hydrochloric  acid.  Kussmaul,  Uffelmann,  Leube,  and  von  den 
Velden  have  confirmed  this  subacidity  in  cases  of  fever  in  the 
human  being.  It  is  not  surprising,  therefore,  if  we  find  acute  gas- 
tritis developing  in  convalescents  from  severe  diseases;  also  in 
tuberculous,  cancerous,  and  syphilitic  patients.  Functional  gastric 
disturbances  predispose  to  acute  gastritis  as  well  as  preexisting 
or  concomitant  diseases  of  the  heart,  lungs,  liver,  and  kidneys. 
Ewald  believes  in  hereditary  predisposition  to  gastritis,  as  some 
families  show  numerous  cases  of  the  trouble  in  spite  of  the  best 
care  they  take  of  their  stomachs. 

Idiosyncrasy . — It  is  a very  perplexing  fact  that  some  persons  in 
good  health  acquire  acute  gastritis  after  eating  certain  articles  of 
food.  While  the  author  was  physician  in  charge  of  Bay  View 
Hospital,  Baltimore,  he  had  a colleague,  a perfectly  robust,  vigorous 
man,  not  at  all  neurasthenic,  who  developed  the  disease  every  time 
he  ate  oysters.  He  could  not  be  induced  to  eat  them  after  he  had 
established  the  casual  relation,  but  convinced  us  by  consenting  to 
an  experiment. 

Influence  of  Sex  and  Age. — Acute  gastritis  occurs  more  frequently 
in  men  than  in  women  ; of  60  cases  observed  by  the  author,  of 
which  records  were  taken,  16  occurred  in  females  and  44  in  males. 
Females  are  more  frequently  attacked  during  menstruation  and 
puerperium.  Old  persons  and  very  young,  feeble  children  are  more 
likely  to  be  attacked  than  those  in  middle  age.  In  nursing  infants 
a very  slight  change  in  the  milk  may  be  enough  to  cause  it.  Ac- 
cording to  Booker,  of  Baltimore,  acute  gastritis  in  infants  is  accom- 
panied by  prolongation  of  the  time  that  the  milk  is  retained  in  the 
stomach,  at  times  over  five  hours.  The  gastric  contents  occa- 
sionally show  epithelial  and  pus  cells. 

Rotch  (“Pediatrics,”  p.  854)  holds  that  the  acute  form  is  more 
common  in  infants,  and  that  the  chronic  form,  while  it  does  occur 
in  them,  is  more  frequent  in  children  toward  puberty.  The  frequent 
attacks  of  gastritis  occurring  during  the  hot  summer  months  are 
undoubtedly  largely  due  to  the  consumption  of  unripe  fruit.  Bou- 


422 


ACUTE  GASTRITIS. 


veret,  however  (“Traite  des  Maladies  de  1’  Estomac,”  p.  384,  Paris, 
1893),  attributes  them  to  the  abusive  consumption  of  water.  Ac- 
cording to  Pick,  the  disease  has  been  observed  to  develop  after 
taking  cold. 

The  effect  of  fever  on  the  secretions  of  the  stomach  is  not  al- 
ways evident.  Edinger  found  the  secretion  of  hydrochloric  acid 
normal  in  five  cases  of  fever ; having  examined  hectic,  recurrent, 
intermittent,  and  typhoid  fever  patients  (L.  Edinger,  “ Zur  Physiol, 
u.  Path.  d.  Magens,”  “ Deutsch.  Archiv  f.  klin.  Medizin,”  Bd.  xxix, 
S.  555).  G.  Klemperer  (“  Dyspepsie  d.  Phthisiker,”  “Berlin,  klin. 
Wochenschr.,”  i889)and  Schetty  (“  Untersuch.  u.  Magenfunction. 
bei  Phthisis,”  “ Deutsch.  Archiv  f.  klin.  Med.,”  Bd.  xliv,  S.  516) 
confirm  the  finding  of  Edinger.  Ewald  (loc.  cit .,  p.  301)  found  almost 
normal  digestive  power  in  a case  of  facial  erysipelas.  From  these 
studies  it  is  plain  that  not  in  all  cases  of  secondary  acute  gastritis 
can  we  attribute  the  stomach  affection  to  the  functional  disturbances 
which  the  primary  disease  produces ; for,  in  the  first  place,  these  may 
be  entirely  absent:  secondly,  the  frequency  of  the  gastritis  is  not 
at  all  dependent  upon  the  height  or  intensity  of  the  fever;  thirdly, 
the  secondary  sympathetic  gastritis  may  set  in  concomitant  with 
the  fever  or  even  before  it,  ushering  in  the  main  infectious  symp- 
toms as  a prodromal  affection. 

The  secondary  sympathetic  gastritis  is  therefore  more  likely  to  be 
originated  by  localization  of  the  specific,  organized  disease-pro- 
ducers of  the  fundamental  disturbance — in  the  mucosa  of  the  stom- 
ach, or  even  by  the  toxic  metabolic  products  of  these  microbes. 
In  addition  to  the  infectious  diseases  already  mentioned,  this  sym- 
pathetic form  may  be  a consequence  of  diseases  of  the  heart,  lungs, 
kidneys,  and  liver,  causing  venous,  passive  congestion  of  the  gastric 
mucosa  (Stauungskatarrh).  In  cardiac  and  nephritic  diseases  the 
passive  gastric  congestion  may  be  relieved  by  appropriate  medica- 
tion directed  to  the  fundamental  disorder — i.  e .,  the  use  of  digitalis, 
strychnin,  and  diuretics. 

Pathological  Histology. — According  to  Orth  (“Specielle  patho- 
log.  Anatomie,”  Bd.  1,  S.  702),  our  knowledge  concerning  the 
pathological  histology  of  the  exudative  inflammation  of  the  stomach 
is  very  limited  ; in  the  first  place,  because  uncomplicated  simple 
acute  gastritis  rarely  ends  in  death,  and,  secondly,  because  post- 
mortem changes  and  autodigestion  exert  a most  disturbing  and 
disfiguring  effect,  particularly  in  these  superficial  diseases.  In  a 
case  which  M.  Laboulbene  observed, — twenty-four  hours  after  death 


PATHOLOGICAL  HISTOLOGY. 


423 


by  rupture  of  an  aneurysm, — there  existed  hyperemia  of  the  mucosa, 
localized  ecchymoses,  swelling  of  the  mucous  alveoli,  and  augmen- 
tation of  the  mucus. 

Delafield  and  Prudden  give  essentially  these  same  changes 
(“  Text-book  on  Pathology  ”),  also  Ziegler  (“  Lehrbuch  d.  all g.  und 
spec,  patliol.  Anat.,”  Jena,  1890),  which  may  be  summarized  as 
follows  : The  surface  of  the  mucosa  is  covered  by  a tough,  glassy, 
cloudy,  or  reddish  mucus.  The  mucosa  itself  is  injected,  swollen, 
and  characterized  by  a hyperemia,  which  is  limited  generally  to 
the  pyloric  region,  and  rarely  extends  to  the  entire  mucosa.  Red 
spots,  either  well  circumscribed  or  diffuse,  are  very  evident,  and 
ecchymoses  are  scattered  throughout  the  mucous  membrane. 
Larger  suggillations  occur  also,  but  are  rare. 

The  histological  changes  are,  by  most  German  authors,  said  to  be 
out  of  proportion  to  the  degree  and  intensity  of  the  symptoms 
(Fleiner,  loc.  cit.,  p.  233):  that  is  to  say,  they  expect  a greater 
extension  and  degree  of  inflammation  to  correspond  to  the  severity 
of  the  symptoms,  and  are  surprised  not  to  find  it.  Fischl  asserts 
this  particularly  of  the  gastroenteritis  of  children  (Fleiner,  loc.  cit. , 
p.  233).  However,  the  exact  and  very  instructive  investigations  of 
William  D.  Booker  (“  Johns  Hopkins  Hospital  Reports,”  vol.  vi, 
pp.  159-258,  plates  xvi  to  xxi)  show  quite  the  contrary.  Booker’s 
researches  demonstrate  destruction  of  the  superficial  epithelium  in 
parts  and  infiltration  of  the  mucosa  with  polynuclear  leukocytes. 
Many  oxyntic  cells  are  without  nuclei,  and  show  only  loose, 
granular  protoplasm  remaining.  Epithelial  cells  and  fragments  of 
glands  are  collected  in  heaps  on  the  surface,  but  not  to  so  marked 
an  extent  as  in  the  intestine  (Booker,  loc.  cit.,  p.  25 1).  In  a few 
cases  of  acute  gastritis  associated  with  enteritis  he  found  the 
entire  gastric  mucosa  destroyed.  Bacteriological  cultures  were 
made  in  23  cases;  in  19  the  colonies  were  very  numerous,  in  two 
moderately  numerous,  and  in  two  there  were  no  colonies  of  bac- 
teria, but  many  of  o’idium  albicans.  Tabulated,  his  results  appear 
as  follows : 


Predom- 

inant. 

Numer- 

ous. 

Few. 

Absent. 

Pure 

Culture. 

Oidium  albicans,  .... 

Cases. 

3 

Cases. 

3 

Cases. 

I 

Cases. 

14 

Cases. 

0 

Bacillus  coli  communis,  . . . 

5 

8 

4 

6 

O 

Bacillus  lactis  aerogenes,  . . . 

7 

2 

5 

7 

2 

Proteus  vulgaris 

3 

0 

2 

18 

O 

Streptococci, 

0 

4 

3 

16 

O 

424 


ACUTE  GASTRITIS. 


Booker,  like  A.  Czerny  and  P.  Moser,  concludes  that  the  gastro- 
enteritis of  children  is  a general  infectious  disease,  with  auto- 
intoxication, in  which  other  organs  of  the  body  participate,  either 
as  a result  of  an  invasion  of  the  body  by  bacteria,  as  is  often  the  case 
with  the  lungs,  or  from  the  effects  of  poisons  absorbed  from  the 
gastrointestinal  canal.  This  infantile  digestive  affection  is  un- 
doubtedly a more  severe  and  acute  disease  than  any  gastritis  that 
occurs  in  adults,  but  its  study  certainly  aids  our  knowledge  of  the 
allied  pathological  states  of  adults.  There  are  a number  of  inflam- 
mations, occurring  in  adults  as  well  as  children,  that  are  followed  or 
preceded  by  digestive  disorders,  the  etiology  of  which  is  much 
cleared  up  by  the  work  of  the  authors  above  mentioned.  We  refer 
to  the  obscure  attacks  of  parotitis,  tonsillitis,  and  pharyngeal  abscess 
sometimes  following  well-defined  gastric  ulcer,  and  to  the  disorders 
of  the  heart  and  nervous  system  concomitant  or  succeeding  gastro- 
intestinal lesions. 

These  secondary  attacks  at  times  may  be  autointoxications ; 
then,  again,  they  show  the  unmistakable  signs  of  direct  infection 
secondary  to  digestive  trouble,  for  in  the  superficial  epithelium  is 
to  be  found  the  chief  protection  of  the  mucosa  against  the  invasion 
of  bacteria.  When  the  epithelium  is  well  preserved,  bacteria  are 
not  found  in  the  mucosa  beneath,  whereas  they  may  be  seen 
entering  it  where  the  epithelium  has  been  lost  or  injured  (Booker, 
loc.  cit.).  The  first  step  in  the  pathological  process  is  probably  an 
injury  to  the  epithelium  from  abnormal  or  excessive  fermentation 
in  the  stomach,  or  from  toxic  products  of  bacteria  and  the  many 
other  conditions  that  have  already  been  described.  (See  Plate  VI.) 
To  prevent  the  effects  of  autodigestion  and  postmortem  digestion 
on  the  gastric  mucosa,  Ewald  suggested  washing  out  the  stomach 
immediately  after  death  and  filling  it  with  alcohol.  This  may  in 
future  save  a large  number  of  futile  investigations.  Formerly  one 
depended  largely  on  the  studies  of  gastritis  experimentally  pro- 
duced in  animals  for  recognition  of  the  pathological  changes.  Thus, 
Ebstein  produced  gastritis  by  injecting  absolute  alcohol  into  the 
stomachs  of  dogs. 

Ewald  and  Ebstein  describe  a granular,  cloudy  swelling  in  the 
superficial  epithelium.  While  there  is  no  differentiation  possible 
between  the  parietal  or  oxyntic  and  the  central,  chief,  or  ferment 
cells,  both  varieties  are  either  swollen  or  contracted,  granular, 
cloudy,  and  with  very  indistinct  nuclei.  Between  the  different  epi- 
thelia  and  in  the  interglandular  connective  tissue  there  are  consid- 


SYMPTOMS  AND  COURSE. 


425 


erable  masses  of  round  cells.  In  these,  as  well  as  in  the  emigrated 
leukocytes  and  the  cylindrical,  superficial  cells,  numerous  karyoki- 
netic  figures  are  very  evident,  and  were  claimed  by  Sachs  (loc. 
cit.)  to  be  characteristic  of  acute  gastritis,  but  this  is  denied  by 
Ewald. 

Beaumont  [loc.  cit.)  gives  some  strikingly  correct  descriptions  of 
the  conditions  observed  in  the  stomach  of  his  patient,  Alexis  St. 
Martin,  when  it  was  acutely  inflamed  in  consequence  of  overfeeding 
or  of  abuse  of  alcoholic  beverages.  He  states  that  the  mucosa, 
even  when  no  digestion  was  going  on,  was  mostly  very  hyperemic, 
swollen,  and  covered  with  a thick  layer  of  tough  mucus.  After 
ingestion  the  food  was  not  digested,  but  remained  undigested  in  the 
stomach  from  four  to  six  hours.  The  secretion,  which  was  much 
diminished,  was  only  rarely  faintly  acid  ; mostly  it  was  found  alkaline 
or  neutral.  After  a few  days  the  mucus  became  still  thicker,  but  the 
hyperemia  grew  less.  This  and  the  following  account  of  Beaumont 
on  the  state  of  the  mucosa  in  gastritis — “ its  surface  was  marked  with 
numerous  white  spots  and  vesicles  like  coagulated  lymph,  between 
which  were  very  dark  red  spots  ” — are  considered  by  Fleiner  (p.  232, 
loc.  cit)  and  Fleischer  (p.  802,  loc.  cit.)  as  unintelligible  in  the  light 
of  our  present  knowledge.  These  remarks  of  the  American  pioneer 
of  gastric  pathology,  considered  in  that  very  light,  impress  us  as 
a surprisingly  acute  and  exact  description  of  the  mucosa  in  certain 
types  of  gastritis,  and  inspire  the  latter-day  student  with  respect  for 
the  powers  of  observation  in  the  man.  Fisch  (“  Fleiner’s  Lehrbuch,” 
p.  233),  after  what  he  considers  very  detailed  and  careful  investiga- 
tions, differentiates  three  forms  of  gastritis  in  children  : (1)  An 
interstitial  gastritis,  which  he  supposes  to  start  from  the  connective 
tissue;  (2)  a parenchymatous  inflammation  having  its  seat  in  the 
glandular  tubes  ; and  (3)  a combined  parenchymatous  interstitial 
inflammation.  The  interstitial  affection  may  be  interglandular  or 
submucous. 

Symptomatology  and  Course. — Immediately  after  gross  in- 
sults to  the  gastric  physiology,  characteristic  signs  and  symptoms 
appear.  These  are  fullness  in  the  epigastrium,  which  is  distended 
and  painful  on  pressure ; eructation,  which  at  first  may  bring  relief, 
later  on  increases  so  as  to  be  a great  annoyance  ; thirst,  anorexia, 
and  even  disgust  for  food,  may  accompany  this.  The  tongue  is 
often  thickly  covered  with  a tenacious  white  fur,  retaining  the  im- 
pressions of  the  teeth,  and  colored  by  food  or  drugs  ; the  breath  is 
offensive.  The  secretion  of  saliva  is  augmented,  the  pulse  small 
28 


426 


ACUTE  GASTRITIS. 


and  rapid.  There  may  be  painful  contractions  of  the  esophageal 
musculature,  spasmodic  yawning,  and  herpes  labialis.  A burning 
pain  in  the  epigastrium,  which  may  radiate  to  the  hypochondriac 
region,  arises  under  the  sternum  (pyrosis)  toward  the  throat,  caus- 
ing burning  all  the  way,  and  sometimes  raising  sour  or  bitter 
stomach  contents.  As  water  and  other  liquids  diminish  the  gastric 
burning,  the  patients  usually  show  great  thirst.  The  appetite,  how- 
ever, is  absent,  or  there  is  a perverse  craving  for  piquant,  acid,  or 
salty  foods,  while  the  habitual  diet  is  detested.  Taste  is  much  dis- 
turbed. The  nervous  symptoms  are  general  malaise,  indisposition 
to  mental  or  bodily  work,  prostration,  and  frontal  and  occipital 
headache.  Palpitation  of  the  heart,  giddiness,  and  a feeling  of  fear, 
with  profuse  sweating,  are  sometimes  present.  Nervous  and  less 
resistant  patients  (children)  may  have  delirium.  Fleiner  declares 
that  general  convulsions  or  loss  of  consciousness  are  not  rare  in  his 
experience. 

All  these  symptoms  may  arise  directly  from  the  stomach  or 
reflexly  from  the  central  nervous  system,  which  in  these  cases 
suffers  intensely  at  times  through  the  absorption  of  toxins  from  the 
stomach.  If  the  nausea  increases  to  emesis,  there  will  be  at  first 
vomiting  of  food  that  has  been  eaten  many  hours  before.  This 
vomited  material  is  mostly  badly  digested,  and  imbedded  in  mucus. 
After  emesis  the  symptoms  may  ameliorate  and  the  nausea  cease ; 
very  frequently,  however,  the  vomiting  continues  when  no  more 
food  is  in  the  stomach.  Then  saliva,  mucus,  bile,  and  even  blood, 
may  be  forced  up  under  great  retching  and  suffering.  Intestinal 
parasites  have  in  this  way  been  forced  into  the  stomach  and  vomited 
Skoda  first  directed  attention  to  cases  in  which  vomiting  was 
much  impeded  (at  times  prevented)  by  spasm  of  the  sphincters, 
particularly  at  the  cardia. 

If  the  last  meals  contained  an  abundance  of  carbohydrates  or 
fats,  the  vomited  material  will,  on  testing,  show  an  abundance  of 
lactic,  butyric,  and  fatty  acids ; it  will  also  contain  acetic  acid  from 
the  alcohol  which  was  either  the  cause  of  all  the  difficulty  or 
which  has  been  administered  by  sympathizing  laymen.  But  the 
most  characteristic  chemical  condition  is  the  entire  absence  of 
free  hydrochloric  acid  in  the  vomited  matter,  which  is  the  cause 
of  the  perverse  fermentations  and  decomposition  in  the  gastric 
contents. 

The  occurrence  of  hydrogen  sulphid  in  the  contents  of  the 
stomach  and  in  the  urine,  which  has  been  reported  by  Senator, 


DIFFERENTIAL  DIAGNOSIS.  427 

indicates  a degree  of  albuminoid  decomposition  which  is  extremely 
rare. 

State  of  the  Urine. — The  quantity  is,  as  a rule,  diminished;  in 
febrile  cases  the  specific  gravity  is  high,  and  when  constipation  is 
present,  it  contains  an  excess  of  indican. 

Fever. — While  about  one-half  of  the  cases  transpire  without  rise 
of  temperature,  in  the  other  half  fever  is  present,  appearing  sud- 
denly, and  reaching  at  times  105°  F.  (40°  C.).  This  form  may,  in 
the  beginning,  occasion  some  difficulty  in  the  diagnosis,  because  of 
its  strong  resemblance  to  typhoid  fever.  Under  these  circum- 
stances Widal’s  reaction  for  typhoid  fever,  by  the  effect  of  the 
serum  of  such  patients  on  the  clumping  of  the  typhoid  bacillus, 
should  be  carried  out  for  diagnostic  differentiation  (“  Le  Bulle- 
tin Medical,”  1896,  Nos.  59,  61,  64,  78,83;  1897,  No.  4).  Also 
C.  Frankel  (“  Deutsch.  med.  Wochenschr.,”  1897,  No.  3)  and 
Wyatt  Johnson  (“  N.  Y.  Med.  Jour.,”  Oct.,  1896,  and  “Med. 
News,”  Jan.,  1897).  Some  German  writers  still  speak  of  gastric 
fever  as  an  infectious  disease  peculiar  to  itself.  (See  F.  Schmidt, 
“Dissertation,”  Berlin,  1885;  “ Z.  Frage  d.  Existenz  d.  gastrisch. 
Fiebers,  als  einer  eigenartigen  Krankheit  ” ; Hans  Herz,  loc.  cit.y  p. 
95.)  The  cases  described  as  such  are  no  doubt  mild  cases  of 
enteric  fever. 

Though  it  is  difficult  to  furnish  proof  of  a direct  infection  in  these 
febrile  forms  at  present,  it  is  not  at  all  impossible  that  such  a gas- 
tritis may  exist.  Future  bacteriological  studies  in  this  disease  may 
throw  much  light  on  this  point.  The  fever  of  acute  gastritis  is 
usually  preceded  by  repeated  chilly  sensations  or  by  a typical 
shaking  chill. 

Diiration. — If  the  rules  of  hygiene  are  regarded  and  the  patient 
observes  a careful  diet,  the  disturbances  will  disappear  entirely  in 
from  three  to  four  days.  There  are,  of  course,  much  shorter  attacks. 
The  stomach  remains  very  sensitive  to  errors  of  diet,  etc.,  for  a 
varying  time.  A number  of  neglected  cases,  or  those  occurring  in 
very  weakened  individuals,  may,  by  a gradual  transition,  turn  to 
the  subacute  or  chronic  form. 

Diagnosis. — In  cases  that  are  not  accompanied  by  any  fever 
there  should  be  no  difficulty  in  determining  the  nature  of  the  dis- 
ease, especially  as  the  direct  cause  is,  in  most  instances,  apparent. 
The  febrile  form  may  be  confounded  with  beginning  enteric  fever; 
during  the  first  three  days  of  the  attack  it  may  be  impossible  to 
differentiate  the  two,  Widal’s  method  giving  a negative  result  if 


428 


ACUTE  GASTRITIS. 


instituted  before  the  second  week  of  typhoid  fever.  The  existence 
of  fever  blisters  (herpes  labialis),  which,  according  to  Leo  (loc.  cit ., 
p.  66),  speaks  against  typhoid,  is,  in  our  experience,  an  unreliable 
sign ; the  results  of  the  blood  examinations  are  contradictory,  and 
in  the  urine  no  diagnostic  feature  is  known.  The  diazo  reaction  of 
Ehrlich,  even  when  performed  in  the  originator’s  latest  method 
(“  Charite  Annalen,”  1886,  Bd.  11),  has,  in  our  experience,  been  of  no 
diagnostic  value.  In  this  respect  we  can  confirm  the  opinions  of 
von  Jaksch  and  Eichhorst  (“  Klinische  Untersuchungsmethoden,” 
p.  177).  Most  infectious  diseases  (see  above)  are  in  the  beginning 
accompanied  by  an  acute  gastritis  ; in  most  of  them,  particularly 
the  exanthemata,  a differentiation  is  not  difficult.  It  is  good  advice 
that  von  Leube  (“  Specielle  Diagnose,”  1.  Theil,  Leipzig)  gives 
when  he  says : “ In  all  cases  with  high  fever  think  of  other  sources 
and  causes  before  settling  upon  gastritis.”  There  are  two  condi- 
tions which,  so  far  as  can  be  judged  at  present,  are  reliable  factors 
in  the  early  diagnosis  between  acute  gastritis  and  enteric  fever. 
(The  early  diagnosis  is  the  only  one  we  are  discussing;  the 
element  of  time  is  very  important  here,  as  simple  gastritis  is  only 
of  three  days’  duration.)  The  differentiating  factors  are  the  manner 
and  rise  of  the  fever  and  the  state  of  the  spleen. 

In  enteric  fever  we  mostly  meet  with  a gradual  rise  of  tempera- 
ture and  a gradual  fall  when  the  fever  subsides.  In  gastritis  the 
temperature  rises  abruptly,  the  remissions  are  slighter,  and  the  fall 
is  more  sudden.  (See  Osier,  “ Prin.  and  Prac.  of  Med.,”  p.  349.) 

Therefore  frequent,  regular,  thermometrical  studies  are  not  to  be 
omitted.  The  second  diagnostic  sign  of  value  is  the  presence  or 
absence  of  splenic  tumor ; its  presence  points  to  enteric  fever. 
Unfortunately,  the  splenic  enlargement  is  not  invariably  present  in 
enteric  fever  at  the  outset.* 

Prognosis. — Speaking  generally,  the  prognosis  of  simple  acute 
gastritis,  except  in  very  old  patients  and  in  young  children,  is 
favorable. 

Treatment. — 1.  Prophylactic.  2.  Dietetic.  3.  Medicinal. 

Prophylactic  treatment  will  especially  be  applicable  to  cases  that 


* Dr.  Edward  L.  Whitney  and  myself  observed  in  1897  that  the  Widal  test  for  typhoid 
fever  failed  when  instituted  during  the  first  week.  Apparently,  a certain  time  is  required 
before  the  serum  acquires  the  characteristic  effect  on  the  typhoid  bacilli.  This,  of  course, 
— if  confirmed  by  further  observations, — would  render  it  useless  in  the  early  differential 
diagnosis  between  typhoid  fever  and  acute  gastritis,  because  the  duration  of  the  latter  is 
only  a few  days. 


ADULTERATION  AS  A CAUSE  OF  GASTRITIS.  429 

are  known  to  have  enfeebled  digestive  organs  or  in  which  attacks 
of  digestive  disease  have  repeatedly  occurred.  Attention  must  be 
directed  to  avoidance  of  injurious  influences  that  may  affect  the 
stomach  direct  from  external  causes  and  those  that  affect  it  from 
internal  causes. 

(a)  The  external  causes  are,  of  course,  the  manifold  varieties  of 
trauma  that  are  possible  in  modern  life;  not  only  those  that  can 
occur  accidentally,  but  those  that  occur  gradually  by  pressure  upon 
the  abdomen  from  without,  such  as  are  requisite  in  the  execution 
of  certain  trades,  the  manipulation  and  handling  of  machines,  and 
even  the  continuous  pressure  of  tables. 

A very  important  matter  in  this  respect  is  clothing,  particularly 
that  of  the  female  sex.  Their  clothing  of  to-day,  as  far  as  the 
maintenance  of  healthy  digestive  organs  is  concerned,  is  not  at  all 
conformable  to  this  object.  The  much-condemned  corset  is  not 
even  the  worst  part  of  the  female  outfit,  for  a properly  constructed 
and  correctly  applied  corset  does  not  necessarily  effect  damage ; 
but  it  would  be  more  hygienic  to  discard  it  altogether,  and 
preserve  form  and  insure  support  to  the  breast  and  graceful  car- 
riage in  the  style  of  the  ancient  Greeks  (Grecian  corset),  or  by 
broad,  soft  bandages  applied  immediately  to  the  skin,  over  the 
underwear,  or  even  externally  (Julia  Marlowe  style).  More  harm- 
ful than  the  corset  is  the  tying  of  the  skirts  and  dresses  around 
the  waist. 

The  most  judicious  clothing  conformable  to  the  object  of 
relieving  the  abdominal  organs  of  pressure  is  represented  by  gar- 
ments made  in  one  piece,  of  which  the  upper  part  supports  the 
lower  from  the  shoulders  (Kleinwachter,  “ Deut.  Med.  Zeitschr.,” 
1894,  S.  82  ; also  Meinert,  “ Volkmann’s  klin.  Vortrage,”  115,1 16). 

The  abdomen  should  always  be  kept  warm,  not  by  special  ban- 
dages, but  by  garments  that  are  made  of  wool,  fitting  quite  com- 
fortably to  the  skin,  and  closed  below — i.  e.f  over  the  genito-urinary 
organs  and  rectum.  All  digestive  sufferers  should  take  special 
care  against  cooling  or  sudden  chilling  of  the  surface. 

(1 b ) The  internal  causes  or  injurious  influence  must  chiefly  be 
avoided  in  the  food.  Exclusive  of  corrosive  and  irritant  poisons 
that  may  be  swallowed  accidentally,  the  food  articles  may  contain 
adulterations  in  the  form  of  organic  or  inorganic  additions  that  are 
incompatible  with  sound  digestion,  or  the  food  may  be  decayed, 
fermenting,  or  decomposed.  Among  the  adulterations  might  be 
mentioned  that  of — 


430 


ACUTE  GASTRITIS. 


Milk , with  water,  sodium  carbonate  and  bicarbonate,  borax,  and 
salicylic  acid ; or  it  may  contain  bacteria  (tubercle  and  typhoid 
bacilli). 

Cheese , adulterated  with  decomposable  gelatins,  and  may  con- 
tain lead  and  tin  from  the  packing,  and  also  mineral  impurities. 

Sausages  may  contain  flour,  fuchsin  (for  coloring),  organic  poi- 
sons, bacteria,  ptomains.  (Botulismus  : poisoning  by  sausage.) 

Butter  may  be  adulterated  by  mineral  substances,  gypsum,  lime, 
coloring  matters,  lead  chromate,  cresol,  dinitronaphthol,  and  the 
caustic  alkalies. 

Vegetable  Food. — Flour  has  been  found  adulterated  by  sand, 
gypsum,  and  alum,  and  also  mixed  with  the  fungi  of  rye  or  wheat ; 
ergot  poisoning  by  rye  flour  has  been  observed  in  Russia.  Some 
confectioners  use  dye-stufls  of  various  kinds,  all  of  which  are  dan- 
gerous. Coffee  is  sometimes  adulterated  with  copper  or  lead  salts 
to  give  it  the  desired  color.  Wine,  beer,  and  whisky  are  subject  to 
numerous  adulterations  to  effect  cheaper  manufacture,  to  preserve 
or  color,  or  to  give  any  desired  taste.  In  beer,  picric  acid,  colchicum, 
and  strychnin  have  been  found  as  substitutes  for  hops  ; impure 
grape-sugar  for  malt;  alkalies  to  prevent  souring,  and  salicylic  acid 
to  preserve  it  or  check  fermentation. 

Furthermore,  the  prophylaxis  must  be  directed  to  the  (i)  quality, 
(2)  quantity  of  the  food,  (3)  the  proper  preparation  of  the  food  by 
chewing  and  insalivation,  and  proper  conduct  after  eating. 

These  subjects  are  best  studied  in  the  section  on  Dietetics. 

Dietetic  Treatment. — Acute  inflammation  of  any  structure  is 
best  treated  by  rest,  and  the  stomach  forms  no  exception.  Hence, 
total  abstinence  from  food  and  great  reduction  of  the  quantity  of 
fluid  imbibed  is  often  curative  after  an  interval  of  thirty-six  hours. 
So,  for  the  first  two  days  as  little  food  as  possible  should  be  allowed. 
To  accomplish  this  very  simple  and  logical  object  is,  in  private 
practice,  a most  difficult  thing.  There  is  an  incorrigible  custom 
among  relatives,  which  it  is  hard  to  combat,  of  stuffing  the  patient 
with  all  manner  of  articles.  At  the  bottom  of  all  this  probably  lies 
the  popular  superstition  that  a human  being  can  not  exist  twenty- 
four  hours  without  food.  A total  abstinence  from  food  is  borne  very 
well,  and  leads  most  rapidly  to  recovery.  For  the  intolerable  thirst, 
cracked  ice  should  be  given,  a wineglassful  in  two  hours.  If  there 
are  signs  of  collapse,  champagne  or  brandy  may  be  added  with 
safety,  even  if  alcohol  was  the  cause  of  the  trouble. 

After  the  twenty-four  hours  of  total  abstinence,  the  first  food  to 


MEDICINAL  TREATMENT. 


431 

be  given  is  milk  or  beef  bouillon,  with  soft  rice  or  an  egg  beaten  up 
in  it.  A good  stimulating  food,  when  there  are  signs  of  prostration, 
consists  of  one  raw  egg  beaten  up  with  ^ of  a pint  of  Hochheimer, 
or  a full  pint  if  desired,  and  sweetened  to  taste,  with  a slight  flavor 
of  lemon  added.  The  wine  may  have  to  be  diluted  if  the  gastric 
mucosa  is  very  sensitive.  Of  the  above,  a small  wineglassful  (two 
ounces)  may  be  given  every  two  hours  or  it  may  safest  be  given  by 
enema  (quite  warm,  if  preferred).  On  the  third  day  a few  soda 
crackers  or  cakes  may  be  allowed.  On  the  fourth  day  a gradual 
return  to  more  reconstructive  food  is  advisable,  such  as  calf’s  brain, 
free  from  all  stringy  and  membranous  parts,  boiled  first  in  bouillon, 
then  rapidly  broiled  ; sweetbread  or  thymus  gland  broiled  ; breast 
meat  of  broiled  squab,  pigeon,  or  chicken.  Finally,  on  the  sixth 
day  after  the  attack,  finely  scraped  broiled  beef,  potato  puree, 
stewed  apples,  rice,  tapioca,  very  soft  omelet.  A plan  that  is 
generally  successful  is  to  follow  out  the  Penzoldt  diet  order  given 
on  p.  228. 

Medicinal  Treatment. — Acute  gastritis  should  be  treated  with- 
out drugs  whenever  it  is  possible.  If  the  dietetic  rules  of  total 
abstinence  from  all  food  for  twenty-four  hours  and  cautious  return 
to  light  diet  are  carried  out,  three-fourths  of  the  cases  will  recover 
without  medicines.  Not  a few  patients,  even  children,  will  do  this 
instinctively,  and  not  permit  any  cramming  with  food  until  the 
stomach  has  become  rested  and  a natural  desire  therefor  returns. 
We  have  consistently  carried  out  the  starvation  treatment  in  twenty 
cases  of  acute  simple  gastritis,  allowing  nothing  but  water  or 
cracked  ice  for  forty-eight  hours;  they  all  recovered  without  the 
use  of  drugs.  The  most  important  indication  of  treatment  is  usually 
done  by  the  organ  itself — i.  e.,  evacuation. 

If  emesis  does  not  occur  easily  at  the  outset,  both  Ewald  and 
Boas  recommend  the  following  emetic : 

R.  Pulvis  ipecacuanhae, 1.5  gr.  xxiij 

Antimonii  et  potassii  tartras, 0.05  gr.  |.  M. 

Sig. — P'iat  chart.  No.  1.  To  be  taken  at  once  or  in  divided  doses. 

In  children,  Ewald  favors  a teaspoonful  of  the  syrup  of  ipecac. 
I have  so  far  been  able  to  accomplish  all  that  was  necessary  with- 
out emetics,  and  am  loath  to  advise  their  use.  Apomorphin  hydro- 
chlorate may  be  used  hypodermically  in  doses  of  of  a gr.,but  in 
some  cases  it  has  been  known  to  cause  syncope  and  collapse.  A 
drug  which  gives  satisfaction  to  both  patient  and  physician  in 
these  attacks,  particularly  when  there  is  constipation,  is  calomel. 


432 


ACUTE  GASTRITIS. 


Sometimes,  when  persistent  nausea  follows  through  emesis,  it  may 
even  act  as  a gastric  sedative.  Ewald  advises  six  grs.,  repeated  in 
an  hour.  While  this  dose  seems  large,  it  is  by  no  means  too  large, 
and  will  produce  a cholagog  and  sterilizing  effect  that  sometimes 
terminates  the  gastritis  then  and  there.  Formerly  we  used  tablet 
triturates  of  of  a gr.  of  calomel  every  hour  until  purgation  ; they 
are  more  pleasant  to  administer.  The  larger  dose  recommended 
by  Ewald  produces  more  of  an  antiseptic  action,  since  a portion  of 
it  is  converted  into  mercuric  chlorid. 

Calomel  can  not  be  given  at  the  beginning  of  the  gastritis  very 
well ; the  second  day  is  best  suited  for  its  administration.  Although 
I mention  these  drugs,  it  is  not  with  a view  to  routine  treatment, 
but  to  aid  in  meeting  special  indications.  When  pain  in  the  stomach 
is  attended  by  chilliness,  we  advise  hot  poultices  over  the  entire 
abdomen,  turpentine  stupes,  or  spongiopilin  dipped  in  hot  water, 
and  ten  to  twenty  drops  of  tincture  of  opium  sprinkled  over  before  it 
is  applied  to  the  epigastrium.  But  when  there  is  gastric  pressure  that 
seems  to  embarrass  respiration,  associated  with  explosive  eructa- 
tion, cold  hydropathic  applications  are  more  effective  than  hot 
ones.  (For  the  technic  of  these  applications  see  Baruch,  “ Hydro- 
therapy.”) When  there  is  fever,  these  applications  should  be  made 
with  ice-water  or  the  ice-bag.  Intense  pain  is  met  with  hypodermic 
injections  of  morphin,  of  a gr.,and  atropin  sulphate,  yj-g  of  a gr. 
The  following  suppositories  of  Boas  may  be  applied: 

B . Codein  phosphoric, 0.05  gr. 

Ext.  belladonnse, 0.03  gr.  f. 

Enough  cacao  butter  to  make  ten  suppositories. 

Sig. — One  every  hour  until  relieved.  When  the  pain  must  be  relieved,  and  the 
hypodermic  injection  is  not  permitted  and  medication  per  os  not  retained,  they 
are  very  useful. 

By  the  mouth,  codein  is  best  given  in  the  following  manner: 

B.  Codein  phosph., 0.4  gr.  vj 

Aqua  menth.  pip., 40.0  fjiss.  M. 

Sig. — One  teaspoonful  every  three  hours. 

If  symptoms  of  hyperacidity,  keeping  up  the  annoying  pyrosis 
and  thirst,  are  predominant,  it  may  be  impossible  to  avoid  alkalies. 
They  are  expediently  prescribed  in  the  succeeding  formula: 

B • Magnesia,  calcined, 

Sodium  bicarbonate, aa  10. o ^iiss 

Menthol, 2.0  gr.  xxx. 

Mix  thoroughly. 

Sig. — One-half  teaspoonful  pro  re  nata,  followed  by  ^iij  water. 


LAVAGE  OF  STOMACH  AND  COLON  IN  ACUTE  GASTRITIS.  433 

It  is  not  rational  to  give  purgatives,  because  they  irritate  the 
inflamed  mucosa;  calomel  is  the  only  drug  of  this  nature  that  can 
safely  be  given,  but  not  before  the  fermenting  stomach  contents 
have  been  removed  by  emesis  or  lavage.  To  effect  purgation  be- 
fore the  stomach  is  emptied  exposes  the  intestine  to  infection  from 
the  septic  mass  forced  through  it.  Persistent  vomiting  may  call 
for  especial  treatment;  here,  morphin  hypodermically,  mustard 
plasters  to  the  epigastrium,  and  small  pieces  of  ice  will  be  suffi- 
cient. A singular  case  of  very  exhausting  and  persistent  vomiting 
was  in  my  practice  relieved  by  bismuth  salicylatis  gr.  x;  cocain 
hydrochlorate,  gr.  y2\  menthol,  gr.  ij ; aqua  camphor.,  fgss.  M. 
Every  two  hours  until  relieved.  Vomiting  of  this  character  is 
bound  to  bring  on  collapse.  It  is,  fortunately,  a rare  complication, 
but  must  be  met  energetically  if  it  develops.  In  concluding  the 
medicinal  treatment,  we  desire  to  refer  to  a successful  therapeutic 
measure  which  does  not  properly  belong  under  this  heading,  be- 
cause it  is  not  medicinal,  but  mechanical. 

This  consists  of  evacuating  the  stomach  with  the  tube,  and  im- 
mediately thereupon  disinfecting  it  by  washing  it  out  with  a solution 
of  the  following  composition  : 

R.  Thymol, 0.5  gr.  viij 

Boric  acid, 16.  25  ss 

Warm  water, 1000.  one  quart.  M. 

SiG. — Lavage  fluid. 

The  water  during  lavage  must  be  used  quite  warm  and  the  an- 
tiseptic not  used  until  the  plain  water  runs  out  clear.  Use  one  pint 
or  500  c.c.  at  a time.  Catch  up  the  outflowing  antiseptic  fluid  and 
ascertain  that  it  approximates  one  pint ; a few  ounces  retained  will 
not  do  harm.  Vomiting,  as  a rule,  ceases  entirely  after  this.  Six 
hours  later  wash  out  the  colon  by  large  enemata  of  ten  per  cent, 
solution  of  boric  acid,  no  matter  whether  the  patient  has  diarrhea 
or  constipation.  If  diarrhea  exist,  it  is  absolutely  rational  to  effect 
the  removal  of  the  putrefying  colonic  contents  by  large  enemata 
(given  in  the  knee-chest  posture),  and  if  constipation  exist,  the 
stagnation  of  feces  certainly  aggravates  the  symptoms  by  increas- 
ing flatulence  and  abdominal  pressure.  If  there  is  any  therapeutic 
measure  in  addition  to  abstinence  from  food  that  merits  confidence, 
it  is  this  mechanical  cleansing  of  stomach  and  colon.  Rare  cases 
of  high  temperature  may  need  special  therapeutic  measures  for 
the  fever.  Here,  also,  drugs  must  be  avoided  and  the  temperature 
reduced  by  sponging  with  cold  water  or  the  cold  bath. 


434 


PHLEGMONOUS  OR  PURULENT  GASTRITIS. 


In  case  the  appetite  fails  after  the  attack,  or  there  is  protracted 
weakness  with  timidity  and  aversion  to  food,  the  following  tonic 
will  prove  useful : 

R . Strychnin,  sulphatis,  0.021  gr.  */£ 

Acidi  hydrochloric!  dilut., 12.  f^iij 

Elixir  gentianse, q.  s.  ad  mis.,  192.  f:|vj.  M. 

SiG. — One  tablespoonful  diluted  with  two  ounces  H20  three-quarters  of  an  hour 
before  meals,  through  a glass  tube. 

Forms  of  acute  gastritis  associated  with  copious  vomiting  of  bile 
are  frequently  seen  in  our  latitude  and  termed  “ bilious  attacks.” 
There  is  no  liver  disease  associated  with  the  attacks,  and  they  are 
generally  brought  on  by  errors  in  diet  and  mental  strain. 

PHLEGMONOUS  OR  PURULENT  GASTRITIS— SUPPURATIVE  IN- 
FLAMMATION OF  THE  STOMACH— GASTRIC  ABSCESS. 

This  is  a very  acute,  fatal,  and,  fortunately,  very  rare  affection  of 
the  gastric  walls,  apparently  set  up  by  an  invasion  of  pyogenic 
cocci.  It  is  a purulent  inflammation  invariably  originating  in  the 
submucous  connective  tissue,  and  from  here  extending  to  the 
mucosa.  Ziegler  (“  Lehrbuch  d.  allgem.  u.  spec.  path.  Anat.,” 
1887,  Bd.  11,  S.  516)  describes  large  numbers  of  streptococci  oc- 
curring partly  free  in  the  tissues  and  partly  in  the  protoplasm  of 
the  cells.  In  case  the  serosa  is  invaded,  the  disease,  as  a rule, 
produces  a general  fatal  peritonitis  by  perforation,  unless  an 
infection  of  the  peritoneum  is  prevented  by  an  agglutination  with 
adjacent  organs.  We  have  seen  but  one  case  of  this  sort ; it  was 
not  diagnosed,  but  discovered  at  the  autopsy.  It  had  followed 
ulcus  carcinomatosum  of  the  pylorus.  The  submucosa  and  mus- 
cularis  mucosae  were  pushed  apart  by  numerous  miliary  abscesses. 
(See  Hemmeter  and  Ames,  “ N.  Y.  Med.  Record,”  Sept.,  1897, 
“ A Case  of  Phlegmonous  Gastritis,”  etc.)  We  submit  an  excellent 
drawing  showing  four  small  abscesses  forcing  apart  the  fibers  of 
the  muscularis  mucosae.  As  far  as  one  is  able  to  judge  from  the 
literature  on  this  subject,  the  disease  is  inevitably  fatal,  running 
most  always  an  acute,  rarely  a subacute,  course.  Ewald  ( loc . cit., 
p.  303)  has  seen  only  one  case,  and  that  at  the  clinic  of  his 
teacher,  Frerichs.  It  occurs  much  oftener  in  men  than  in  women; 
of  41  cases,  33  were  men  and  eight  women.  In  a report  by 
Glax  (“  Die  Magenentziindung.,”  “ Deutsche  med.  Zeit.,”  1884, 
No.  3)  it  is  stated  that  but  51  cases  had  been  observed  up  to  that 


PLATE  V. 


Phlegmonous  Gastritis  in  the  Sequence  of  Ulcus  Carcinomatosum.  Section 
Showing  the  Lower  Part  of  the  Mucous  Coat  with  the  Ends  of  Some 
of  the  Gastric  Glands,  the  Muscularis  Mucosa,  and  a 
Small  Portion  of  the  Upper  Part  of  the  Submucosa. 

— ( Original  observation  from  the  Author' s Clinic .) 

Objective,  one-sixth.  Eyepiece,  one  inch.  Stained  with  hematoxylon  and  orange  G. 
Magnification  about  320  diameters. 

In  all  sections  the  small  round-cell  infiltration  is  well  marked,  the  cells  chiefly  filling 
up  the  muscularis  mucosae  and  invading  the  lower  portion  of  the  mucous  coat.  In  the 
muscularis  mucosae  these  cells  are  aggregated  into  a number  of  small,  circular,  dense 
masses  (£>),  miliary  abscesses,  between  which  they  are  but  little  less  numerous.  The 
fibers  of  the  muscularis  mucosae  have  been  widely  separated  by  these  cells.  Few  cancer 
cells  are  to  be  seen  in  this  portion  of  the  tissue,  but  in  one  place  (C)  they  afe  found  plug- 
ging completely  a small  vessel.  In  the  upper  part  of  the  submucosa  a few  of  the  cancer 
cells  can  also  be  seen  (Z>). 


PATHOLOGY  OF  PHLEGMONOUS  GASTRITIS. 


435 


time.*  Most  authors  who  have  had  experience  with  the  disease 
distinguish,  first,  an  idiopathic  primary  purulent  gastritis,  the  eti- 
ology of  which  is  obscure;  and,  secondly,  a secondary,  metastatic, 
phlegmonous,  or  purulent  gastritis,  which  is  an  accompaniment  or 
a sequence  of  other  infections,  such  as  pyemia,  puerperal  fever, 
anthrax,  typhus,  or  variola.  Anatomically,  one  may  distinguish  a 
diffuse  and  a circumscribed  purulent  inflammation  of  the  submu- 
cosa ; the  latter  is  spoken  of  as  a stomach  abscess. 

Etiology. — The  direct  cause  of  the  rarer  idiopathic  phlegmon- 
ous gastritis  is  unknown.  The  predisposing  causes  may  be  the 
same  as  stated  under  the  etiology  of  simple  gastritis.  The  direct 
causes,  judging  from  anatomical  specimens,  are  undoubtedly  bac- 
terial invasions  of  the  submucosa,  principally  by  pyogenic  cocci 
that  find  portals  of  entry  through  lesions  in  the  superficial  epithe- 
lium of  the  stomach,  such  as  occur  in  most  gastric  diseases,  espe- 
cially in  so-called  exfoliation  in  carcinomata  and  old  ulcers,  or  after 
trauma  caused  by  fish-bones, seeds,  foreign  bodies, etc.  Ziegler’s  bac- 
teriological ( loc . cit.)  studies  have  already  been  mentioned.  The  sec- 
ondary metastatic  phlegmonous  gastritis,  which  seems  most  fre- 
quent, is  that  following  puerperal  fever,  and  owes  its  origin  to  locali- 
zation in  the  stomach  of  the  specific  organisms  producing  the  funda- 
mental disease.  Whatever  they  may  be,  it  is  self-evident  that  only  an 
enfeebled  organ  is  liable  to  such  an  inflammation,  since  pyogenic 
cocci  can  not  resist  the  action  of  the  free  HC1  of  the  gastric  juice. 

Pathological  Anatomy. — The  diffuse  inflammation  rarely  in- 
vades all  parts  of  the  stomach  with  the  same  intensity,  even  if  the 
whole  organ  is  involved.  The  pyloric  portion  is  generally  invaded 
more  than  the  others  ; toward  the  cardia  the  inflammatory  process 
is  less  and  less  marked,  while  the  esophagus  is  rarely  attacked. 
The  submucous  layer  is  most  extensively  altered  ; on  cross-section 
it  is  swollen,  showing  an  edematous,  purulent,  or,  at  times,  a bloody 
infiltration.  From  here  the  inflammation  spreads  along  the  inter- 
glandular  tissue  between  the  glandular  tubules,  effecting  fine  or 
larger  perforations  in  the  mucosa,  which  may  assume  a sieve-like 
appearance.  Pus  wells  up  through  these  cribriform  perforations  as 
out  of  a swollen  sponge.  It  may  occur  that  the  mucosa  is  lifted 
from  the  submucosa  by  accumulations  of  pus.  Rokitansky  has 
described  a case  in  which  the  mucosa  was  only  strikingly  anemic 


* We  have  collected  the  entire  literature  on  the  subject  of  phlegmonous  gastritis,  which 
is  appended. 


436 


PHLEGMONOUS  GASTRITIS. 


otherwise  unaltered.  Macleod  (“  Lancet,”  1887,  vol.  11,  p.  1166)  de- 
scribes a gastric  abscess  in  which  mucosa  was  said  to  be  unaltered. 

Toward  the  deeper  portions  of  the  engorged  layers  the  process 
spreads  along  the  bundles  of  muscular  fibers  in  the  muscularis, 
which  undergo  fatty  degeneration,  and  show  infiltration  with  pus 
cells  and  proliferation  of  nuclei.  The  serous  or  peritoneal  layer 
may  also  be  lifted  from  the  subserous  or  muscular  layers,  and  per- 
foration, as  a rule,  rapidly  follows  inflammation  of  this  layer. 
Circumscribed  abscesses,  which  must  be  differentiated  from  the 
diffuse  inflammation,  are  usually  small,  varying  from  the  size  of  a 
hazelnut  to  that  of  a goose  egg  (Leube,  loc.  cit.).  On  cutting  into 
the  swollen  elevated  areas  of  mucous  membrane,  the  abscess  is 
found  in  the  submucosa,  but  may  extend  through  the  muscularis 
to  the  serosa. 

Symptomatology. — The  symptoms  are  very  much  like  those  of 
a very  intense  simple  acute  gastritis ; the  pain  of  gastric  phlegmon 
is  not  materially  increased  by  change  of  position  or  pressure. 
There  is  very  rarely  any  vomiting  of  pus  in  diffuse  purulent  gas- 
tritis. Gastric  abscess  may  be  attended  by  copious  vomiting  of 
pus,  after  which  a tumor  that  may  have  been  palpable  before  may 
become  much  smaller,  or  disappear  entirely ; this  phenomenon 
might  be  significant  for  the  diagnosis  of  gastric  abscess  if  it  were 
not  for  the  fact  that  pus  tumors  of  the  neighboring  organs  some- 
times break  through  into  the  stomach  and  cause  the  same  symp- 
toms. The  fever  reaches  I04°-I05°  F.,  the  patient  being  aware 
from  the  outset  that  he  is  very  seriously  ill.  The  sensorium  is 
much  disturbed  by  great  restlessness,  headache,  insomnia,  delirium. 
To  the  symptoms  of  acute  gastritis  those  of  a sudden  peritonitis 
may  be  added  at  any  time. 

Diagnosis. — The  important  conditions  for  diagnosis  are  the  pain, 
vomiting,  meteorism,  fever,  diarrheas,  and  general  phenomena. 
The  pain  is  localized  in  the  epigastrium,  but  is  said  to  have  been 
absent  in  some  cases.  The  emesis  is  always  present,  and  consists 
of  bile,  mucus,  and  food  debris;  in  diffuse  purulent  gastritis,  pus 
has  not  been  noticed  in  the  vomit,  which  strongly  resembles  so- 
called  peritoneal  vomiting. 

The  fever  is  very  high,  and  the  temperature  curve  is  said  to 
resemble  those  of  pyemic  fevers,  with  marked  remissions  and  ex- 
acerbations. Tympanites  and  diarrhea  are  more  frequent  than  con- 
stipation. Other  symptoms  are : rapid,  compressible  pulse,  cold 
peripheral  parts,  hurried  respiration,  thirst,  and  a much- coated 


PHLEGMONOUS  GASTRITIS. 


437 


tongue.  The  course  of  gastric  abscess  is  not  characteristic,  and 
Leube  states  (“  Spec.  Diagnose  d.  inneren  Krankheiten,”  S.  237) 
that  the  diagnosis  is  a matter  of  chance.  The  attack  may  resemble 
a circumscribed  peritonitis  or  one  of  the  various  perigastric  inflam- 
mations or  abscesses  ; according  to  Ewald  ( loc . cit.)  it  may  so  mimic 
abscess  of  the  spleen  or  left  lobe  of  the  liver  that  a differential 
diagnosis  is  absolutely  impossible.  Deininger(“  Deutsches  Archiv 
f.  klin.  Med.,”  Bd.  xxm,  S.  268)  held  that  high  fever,  constant 
and  intense  gastralgic  pain  that  is  not  increased  on  movement,  and 
increased  resistance  in  the  epigastrium,  should  be  sufficiently  char- 
acteristic to  justify  a diagnosis.  These  symptoms,  however,  occur 
also  in  above  conditions  referred  to  by  Ewald.  Chvostek  (“  Wiener 
Klinik,”  1881,  and  “ Wiener  med.  Presse,”  1877,  Nos.  22-29),  how- 
ever, seems  to  have  made  the  diagnosis  in  one  of  his  cases.  The 
case  reported  by  the  author  (“  A Case  of  Phlegmonous  Gastritis,” 
etc.,  by  Hemmeter  and  Ames,  “ New  York  Medical  Record,”  loc. 
cit.)  was  not  diagnosed  antemortem.  The  condition  of  diffuse 
suppurative  gastric  inflammation  had  followed  an  ulcus  carcinoma- 
tosum,  which  had  been  recognized  and  successfully  treated  as  a 
simple  ulcer  by  my  associate,  Dr.  E.  L.  Whitney,  fourteen  months 
before  death  occurred.  When  there  is  probability  of  diffuse  or  cir- 
cumscribed phlegmonous  gastritis,  the  exploratory  puncture  with 
an  aspirating  needle,  or  the  exploratory  incision,  is,  in  our  opinion, 
justifiable.  In  Penzoldt  and  Stintzing’s  new  “ Specielle  Therapie 
innerer  Krankheiten,”  volume  iv,  page  446,  von  Heinecke  gives 
suggestions  for  the  operative  treatment  of  phlegmonous  gastritis. 

Prognosis  is  almost  always  unfavorable,  especially  in  the  diffuse 
form.  After  the  circumscribed  form  and  evacuation  of  the  abscess, 
several  clinicians  have  reported  recoveries  (Deininger,  loc.  cit.,  Glax, 
loc.  cit.,  Kirchmann,  loc.  cit.,  also  Buckler,  “ Idiopathic  Phlegmon. 
Gastritis,”  “ Bayerisch.  Aerztliches  Intelligenzblatt,”  1880,  No.  37), 
but  it  is  impossible  to  confirm  whether  they  were  really  gastric 
abscesses.  Dittrich  has  found  cicatrices  in  the  submucosa  pointing 
to  the  possibility  of  healing. 

Treatment. — If  a diagnosis  could  be  made,  it  seems  to  me  that 
these  cases,  the  diffuse  as  well  as  the  circumscribed  forms,  had 
best  be  treated  surgically.  Under  the  existing  difficulty,  the  treat- 
ment can  be  only  symptomatic  and  limited  to  relieving  pain  by 
hypodermic  injections  of  morphin,  applications  of  ice, — ice-bag  to 
the  stomach,  crushed  ice  by  the  mouth.  To  counteract  collapse, 
wine  enemata  and  hypodermic  injections  of  strychnin  may  be  rec- 
ommended. Medicines  by  the  mouth  are  worse  than  useless. 


43» 


INFECTIOUS  GASTRITIS. 


INFECTIOUS  GASTRITIS. 

(i Gastritis  infeciiosa , diphtheritica , crouposa,  mycotica , parasiiaria.) 

As  Penzoldt  correctly  remarks  (/0c.  cit.),  every  gastritis  is  to  a 
certain  extent  infectious  ; for  this  reason  a number  of  authors  reject 
the  conception  of  infectious  gastritis  as  a separate  and  distinct  dis- 
ease. Lebert  ( loc . cit.)  and  Oser  (article  on  Gastric  Diseases  in 
“ Eulenburg’s  Realencyclopadie,”  second  edition,  volume  xii,  p. 
410)  believe  that  there  is  a characteristic  infectious  gastritis  peculiar 
to  itself.  Boas  (“  Spec.  Therapie  d.  Magenkrankh.,”  p.  6)  is  of  the 
opinion  that  there  is  a form  of  acute  gastroenteritis,  well  character- 
ized clinically,  which  differs  from  simple  gastritis  by  the  gravity  of 
the  symptoms,  and  particularly  the  course  of  the  fever,  so  that  it 
merits  separate  consideration.  Ewald,  on  the  other  hand,  holds 
that  there  is  no  sufficient  specificity  of  inflammatory  processes 
affecting  the  stomach  for  establishing  a separate  class  of  infectious 
gastritis.  Fleiner,  Penzoldt,  and  Einhorn  give  no  separate  consid- 
eration to  infectious  gastritis.  Those  that  establish  a separate 
category  for  this  affection  class  under  this  head  all  gastric  inva- 
sions by  infectious  germs,  so  that  all  forms,  as  remarked  before,  are 
to  a certain  extent  infectious. 

The  symptoms  are  said  to  be  very  similar  to  acute  simple  gas- 
tritis, and  therefore  require  no  further  description.  The  course  is 
more  protracted,  as  it  may  last,  according  to  Boas,  three  to  ten 
days.  According  to  Lebert  (loc.  citl),  some  cases  may  have  fever 
for  two  to  three  weeks.  In  this  case  the  Widal  method  (loc.  citl) 
should  be  made  use  of  under  such  conditions  to  distinguish 
them  from  enteric  fever.  Gaffky  (“  Deutsch.  Med.  Wochenschr.,” 
1892,  No.  14)  gives  an  account  of  severe  gastroenteritis  in  three 
persons  who  drank  the  unboiled  milk  of  a cow  affected  with 
hemorrhagic  enteritis.  He  believes  that  the  infecting  germ  was  a 
particularly  virulent  type  of  the  bacillus  coli  communis.  A num- 
ber of  similar  mass  epidemics  are  on  record  (Husemann,  “ Deutsch. 
med.  Wochenschr.,”  1889,  S.  960)  that  tend  to  strengthen  the 
conception  of  a special  infectious  gastritis.  There  seems  no  neces- 
sity as  yet  for  a separate  classification  of  this  kind;  the  subject  is 
still  too  hypothetical  to  be  ranked  as  equal  in  importance  with 
other  well-characterized  forms  of  gastritis.  The  diagnosis,  prog- 
nosis, and  treatment  are  said  by  Boas  to  be  the  same  as  for  acute 
simple  gastritis. 

Diphtheric  gastritis  is  a rare  affection,  occurring  not  only  as 


PLATE  VI. 


Bacterial  Invasion  of  Gastric  Epithelium.  From  a Case  of  Diphtheric 
Gastritis. — ( Hemmeter . ) 


29 


MYCOTIC  GASTRITIS. 


439 


a sequence  to  laryngeal  and  pharyngeal  diphtheria,  but  also  as  an 
accompaniment  to  pyemia,  septicemia,  puerperal  fever,  scarlatina, 
variola,  endocarditis,  ulcerosa,  typhus,  etc.  The  disease  is,  as  a 
rule,  not  discovered  until  the  autopsy  is  made,  and  for  that  reason 
has  more  of  a pathological  than  clinical  interest. 

Mycotic  Gastritis* — When  the  vitality  of  the  mucosa  and  the 
secretion  of  hydrochloric  acid  have  been  reduced,  suppressed,  or 
destroyed,  certain  pathogenic  fungi  are  known  to  invade  the 
mucosa,  producing  ulcerations  and  necrosis. 

Most  of  these  mycotic  gastritic  inflammations  can  not  be  recog- 
nized during  life  as  such.  Among  those  that  have  been  described 
are  the  anthrax  gastritis,  produced  by  spores  or  bacilli  of  anthrax 
lodging  in  the  mucosa  or  submucosa,  and  giving  rise  to  inflamma- 
tion, ulceration,  and  necrosis. 

Sidney  Martin  observed  a case  of  anthrax  of  the  anterior  wall  of 
the  stomach  at  Guy’s  Hospital ; the  primary  infection  was  in  the  left 
cheek,  where  a malignant  pustule  developed  (“  Journal  of  Pathology 
and  Bacteriology,”  vol.  i). 

Gastritis  caused  by  the  favus  fungus  (achorion  Schonleinii)  has 
been  reported  by  Kundrat  (“  Ueber  Gastro-enteritis  Favosa,” 
“ Wien.  med.  Blatter,”  1884,  No.  49).  The  case  was  that  of  a drunkard 
whose  gastric  mucosa  was  predisposed  by  alcoholic  chronic  gas- 
tritis; he  had  favus  universalis,  and  in  the  stomach  and  intestines 
the  fungi  had  caused  diphtheric  inflammations,  with  fibrous  exuda- 
tions, ulceration,  and  sloughing ; death  was  caused,  it  appears, 
by  a terminal  colitis. 

The  thrush  fungus  (German,  Soor ; Latin,  Oidium  albicans')  has 
been  reported  as  setting  up  a mycotic  gastritis  ; in  some  cases  the 
stomach  alone  appeared  infected,  throat  and  esophagus  being 
intact. 

The  yeast  fungus  (torulae  or  saccharomyces  cerevisiae),  sarcinae, 
the  common  molds  (penicillium  glaucum  and  mucor)  and  various 
schizomycetes  occur  in  the  gastric  contents  and  set  up  irritation  of 
the  mucosa  : not  by  direct  invasion,  it  appears,  but  by  the  toxic 
products  of  the  fermentation  which  they  cause. 

Sarcinae,  according  to  Huhne,  do  not  bring  about  any  fermenta- 
tion. 

Miller’s  interesting  investigations  concerning  the  bacterial  flora 
of  the  mouth  have  been  referred  to  on  page  63.  Orth,  in  the  first 
volume  of  his  excellent  text-book  (“  Specielle  pathol.  Anatomie,” 
Bd.  1,  p.  704),  describes  an  interesting  bacterial  invasion  near  an 


440 


PARASITIC  GASTRITIS. 


old  chronic  gastric  ulcer  which  had  largely  healed.  At  several 
places  there  were  grayish,  bran-like  incrustations,  partly  adherent, 
which  anatomically  had  to  be  designated  as  diphtheric.  In  the 
scabs  or  crust,  and  in  the  deeper  parts  of  the  mucosa,  and  partly 
lodged  distinctly  in  lymph  vessels,  were  numerous  bacilli  that 
had  some  morphological  resemblance  to  those  of  anthrax;  this 
supposition  could  not,  however,  be  confirmed  by  cultures.  The 
case  was  complicated  by  the  fact  that  a fatal  hemorrhage  had 
occurred  from  a very  small  arteriole  at  a place  where  only  a very 
tiny  defect  in  the  mucosa  was  observable.  In  the  immediate  neigh- 
borhood of  this  defect  the  bacilli  were  found  also,  but  not  in  suffi- 
cient numbers  to  attribute  to  their  destructive  agency  the  tearing 
of  the  arteriole,  which  was  not  aneurysmatic. 

Orth  then  refers  to  the  bacillus  gastricus,  or  polysporus  brevis 
of  Klebs  (“  Ueber  Infectiose  Magenaffectionen,”  “Allgemein. 
Wien.  med.  Zeit.,”  1881,  Nos.  29  and  30),  which  this  pathologist 
claims  to  have  found  free  in  the  lumen  of  the  glands  as  well  as 
between  the  cells  of  the  glands  and  the  tunica  propria  ; there  was 
also  an  interglandular,  small  round-cell  infiltration. 

Bottcher  (“  Dorpater  med.  Zeitschr.,”  1875,  p.  184)  also  de- 
fended the  view  that  gastric  ulcers  are  in  part  due  to  mycotic  and 
bacterial  invasions.  Unfortunately,  Klebs’  and  Bottcher’s  state- 
ments have  not  been  confirmed  by  later  investigators. 

Animal  parasites  are  also  on  record  for  producing  gastritis.  C. 
Gerhardt  (“  Magenkatarrh  durch  lebende  Dipterenlarven,”  “Jenaer^ 
med.  Zeitschr.,”  Bd.  in,  S.  522)  gave  an  account  of  acute  gastritis 
set  up  by  larvae  (maggots)  of  diptera,  a class  of  insects  of  which  the 
common  fly,  the  flea,  etc.,  are  examples.  The  eggs  of  these  larvae 
were  said  to  have  been  swallowed  with  raspberries.  Meschede 
(“  Ein  Fall  von  Erkrank.  durch  im  Magen  weilende  lebende 
Maden,”  “ Virchow’s  Archiv,”  Bd.  xxxvi,  S.  300)  reports  gastritis 
caused  by  maggots  eaten  with  cheese.  Senator  reported  gastritis 
set  up  by  living  maggots  of  the  common  fly,  which  occurred  in 
the  mouth  and  stomach  (“  Berlin,  klin.  Wochenschr.,”  1890,  No. 
7)  ; the  same  observation  was  made  by  Hildebrandt  (“  Berlin,  klin. 
Wochenschr.,”  1890,  No.  19).  Fermaud  observed  a case  of  gas- 
tritis and  gastralgia  caused  by  an  earthworm  (“Journal  de  Med. 
Practique  de  Paris,”  1836,  tome  vn,  p.  57).  It  is  known  also  that 
ascarides  and  tape-worms  may  reach  the  stomach  in  rare  cases  and 
give  rise  to  severe  inflammations,  which  may  subside  at  once  as 
soon  as  the  offending  parasite  is  vomited. 


TOXIC  GASTRITIS. 


44 


Toxic  Gastritis  ( Gastritis  Venenata). — This  form  of  acute  gastric 
inflammation  is  caused  by  poisons  or  corrosive  chemical  bodies. 
The  poisons  that  have  been  taken,  either  by  mistake  or  with 
suicidal  intentions,  are  mercuric  chlorid  or  corrosive  sublimate, 
phosphorus,  arsenic,  chloroform,  creasote,  potassium  chlorate, 
oxalic  acid,  nitrobenzol,  carbolic  acid,  the  concentrated  inorganic 
acids,  sulphuric,  hydrochloric,  and  nitric  acids;  the  caustic  alkaline 
hydroxids  in  strong  solution,  and,  furthermore,  alcohol  in  all  its 
forms,  and  some  substances  used  as  medicines  (see  etiology  of 
acute  gastritis),  particularly  croton  oil,  antimonium  and  potassium 
tartrate  (tartar  emetic) ; also  ammonia. 

The  pathology  will  necessarily  vary  considerably,  as  it  is  not 
only  dependent  upon  the  kind,  but  upon  the  quantity  and  con- 
centration of  the  poison  ; and  also  upon  the  circumstance  whether 
the  poison  is  taken  on  a full  or  an  empty  stomach,  as  food  and  drink 
dilute  the  drugs.  There  may  be  only  a slight  superficial  inflam- 
mation, or  a very  penetrating  corrosive  effect  involving  the 
entire  gastric  wall  and  even  leading  to  perforation.  Different  drugs 
produce  different  effects  upon  the  mucosa.  Phosphorus,  arsenic, 
antimony,  and  alcohol  produce,  in  excessively  large  toxic  doses,  a 
milky,  yellowish-white,  or  opaque  appearance.  The  epithelia  of  the 
alveoli  of  the  tubular  glands  are  partly  in  a state  of  mucoid  degen- 
eration, partly  finely  granulated,  cloudy,  and  showing  fatty  degen- 
eration ; the  same  is  the  case  with  the  secreting  cells.  The  tissue 
between  the  cells  is  crowded  with  a small  round-cell  infiltration. 
In  this  condition  auto-digestion  by  the  gastric  juice  may  cause 
peptic  ulcers — i.  e.y  when  the  poisons  are  not  taken  sufficiently 
strong  to  effect  ulceration  or  to  destroy  secretion. 

Dilute  acids  and  alkalies  induce  the  clinical  picture  of  a simple 
acute  gastritis  ; while,  in  concentrated  form  the  same  agents 
cause  a deeply  penetrating  necrosis,  formation  of  crusts  and  intense 
reactive  inflammation  with  serous  infiltration,  suppuration,  and 
blood  extravasation.  The  scabs  or  crusts  show  different  colors  with 
different  corrosives.  Under  the  effect  of  sulphuric  acid  they  are 
black;  of  nitric  acid,  yellow ; of  alkalies,  brown ; of  copper  salts, 
green  or  blue  ; of  silver  salts,  black.  Dislodgment  of  these  crusts 
leads  to  fatal  bleeding,  tearing  of  the  serosa,  or  perforation,  with 
peritonitis.  Oxalic  acid  is  said  to  produce  a jelly-like,  semitrans- 
parent swelling.  Ammonia  causes  a pustular  inflammation. 

Symptoms . — After  taking  the  poison  there  is  generally  an  inde- 
scribably severe  pain,  intolerable  burning,  and  vomiting  which  in- 


442 


TOXIC  GASTRITIS. 


creases  the  pain  and  at  times  causes  fainting.  The  vomit,  as  a rule, 
contains  blood  or  bloody  mucus.  The  thirst  is  great.  There  is  most 
frequently  diarrhea  containing  blood.  Severe  general  symptoms 
follow  : small,  very  fast  pulse  ; jactitation  ; delirium.  In  case  much 
of  the  poison  has  reached  the  general  circulation,  hematogenous 
icterus,  petechiae,  albuminuria,  and  hematuria  may  follow.  Death 
may  follow  in  a few  hours  or  a few  days  from  collapse;  or  later  by 
perforation  peritonitis.  Even  if  the  patients  are  tided  over  the  first 
period  of  acute  gastric  symptoms,  they  may  die  later  from  hemorr- 
hage when  the  scabs  and  crusts  are  sequestrated,  or  by  sequelae — 
i.  e.,  stenosis  of  the  esophagus,  cardia,  pylorus,  or  atrophy  of  the 
mucosa. 

The  diagnosis , after  learning  the  history  of  the  case,  will  not  be 
difficult.  ..One  should  not  fail  to  make  a thorough  examination  of 
the  mouth  and  throat,  where  the  corrosive  effect,  if  any,  will  be 
evident. 

The  prognosis  of  severe  toxic  gastritis  is  necessarily  grave ; if 
not  from  the  direct  poisoning  or  first  destructive  effect  of  the  drug, 
certainly  from  the  severe  secondary  effects. 

The  treatment  will  vary  with  the  nature  of  the  poison.  In  recent 
poisoning  with  strong  acids,  magnesia  usta  (calcined)  should  be 
given  as  soon  as  possible.  If  no  drug-store  is  near,  chalk,  or  even 
powdered  lime,  which  can  be  scraped  from  the  wall,  should  be  given. 
Whenever  possible,  the  stomach-tube  should  be  used  at  onceffor 
all  poisoning  of  recent  date. 

Boas,  Fleischer,  and  Pick  advise  that  the  tube  should  not  be  used 
in  severe  acid  or  caustic  alkali  poisoning,  because  of  the  danger  of 
perforating  the  stomach.  In  six  cases  of  poisoning — one  with  lye 
(KOH),  two  with  oil  of  vitriol  (H2S04),  one  with  strong  ammonia 
(NH3),  and  two  with  carbolic  acid — the  tube  was  used  immediately 
after  the  patients  reached  the  hospital.  As  such  cases  run  great 
danger  of  a corrosive  perforation,  we  have  personally  used  the  tube 
and  let  the  patient  take  his  chances,  which  were  better  in  these  cases 
than  in  those  where  the  tube  was  not  used.  About  250  c.c.  of  water, 
with  sodium  bicarbonate  in  case  acids  h'ave  been  taken,  or  vinegar 
in  case  of  alkalies,  is  indicated  to  dilute  and  combine  with  the 
destructive  agent  present.  Lemon  juice  will  also  answer  for  the 
alkaline  caustics.  In  all  other  poisonings  the  stomach-tube,  or, 
if  convenient,  the  pump,  should  be  used  as  soon  as  possible,  and 
the  stomach  washed  out  thoroughly.  The  approved  antidotes 
should  be  given  (freshly  prepared  hydrated  oxide  of  iron  for 


TREATMENT  OF  CHRONIC  GASTRITIS. 


445 


arsenic,  etc.),  that  will  be  found  in  various  text-books  on  toxi- 
cology and  therapeutics  (H.  A.  Hare’s  system;  H.  C.  Wood; 
Lauder  Brunton ; Binz,  Schmiedeberg  ; Penzoldt  and  Stintzing’s 
system,  vol.  iv).  After  carbolic  acid  ingestion,  wash  out  the  stomach, 
and  then  pour  in  250  c.c.  olive  oil.  In  all  corrosive  poisoning  cases 
the  pouring  in  of  olive  oil  or  molten  vaselin,  after  neutralization 
and  washing  out,  will,  if  possible,  diminish  the  corrosive  effect. 
When  not  too  much  acid  or  alkali  has  been  taken,  the  subnitrate 
of  bismuth  or  subgallate  of  bismuth,  one  dram  twice  a day, 
swallowed  with  oil,  will  favor  rapid  cicatrization  and  inhibit  bac- 
terial infection  of  the  necrosed,  charred  areas.  A suspension  of 
bismuth  subnitrate,  three  drams  to  one  pint  mucilage  and  water, 
has  proved  advantageous  in  a case  of  carbolic  acid  poisoning  in  our 
practice ; it  was  used  in  form  of  lavage.  Another  was  healed  of 
long  standing  gastric  ulcerations  by  blowing  in  bismuth  subnitrate 
and  subgallate  through  a stomach-tube — dry,  not  in  suspension. 

If  the  pain  is  severe,  morphin  must  be  promptly  given,  hypoder- 
mically, in  to  of  a grain  doses,  repeated  until  relief  comes.  It 
is  our  duty  to  give  relief  of  the  pain  at  any  risk,  even  if  chloroform 
anesthesia  is  required  ; for  after  the  suffering  ceases  our  efforts  to 
save  the  patient  can  be  more  easily  executed.  Nutrition  must  be 
carried  on  by  rectal  enemata  only.  By  the  mouth,  ice  is  about  all 
that  is  permissible  ; it  will  tend  to  diminish  the  pain,  fever,  and 
inflammation.  We  make  so  explicit  a statement  of  treatment 
because  we  had  experience  with  two  cases  where  the  autopsy 
showed  that  recovery  might  have  been  possible  (as  not  much  sul- 
phuric acid  had  reached  the  stomach)  if  the  treatment  had  been  more 
heroic — i.  e.,  if  the  tube  had  been  used  for  timely  removal  of  the 
poison. 


CHAPTER  II. 

CHRONIC  GASTRITIS. 

Little  over  a decad  ago  it  was  customary  to  designate  all 
stomach  diseases  that  were  not  acute,  and  that  could  not  be  diag- 
nosed as  dilatation,  ulcer,  or  carcinoma,  as  “ chronic  gastric 
catarrh.”  We  agree  with  Ewald  and  Penzoldt  in  the  objections  to 
the  word  “ catarrh,”  and  have  given  the  reasons  under  the  chapter 
on  Simple  Acute  Gastritis.  Even  at  the  present  day  there  is  no 


444 


CHRONIC  GASTRITIS. 


absolute  uniformity  in  the  conception  and  limitations  of  the  term 
“ chronic  gastritis.” 

With  the  aid  of  improved  methods  of  diagnosis,  particularly 
such  methods  as  permit  of  an  exact  study  of  the  various  gastric 
functions,  the  so-called  gastric  neuroses  have  been  recognized  as 
separate  and  distinct  diseases  ; formerly  they  were  believed  to  be 
symptoms  of  chronic  gastritis.  This  chronic  inflammation  of  the 
mucosa  affects  all  the  important  functions,  although  one  or  the  other 
of  these  is  generally  most  involved.  There  are  observed  many  varia- 
tions in  kind  and  intensity  of  disturbed  function,  from  a trivial 
reduction  of  secretion  of  gastric  juice  or  interference  with  motility, 
to  complete  suppression  of  glandular  activity  and  pronounced 
insufficiency  of  peristalsis.  There  are  two  pathological  processes 
inseparable  from  every  chronic  gastritis  ; these  are : degeneration 
and  desquamation  of  the  glandular  cells,  and  infiltration  of  con- 
nective tissue.  Bearing  in  mind  these  conditions,  we  may  distin- 
guish two  main  types  of  chronic  gastritis:  first,  the  hypertrophic; 
and,  secondly,  the  atrophic.  The  hypertrophic  form  consists  of 
proliferation  of  the  connective  tissue,  leading  to  change  of  form 
and  folding  or  warty  elevations  of  the  mucosa  (“  etat  mammelone,” 
or  polyposis).  The  result  of  this  process  is,  first,  either  complete 
destruction,  or,  secondly,  cystic  degeneration  of  the  glands.  A 
grayish-brown,  or,  in  places,  a dark  brown,  color  is  peculiar  to  this 
swollen  and  proliferated  mucosa,  which  is  covered  with  an  adherent, 
gray  coating  of  mucus. 

The  atrophic  form  consists  of  contraction  of  the  connective 
tissue,  loss  of  epithelium,  and  more  or  less  complete  destruction 
of  the  glands;  in  rare  instances,  superficial  ulcerations.  The  mu- 
cous membrane  is  much  thinned  out,  very  smooth,  and  of  a grayish- 
white  or  pale  slate-gray  color.  If  this  process  attacks  the  muscu- 
laris  and  submucosa,  it  may  cause  atrophy  of  the  muscle  fibrils, 
with  or  without  thickening  of  the  entire  gastric  wall  due  to  new 
formation  of  connective  tissue.  Then,  again,  we  may  meet  with 
a genuine  hypertrophy  of  the  muscularis,  particularly  at  the  pyloric 
portion,  or  in  the  pylorus  itself  (hyperplastic  stenosis  of  the 
pylorus).  The  lumen  of  the  stomach  in  these  forms  may  show  a 
normal  capacity;  or  it  may  be  much  diminished  in  size  by  con- 
nective-tissue thickening  of  the  gastric  walls  and  subsequent  con- 
traction. This  process  is  known  as  “ gastric  cirrhosis  ” (Brinton). 
By  French  writers  it  is  termed  “hypertrophic  sclerosis  of  the 
stomach  ” (Hanot  and  Gombauldt,  “ Archiv  de  Physiol.,”  ix,  p.  412  ; 


ETIOLOGY. 


445 


also  Dubey,  “ Gazette  Hebdomin.”  1883,  p.  198),  and  it  may  reduce 
the  normal  capacity  to  160  c.c.  (Leube,  Penzoldt).  Or,  again,  the 
capacity  is  much  increased  by  a dilatation  in  consequence  of 
chronic  gastritis  and  hypertrophic  pyloric  stenosis.  So  the 
anatomical  picture  may  present:  {a)  atrophy  of  the  mucosa  with 
wasting  of  the  peptic  glands  and  of  the  muscularis  ; thinning  of  the 
entire  gastric  wall,  and,  very  frequently,  dilatation;  or,  on  the  other 
hand,  ( b ) inflammatory  hyperplasia  of  the  layers  of  the  stomach, 
with  excessive  connective-tissue  proliferation  (cirrhosis  ventriculi) ; 
hypertrophic  pyloric  stenosis;  atrophy  of  the  glandular  layer  and 
sometimes  of  the  muscularis.*  This  form  may  lead  to  marked 
reduction  of  the  lumen  if  the  hypertrophy  invade  all  layers 
uniformly.  But  if  it  attack  the  pyloric  portion  only,  there  may  be 
a dilatation.  Both  forms  produce  grave  disturbances  of  motility, 
secretion,  and  absorption. 

The  cause  of  the  elevated,  warty,  or  polypoid  projections  of  the 
glandular  layer  is  to  be  sought  in  the  fact  that,  in  certain  forms  of 
the  disease,  the  mucous  layer  grows  much  more  rapidly  than  the 
submucous  layer,  bringing  about  a rough,  wrinkled,  mammillated 
surface  that  has  been  described  as  “ gastritis  polyposa,”  and  by  some 
French  writers  is  termed  “ etat  mammelone”  (see  Orth,  “ Specielle 
pathol.  Anat.,”  Bd.  1,  p.  709).  A number  of  Germans  describe  a 
variety  of  special  forms  of  chronic  gastritis  under  the  names  of 
“ saurer  Katarrh  ” (sour,  or  acid,  gastritis),  “ Schleimkatarrh”  (slimy, 
or  mucous,  gastritis),  also  termed  “ gastritis  atrophicans,”  and  a 
simple  chronic  gastritis,  or  “ einfacher  Katarrh.”  All  of  these 
terms  are,  unfortunately,  chosen  and  unscientific  because  they  are 
artificial.  The  so-called  “ saurer  Katarrh  ” is  not  a gastritis  at  all 
(Ewald),  but  a neurosis  of  secretion  : a hyperacidity,  the  result  of 
secondary  irritation  of  the  mucosa. 

Etiology. — Chronic  gastritis  is  a wide-spread  disease,  occurring 
in  all  stations  of  life,  but  most  frequently  among  the  poorer  classes, 
where  the  quality  of  the  food  may  be  so  inferior  as  to  keep  the  stom- 
ach in  a state  of  constant  irritation.  All  the  numerous  injurious 
influences  which  arise  from  a defective  and  inappropriate  diet  have 
been  referred  to  under  the  head  of  the  pathogenesis  of  acute  gas- 
tritis. It  may  evolve  from  the  acute  or  subacute  form,  where  the 
mucosa  has  been  damaged  by  the  altered  circulation  and  its  resist- 

*See  Hemmeter  and  Stokes,  “Chronic  Hypertrophic  Gastritis,”  etc.,  “Jubilee 
Memorial  Volume,”  on  occasion  of  twenty-fifth  anniversary  of  Doctorate  of  Prof. 
William  H.  Welch,  M.D.,  John  Hopkins  University,  1900. 


446 


CHRONIC  GASTRITIS. 


ance  to  disease  lessened.  It  may  arise  from  all  processes  that  lead 
to  venous  congestion  of  the  stomach — i.  e.>  affections  of  the  organs 
of  the  portal  system,  especially  of  the  liver  and  spleen  ; it  may  also 
be  caused  by  diseases  of  the  heart.  There  are  certain  conditions 
which  may  bring  about  a chronic  gastritis  by  effecting  alterations 
in  the  composition  and  structure  of  the  blood ; among  these  are : 
anemia,  chlorosis,  scrofula,  secondary  anemias  following  typhus 
and  typhoid  fevers,  the  exanthemata,  pregnancy,  tuberculosis,  dia- 
betes, gout,  and  nephritis.  Irritating  substances  brought  continu- 
ously in  contact  with  the  mucosa,  either  from  without  or  within, — 
i.  e.}  from  the  blood, — are  believed  to  cause  the  disease.  Ewald 
states  that  it  may  result  from  direct  local  irritation  of  alterations  in 
the  mucosa  itself,  such  as  cicatrices  and  neoplasms.  Our  experi- 
ence is  that  in  the  vicinity  of  such  structural  changes  preexisting 
in  the  mucosa  there  is  indeed  a gastritis  observed,  but  it  partakes 
mostly  of  an  acute  or  subacute  type.  Among  the  most  pronounced 
causes  of  the  frequency  of  chronic  gastritis  are  : defective  chewing 
and  insalivation,  hurried  eating  and  swallowing  of  large  pieces  of 
food,  putrefaction  of  the  mouth  from  carious  teeth,  or  the  manifold 
forms  of  stomatitis  and  gingivitis,  and,  in  this  country,  excessively 
hasty  eating,  with  the  abuse  of  ice-water  at  meals  and  of  tobacco 
and  alcoholic  liquors  between  meals.  The  majority  of  American 
people  residing  in  cities  live  under  commercial  and  social  customs 
pernicious  to  the  digestive  organs.  Foremost  among  these  con- 
ditions are  the  high  mental  pressure  evoked  by  the  demands  of 
business,  the  constant  worry  and  nervous  tension  caused  by  force 
of  competition,  the  anxiety  to  get  rich  rapidly  by  straining  all 
mental  and  physical  powers ; all  these  things  bring  about  a hasty 
nervous  manner  of  taking  food.  Chewing  is  a process  which  most 
business  men  execute  in  a perfunctory  manner  only,  allowing  no 
time  for  insalivation.  If  it  were  possible,  they  would  gulp  the  food 
down  dry  ; as  it  will  not  go  down  that  way,  it  is  washed  down  with 
ice-water.  Tobacco  juice  is  responsible  for  much  of  this  disease; 
also  condiments  used  habitually  (pepper,  ginger,  mustard,  horse- 
radish), and  the  habitual  use  of  drugs  (arsenic,  silver  salts,  iodids). 

Chronic  gastritis  is  most  frequent  among  habitual  consumers  of 
alcoholic  liquors.  From  what  was  said,  under  acute  gastritis,  of 
the  experimental  production  by  Ebstein  of  this  disease  with  alco- 
hol, the  frequency  of  the  chronic  form  among  the  devotees  to 
Bacchus  and  Gambrinus  is  very  intelligible.  As  Ewald  correctly 
remarks,  the  disease  may  be  classified  among  those  in  which  the 


PATHOLOGY  OF  CHRONIC  GASTRITIS. 


44/ 


patient’s  indiscretions  play  a very  important  role.  But,  as  most 
persons  treat  their  stomachs  badly,  and  neither  eat  with  proper 
mastication  nor  are  able  to  resist  culinary  temptations,  gastritis  is 
one  of  the  “ best  nourished  ” and  most  prevalent  diseases  in  the 
world.  “ Indigestion  is  the  remorse  of  a guilty  stomach,”  says 
Ewald ; and  F.  Albin  Hoffmann  (“  Vorlesungen  fiber  allgemeine 
Therapie,”  Leipzig,  1885)  expresses  a sentiment  that  deserves  to  be 
an  apothegm  : “ Jeder  Mensch  hat  den  Magen  den  er  zu  liaben 

verdient ” (“every  one  has  the  stomach  which  he  deserves”).  It 
is  not  intended  here  to  do  injustice  to  a large  number  of  sufferers 
from  weak  stomachs  who  take  the  greatest  possible  care  to  avoid 
dyspepsia,  and,  nevertheless,  are  liable  to  acute  or  chronic  gastritis. 
The  etiology  explains  why  the  male  sex  is  much  more  frequently 
affected  than  the  female. 

The  Pathological  Anatomy. — The  changes  are,  as  in  the 
acute  formx  most  pronounced  in  the  pyloric  region,  and  from  here 
extend  to  the  fundus.  The  alterations  of  structure  occurring  in 
the  course  of  chronic  gastritis  present  varying  pictures,  according 
to  the  duration  of  the  disease.  In  the  later  stages  the  variations  are 
considerable,  since,  at  this  period,  the  connective-tissue  changes  may 
atone  time  incline  to  inflammatory  hyperplasia ; at  another,  may 
show  an  atrophic  character  ; again,  either  the  mucosa  or  submucosa 
only,  or,  in  other  instances,  the  deeper  layers  may  be  involved,  with 
alternating  intensity  and  extent.  The  inflammatory  process  is  not 
at  all  limited  to  mucoid  degeneration  and  desquamation  of  the 
surface  epithelium,  but  preeminently  affects  the  glandular  elements 
and  interstitial  tissue,  whence  it  attacks  the  deeper  layers  of  the 
gastric  wall.  In  early  stages  there  is  a general,  diffuse  redness, 
due  to  hyperemia;  in  later  stages  this  color  exhibits  a peculiar  pig- 
mentation, which  first  assumes  a bluish  or  brownish  shade,  and 
finally  gets  to  be  of  a dirty  red-brown,  or  slate-gray,  or  both.  This 
pigmentation  is  generally  limited  to  the  pyloric  region,  but,  in 
spots,  it  may  be  spread  over  other  sections  of  the  inner  surface  of 
the  stomach.  The  color  is  caused  by  blood  pigments  which  have 
become  stored  up  in  the  cells  and  interstitial  tissue  ; also  by  blood- 
corpuscles  that  have  left  the  vascular  channels  and  undergone 
pigment  metamorphosis  during  the  long-standing  chronic  hyper- 
plasia. This  pigmentation  must  not  be  confounded  with  post- 
mortem discoloration. 

Inflammatory  Hyperplasia. — In  this  form  the  gastric  mucosa  may 
either  preserve  the  velvety  appearance  peculiar  to  the  normal 


448 


CHRONIC  GASTRITIS. 


inner  surface  of  the  contracted  stomach,  or  it  may  be  covered  with 
irregular  warty  projections,  and  exhibit  immense  development  of 
the  pyloric  “ plicae  villosae.”  This  is  due  generally  to  inflamma- 
tory infiltration  of  the  interglandular  and  subglandular  connective 
tissue,  but  particularly  to  the  same  process  occurring  in  the  con- 
nective-tissue ridges  (“  Leisten  ”)  existing  between  the  vestibular 
entrances  to  the  gland-ducts  (“  Vorraume  ” of  the  Germans),  or 
peptic  duct  alveoli,  as  we  prefer  to  call  them.  If  these  hypertro- 
phic hyperplastic  processes  are  confined  to  circumscribed  areas, 
they  may  assume  exaggerated  degrees,  forming  polypoid  prolifera- 
tions which,  as  a rule,  are  attached  by  broad  bases  ; in  conse- 
quence, however,  of  connective-tissue  contraction,  they  may  also 
occur  pedunculated.  In  this  way  papillomatous  excrescences 
may  be  developed  which  project  into  the  lumen  of  the  stomach 
(Orth,  “ Gastritis  Polyposa,”  loc.  710).  When  the  submucosa 

is  attacked  with  inflammatory  infiltration  and  new  formation  of 
connective  tissue,  the  loose  tissue  is  first  transformed  into  one 
much  richer  in  cells,  subsequently  into  a tougher,  more  inelastic 
layer,  resulting  naturally  in  a much  reduced  movability  of  the 
mucosa  upon  its  substratum.  When  this  chronic  process  results 
in  cicatricial  contraction  in  the  hyperplastic  submucous  tissue,  it 
may  lead  either  to  partial,  localized  change  of  form,  or  to  a more 
or  less  general  uniform  contraction  (“  Schrumpfung,”  “ cirrhosis 
ventriculi  ” ; “ linitis  plastica,”  Brinton).  In  the  pyloric  portion  this 
process  may  lead  to  stenosis.  Frequently,  the  muscularis  also  is 
hypertrophied,  as  a consequence  of  the  chronic  inflammation 
transmitted  through  the  submucosa.  This  muscular  hypertrophy 
is  most  pronounced  at  the  pylorus.  The  localization  at  the  pylo- 
rus of  the  maximal  intensity  of  the  inflammatory  process  in  the 
mucosa,  submucosa,  and  the  muscularis,  makes  the  origin  of  a 
pyloric  stenosis  in  consequence  of  chronic  gastritis  intelligible. 
This  kind  of  stenosis  is  usually  spoken  of  as  benign  (hyperplastic 
stenosis),  in  contradistinction  to  the  malignant  stenosis  of  car- 
cinoma (Hemmeter  and  W.  R.  Stokes,  loc.  cit .). 

Much  diversity  of  opinion  exists  concerning  the  origin  of  the 
etat  mammelone  (“  mammelon  ” means  the  nipple  of  the  mammary 
gland).  Frerichs  held  that  it  was  due  to  accumulations  of  fat  in 
the  mucosa,  and  inflammatory  hyperplasia  of  its  contained  lymph- 
follicles.  Rindfleisch  maintained  that  a greater  growth  of  the 
mucosa  than  of  the  submucosa  was  the  cause.  Ziegler  explained 
the  mucosa  polypi  by  proliferation  of  the  submucosa.  Ebstein 


INFLAMMATORY  ATROPHY. 


449 


assumed  an  inflammatory  hyperplasia  of  the  tissue  between  the 
glands.  Jones  assigned  as  a cause  an  excessive  contraction  of 
single  bundles  of  the  muscularis  mucosae.  Undoubtedly,  this 
gastritis  polyposa,  with  its  mammelonated  appearance,  may  be 
formed  by  a great  diversity  of  processes. 

Inflammatory  Atrophy . — The  progressive  plastic  character  of  the 
inflammation  just  depicted  may  lead  to  retrograde  metamorphosis 
before  it  has  progressed  very  far  ; in  some  cases  it  may  not  de- 
velop at  all,  but  the  disposition  to  break  down  and  atrophy  may 
start  early  in  the  disease.  These  atrophic  changes  are  most  marked 
in  the  glandular  elements,  and  may  be  limited  to  these.  Some- 
times the  inflammations  of  the  mucosa  and  gland-cells  have,  from 
the  outset,  a degenerative  tendency,  and  no  hypertrophy  or  hyper- 
plasia enters  into  the  anatomical  picture.  The  surface  columnar 
epithelium  and  the  cylindrical  epithelium  of  the  vestibular  alveoli 
fall  prey  to  a mucoid  degeneration  and  desquamation.  The  epithe- 
lial cells  of  the  peptic  glands  undergo  fatty  degeneration.  During 
this  atrophy  the  mucosa  changes  to  a thin,  smooth,  pigmented, 
or  slate-gray  membrane.  This  atrophy  may  be  limited  to  the 
mucosa,  while,  at  the  same  time,  hypertrophic  changes  go  on  un- 
hindered in  the  submucosa  and  muscularis;  again,  the  atrophy 
may  extend  to  the  latter  layers,  and  bring  about  a wasting  of  all 
gastric  strata.  This  last  condition  was  formerly  designated  “ tabes 
of  the  stomach  ” (the  “ phthisis  ventriculi  ” of  Rokitansky).  Under 
these  irreparable  atrophic  states  anomalies  in  the  gastric  volume 
may  develop,  but  dilatation  is  here  more  frequent  than  contraction. 

Atrophy  of  the  stomach  may  occur  without  preceding  chronic 
gastritis.  It  then  appears  as  a simple  degenerative  process,  and 
follows  severe  anemic,  cachectic  states,  and  also  grave  infectious 
diseases  and  poisonings. 

When  confronted  with  cases  of  gastric  atrophy,  with  absence  of 
hydrochloric  acid,  the  ferments,  and  enzymes,  and  coexistent 
anemia,  it  is  sometimes  very  difficult  to  decide  as  to  the  primary 
causative  disease.  In  these  cases  it  is  well  to  bear  in  mind  that 
anemias,  even  those  of  a grave  pernicious  character,  may  be  a 
consequence  of,  or  rather  secondary  to,  atrophy  of  the  gastric 
mucosa  which  has  extended  to  the  intestinal  mucosa.  Our 
countryman,  Austin  Flint,  was  the  first  to  call  attention  to  the 
relation  between  anemia  and  atrophy  of  the  gastric  glands.  In 
i860  (“American  Medical  Times,”  i860)  he  expressed  the  opinion 
that  some  cases  of  obscure  and  profound  anemia  are  dependent 


450 


CHRONIC  GASTRITIS. 


upon  degeneration  and  atrophy  of  the  glands  of  the  stomach. 
(Further  contributions  of  Flint  to  this  subject  are  to  be  found 
in  the  “New  York  Medical  Journal,”  March,  1871,  and  in  his 
“ Principles  and  Practice  of  Medicine,”  p.  477,  Philadelphia, 
1881.)  Since  Flint’s  publications,  cases  have  been  reported  by 
Fenwick  (“The  Lancet,”  1877,  July  7th,  etseq.);  Quinke  (“Volk- 
mann’s  Samml.  klin.  Vortrage,”  No.  100,  case  b) ; Brabazon  (“The 
British  Medical  Journal,”  1878,  July  27th);  Nothnagel  (“  Deutsch. 
Archiv  f.  klin.  Med.,”  Bd.  xxiv,  p.  353);  Bartels  (“  Berlin,  klin. 
Wochenschr.,”  1888,  No.  3);  Scheperlen  (“  Nordisch.  Medic. 
Arkiv,”  1879,  Bd.  xi,  No.  3);  Osier  (“  Atrophy  of  the  Stomach, 
with  the  Clinical  Features  of  Progressive  Pernicious  Anemia,” 
“American  Journal  Med.  Sciences,”  1886,  No.  4).  Rosenheim  re- 
ported two  similar  cases  which  appeared  to  be  pernicious  anemia 
(“Berlin,  klin.  Wochenschr.,”  1888,  Nos.  51,  52). 

Inasmuch  as  these  cases  of  atrophy  of  the  gastric  mucosa  are 
accompanied  by  marked  changes  in  the  blood,  signs  of  breakdown 
in  the  red  blood-corpuscles,  increase  in  the  white  corpuscles,  and 
formation  of  macrocytes  and  microcytes,  the  question  may  arise 
whether  pernicious  anemia  is  really  an  independent  disease  or  the 
result  of  gastric  atrophy.  Atrophy  of  the  mucosa — not  secondary 
to  well-known  stomach  or  general  diseases,  but  occurring  as  a 
primary  disease — has  been  claimed  to  exist  by  Fenwick  tyoc.  cit.). 
Professor  William  H.  Welch  (Pepper’s  “ Amer.  System  of  Med- 
icine,” vol.  xi,  p.  616),  however,  was,  at  the  time  of  that  publication, 
of  opinion  that  the  existence  of  atrophy  of  the  stomach  as  a 
primary,  independent  disease  had  not  been  established,  the  histo- 
logical examination  of  many  of  the  cases  reported  as  such  having 
been  defective.  Professor  Welch  has  since  modified  his  views  on 
this  subject.  From  the  statements  of  some  writers  the  impression 
might  be  gained  that  the  hypertrophic  hyperplastic  form  of  chronic 
gastritis  was,  from  its  fully  developed  stage,  changed  into  the 
atrophic  form.  This  would  mean  the  total  disappearance  of  the 
papillary,  polypoid  proliferations  of  the  “ etat  mammelone,”  because 
the  mucosa  of  the  atrophic  form  is  very  smooth.  According  to 
Orth  (loc.  cit.,  p.  710),  this  is  very  improbable.  He  is  of  the 
opinion  that  the  atrophic  form  is  developed  uniformly  by  trans- 
formation of  cellular  interstitial  tissue  into  contracting  cicatricial 
tissue,  bringing  about  thinning  of  the  mucosa  and  degeneration 
of  the  glandular  elements  without  the  intervening  features  of 
hyperplasia  above  referred  to. 


ULCERATIVE  PROCESSES  IN  GASTRITIS.  45  I 

Ulcerative  processes  are  said  to  occur  (Ziegler,  loc.  cit .)  when,  in 
the  course  of  the  disease,  intense  (hemorrhagic)  inflammation  pro- 
duces necrosis  of  the  epithelium  and  submucosa,  and  its  subsequent 
“ sequestration.”  In  this  way  the  so-called  catarrhal  gastric  ulcers 
and  hemorrhagic  erosions  are  formed,  which  may  be  associated 
with  hemorrhage.  Cruveilhier  (*‘  Anatomie  Pathologique  du  Corps 
Humaine”)  records  a follicular  gastritis  in  which  ulcers  were 
said  to  originate  in  the  follicular  glandular  apparatus. 

The  ulcers  of  chronic  gastritis  are  mostly  small,  round,  or 
irregularly  indentate.  They  are  supposed  to  heal  and  form  flat 
pigmented  cicatrices.  Forster  asserts  that  they  may  lead  to  per- 
foration. Orth  (loc.  cit.),  whose  statements  merit  confidence 
because  of  his  scientific  conservatism,  is  of  the  opinion  that  ul- 
cerative processes  in  the  course  of  chronic  gastritis  are  very  rare. 
The  minute  anatomy  of  the  process  is  that  of  a parenchymatous 
and  interstitial  inflammation.  The  glandular  cells  are  partly  de- 
stroyed, partly  granular,  and  partly  shriveled  up;  differentiation 
between  the  chief  (Hauptzellen)  and  the  parietal  cells  (Beleg- 
zellen)  is  impossible.  In  many  places,  especially  in  the  pyloric 
region,  the  ducts  have  lost  their  regular  order  of  lying  alongside 
of  one  another,  and  show  atypical  manifold  ramification  like  glove 
fingers.  Isolated  glands  become  separated  at  the  fundus  and  ap- 
pear as  cysts  at  the  border  of  the  submucosa  ; these  are  either 
empty,  with  a smooth  lining  membrane,  or  are  filled  with  the  re- 
mains of  glistening  hyaline  cuboidal  epithelium.  There  is  an 
abundant  small-celled  infiltration  which  is  especially  marked  near 
the  surface  of  the  mucous  membrane ; the  cells  lie  between  the 
glands,  and,  in  places,  push  their  ducts  far  apart.  In  the  hyper- 
plastic form  we  see  processes  of  connective  tissue  which  proceed 
upward  between  the  glands  from  the  submucosa,  like  the  branches 
of  a tree.  The  free  surface  of  the  glandular  layer  is  covered  with  a 
film  of  mucus  inclosing  many  leukocytes  and  nuclei  (Ewald).  The 
superficial  layer  of  the  epithelium  of  the  ‘mucosa  is  loosened,  and 
can  be  separated  in  adherent  shreds,  which  may  sometimes  be 
found  in  the  wash-water  after  lavage  of  the  stomach.  In  sections 
one  can  readily  see  the  mouths  of  the  glandular  ducts  and  the  sur- 
rounding epithelium.  The  epithelial  cells  of  the  vestibular  alve- 
oli (“  Vorraum  ”)  are,  for  the  greater  part,  filled  with  a pale  mucous 
mass,  which  projects  sharply  against  the  lumen  without  any  inclos- 
ing membrane,  as  described  by  Kupffer  in  the  normal  stomach. 
Ewald  has  been  able  to  study  this  and  the  following  conditions  in 


452 


CHRONIC  GASTRITIS. 


specimens  which  were  obtained  immediately  after  death,  or  from 
living  persons  after  resection  of  the  pylorus.  In  the  conditions 
(to  be  described  presently)  of  gastritis  mucosa  or  mucipara,  this 
mucoid  degeneration  may  be  observed  to  extend  to  the  base  of 
the  glands,  so  that  in  place  of  the  ordinary  chief  and  oxyntic  cells, 
we  find  only  cells  in  the  most  varied  stages  of  mucoid  degeneration 


Fig.  34. — Atrophy  and  Vacuolization  of  Glandular  Elements— Mucoid  Degeneration 
of  Peptic  Cells — Increase  of  Interstitial  Connective  Tissue— Small 
Round-celled  Infiltration. 

In  some  places  the  glandular  elements  have  disappeared,  leaving  empty,  circular  spaces.  From 
a case  of  chronic  (alcoholic)  gastritis  (this  fragment  was  found  in  the  wash-water). 

(see  Fig.  34).  This  condition  is  especially  marked  in  the  pyloric 
region.  Some  isolated  cells  may  be  found  which  are  still  intact, 
the  mucus  filling  only  a small  part  of  them,  while  the  rest  of  the  cell 
is  occupied  by  granular  protoplasm  and  a large  nucleus.  In  others, 
the  mucus  occupies  the  greater  part  of  the  cells,  and  crowds  the 
protoplasm  and  the  flattened  nucleus  against  its  base.  In  still 


SYMPTOMATOLOGY. 


453 


others,  the  cell  membrane  has  ruptured,  and  the  mucus  has  escaped 
into  the  lumen  of  the  duct  of  the  gland,  where  it  has  been  precipi- 
tated in  streaks  by  the  alcohol.  This  gives  rise  to  very  delicate 
figures  which  resemble  a row  of  horseshoes  with  their  openings 
toward  the  lumen  of  the  gland.  That  this  is  really  mucus,  and  not 
the  isolated  formation  of  vacuoles  as  described  by  Stohr  and 
Sachs,  is  easily  proved  by  the  reaction  with  acetic  acid,  and  the 
grayish  color  with  hematoxylin.  Ewald  emphasizes  the  fact  that 
these  features  are  found  only  where  the  mucous  membrane  has 
been  placed  in  alcohol  while  still  warm ; in  old  tissues  he  has 
never  met  them.  Thus  there  is  a mucoid  degeneration  of  the 
protoplasm  of  the  cells,  which  extends  deep  down  into  the  fundus 
of  the  gland. 

Symptomatology. — As  a general  rule,  the  onset  of  gastritis 
can  not  be  determined  with  certainty,  because  it  develops  very 
gradually  and  insidiously,  either  as  a continuation  of  acute  gastritis 
and  of  other  diseases,  or  as  an  independent  disease ; the  initial 
symptoms,  not  being  very  pronounced,  are  generally  ignored. 
Only  the  sudden  aggravation  caused  by  dietetic  errors,  and  other 
injurious  influences,  lead  to  the  conclusion  that  a serious  disease 
is  present.  The  clinical  picture  varies  considerably,  although 
the  signs  of  a disturbed  digestion,  as  indicated  by  absence  of 
appetite,  eructation,  nausea,  vomiting,  pressure  and  fullness  in  the 
gastric  region,  repeat  themselves  in  various  cases ; first  one  symp- 
tom and  then  another  will  manifest  its  presence  or  be  entirely  absent. 
Perhaps  the  most  constant  of  the  early  symptoms  is — 

Absence  of  Appetite  {Anorexia). — Even  in  less  serious  attacks  this 
symptom,  as  a rule,  exists,  and  may  eventuate  in  disgust  for  the 
customary  diet.  After  prolonged  fasting  the  patient  feels  that 
the  stomach  is  empty,  but  there  is  no  desire  to  eat  and  no 
hunger.  There  is,  however,  a strong  craving  for  “ piquante,” 
salty,  or  acid  food.  It  seems  as  if  an  instinctive  knowledge  existed 
that  the  production  of  gastric  juice  is  depressed  and  that  the 
mucosa  requires  a stronger  incentive  to  secretion.  Sometimes  a 
slight  appetite  is,  at  rare  intervals,  developed,  which,  however,  a 
very  few  mouthfuls  of  food  suffice  to  satisfy  completely.  Incident- 
ally the  desire  for  food  will  increase  if  the  patients  force  themselves 
to  eat;  now  and  then  bulimia — an  intense  hunger — may  develop 
at  extraordinary  times, — e.g,  during  the  night, — but  this  is  more  fre- 
quent in  the  neurosis  of  hypersecretion,  which  was  formerly  classed 
as  a gastritis.  Thirst  and  salivation  are  frequently  increased. 

30 


454 


CHRONIC  GASTRITIS. 


Taste. — We  have  rarely  observed  a case  of  chronic  gastritis  of  long 
standing  in  which  there  were  not  present  one  or  more  of  the  follow- 
ing complications  : Pharyngitis,  posterior  nasal  catarrh,  laryngitis, 
or  a form  of  stomatitis  or  glossitis,  the  last  occurring  most  fre- 
quently. This  condition  of  the  mouth  perverts  taste,  rendering  it 
pasty,  sometimes  distinctly  unpleasant,  acid,  bitter,  or  metallic: 
The  breath  is  frequently  offensive,  caused  by  caries  of  the  teeth  and 
by  decomposition  on  and  in  the  lingual  epithelium,  and  eliciting 
the  remark  that  “ food  has  no  taste.”  Almost  all  foods  then  taste 
alike.  Occasionally,  the  breath  will  first  become  offensive  at  the 
height  of  indigestion,  one  or  two  hours  after  meals,  and  especially 
so  after  ill-smelling  eructations ; this  is  suggestive  of  gastric  de- 
composition. 

Nausea  is  an  early  symptom,  generally  preceding  emesis ; it  may 
exist  by  itself  for  many  hours  without  emesis,  and  may  even  occur 
on  an  empty  stomach.  When  it  occurs  after  eating,  it  subsides 
upon  vomiting  the  food.  The  ingestion  of  food  may  diminish  or 
increase  the  nausea,  which  is  not  always  a direct  effect  of  ingesta 
or  fermenting  contents  on  the  stomach  itself.  We  have  observed 
it  when  no  food  has  been  taken  by  the  stomach  for  ten  days,  when 
daily  lavage  has  been  carried  out  and  nutrition  conducted  by  rectal 
feeding.  This  form  of  nausea  may  be  an  effect  of  intestinal  auto- 
intoxication of  a severe  type,  as  these  chronic  caseT  of  gastritis  are 
occasionally  subject  to  “ ptomain  storms.” 

Eructation  is  in  all  cases  present  at  some  time.  The  gases 
brought  up  are  air  and  carbon  dioxid  ; in  some  rare  instances  in- 
flammable gases,  such  as  hydrogen  and  marsh-gas,  CH4,  have  been 
eructated  (Ewald,  Rupstein).  The  gases  may  be  tasteless  and 
odorless,  or  may  have  an  offensive  after-taste  of  rancid  or  bitter 
character,  particularly  when  small  portions  of  ingesta  rise  up  with 
the  belching.  Sometimes  the  contents  of  the  stomach  are  very 
rich  in  organic  acids,  this  being  most  likely  when  the  motility  and 
the  secretion  of  normal  HC1  are  suppressed.  A very  high  total 
acidity,  showing  no  free  nor  combined  HC1  at  all,  will  then  be 
composed  almost  entirely  of  lactic,  butyric,  and  acetic  acids.  This 
is  a very  rare  occurrence  in  chronic  gastritis  in  our  experience,  and, 
as  a rule,  associated  with  some  disturbance  of  motility.  When  this 
acid  mass  is  forced  up  into  the  esophagus  during  the  eructations, 
a very  annoying  heartburn,  or  pyrosis,  ensues,  which  seems 
localized  at  various  parts  of  the  gullet  or  cardia,  and  may  last  for 
hours. 


THE  VOMITING  IN  CHRONIC  GASTRITIS. 


455 


Vomiting , though  not  so  frequent  as  in  acute  gastritis,  neverthe- 
less occurs  quite  often.  In  the  chronic  gastritis  of  drinkers  it  is 
often  a regular  event  each  morning,  and  is  then  known  as  the 
“ morning  vomit,”  or  vomitus  matutinus  (water-brash),  which  Fre- 
richs  attributed  to  the  swallowing  during  the  night  of  saliva  and 
the  secretions  from  the  pharyngeal  catarrh.  The  morning  vomit  is 
usually  alkaline,  as  a rule  it  inverts  starch  to  sugar,  and  gives  the 
red  rhodan-kalium  KCNS  reaction  with  chlorid  of  iron.  A tough, 
glassy,  morning  vomit  occurs  in  some  patients  who  are  not  drinkers  ; 
after  severe  retching,  the  mucus  may  be  found  tinged  with  blood. 
We  have  under  observation  at  present  a female  patient  with 
chronic  gastritis,  who  vomits  this  glassy  mucus  almost  the  moment 
she  raises  her  head  from  the  pillow  in  the  morning.  Vomiting 
which  occurs  after  meals  brings  out  food  in  a more  or  less  partially 
digested  state,  according  to  the  duration  of  its  retention  in  the 
stomach  and  the  condition  of  the  secretions.  The  eructated 
ingesta  are  imbedded  in  tough  mucus,  and  may  be  in  a state  of 
fermentation.  Bile  may  form  part  of  the  admixture.  If  the  gas- 
tritis is  due  to  secondary  passive  hyperemia  (“  Stauungskatarrh  ”) 
accompanying  hepatic  cirrhosis,  the  vomit  may  contain  blood 
from  the  rupture  of  minute  varicosities  on  the  mucosa.  The 
ejected  food  contains  organic  acids  (particularly  after  carbo- 
hydrates have  been  ingested),  but  no  free  acids.  We  have  been 
struck  with  the  frequency  of  the  occurrence  of  excessive  amounts 
of  acetic  acid  when  the  gastritis  has  been  set  up  by  long-standing 
abuse  of  alcohol.  Yeast  cells,  sarcinae,  and  a large  variety  of  bac- 
teria may  be  present.  With  incipient  and  not  very  gr^ve  cases 
the  ferments,  pepsin  and  rennin,  are  yet  to  be  detected  ; but,  in  later 
stages,  they  are  evident  only  after  adding  HC1  slightly  in  excess 
of  the  deficit ; this  really  shows  that  the  proenzymes,  not  the  per- 
fect ferments,  are  present.  Finally,  pepsinogen  and  rennet  zymogen 
are  absent ; and,  in  very  advanced  forms,  even  the  mucus  will  cease 
to  be  secreted.  This  last  symptom  is  an  indication  of  the  com- 
plete atrophy  of  the  mucosa. 

The  tongue  is  very  frequently  coated  with  a grayish-white  deposit, 
most  marked  on  the  back  and  root  of  the  organ.  The  impressions 
of  the  teeth  are  retained  by  it.  At  the  edges  and  apex  the  tongue 
presents  a deeper  red  color,  with  swollen  papillae.  The  coating 
may  disappear  toward  evening,  to  reappear  in  the  morning. 
Henoch  (“  Klinik  der  Unterleibskrankheiten,”  Berlin,  1863,  p.  382) 
holds  that  the  appearance  of  the  tongue  is  really  not  always  a 


456 


CHRONIC  GASTRITIS. 


mirror  of  the  stomach,  but  that  its  condition  is  to  be  regarded 
simply  as  an  index  of  the  existing  state  of  the  oral  mucous  mem- 
brane. Certainly  the  tongue  is  the  more  frequent  organ  of  the  two 
to  first  become  diseased,  as  it  is  nearer  to  the  outer  world  and  its 
infections  than  the  stomach.  Therefore,  it  might  be  supposed  that 
catarrhal  states  of  the  tongue,  mouth,  and  throat  may  occur  more 
frequently  as  independent  diseases,  not  secondary  to  antecedent 
diseases  involving  the  stomach.  Schech  (“  Krankheiten  d.  Mund- 
hohle  ”),  in  addition  to  malformations  and  inherited  or  acquired 
defective  forms  of  the  mouth,  describes  16  distinct  diseases  of  the 
human  mouth,  not  including  neoplasms,  tumors,  and  results  of  ner- 
vous diseases.  Seifert  (Penzoldt  and  Stintzing’s  “ Handbuch  der 
spez.  Therapie,”  Bd.  iv)  describes  23  mouth  diseases.  Kraus 
(“  Erkrank.  d.  Mundhohle,”  etc.,  Bd.  xvi ; “ Spez.  Path.  u.  Therap.,” 
von  Nothnagel)  describes  36  diffuse  and  22  partial  inflamma- 
tions of  the  mouth  and  tongue.  In  the  primary  form  all  these 
arise  in  the  mouth,  and  some  occur  as  secondary  forms  in  acute 
inflammatory  conditions  of  the  digestive  tract,  particularly  after 
infectious  diseases.  We  have  paid  particular  attention  to  the 
state  of  the  tongue,  esophagus,  and  stomach  at  autopsies,  and  also 
during  a large  number  of  analyses  of  stomach  contents,  and  must 
admit  that  the  condition  of  the  tongue  is  one  of  the  most  variable 
signs  in  gastric  symptomatology.  The  cases  of  manifest  disease  of 
the  stomach  where  a primary  disease  of  the  mouth  is  out  of  the 
question  are  extremely  rare.  A critical  review  of  the  etiology  of 
gastric  diseases  can  not  fail  to  evince  the  fact  that  the  prominent 
causes  can,  and  most  often  do,  affect  the  mouth  and  stomach  alike. 
The  gastric  disorders  in  which  the  tongue  is  most  frequently  unaf- 
fected are  those  associated  with  little  or  no  gastric  sepsis,/,  e .,  ulcer, 
hyperacidity,  neurasthenia  gastrica ; whereas  in  diseases  asso- 
ciated with  much  gastric  fermentation  or  histological  changes  in 
the  mucosa  that  may  extend  to  the  mouth,  or  involve  it  through 
circulatory  or  nervous  channels,  the  tongue  is  most  often  affected. 
These  diseases  are  gastritis,  carcinoma,  and  dilatation. 

In  reviewing  the  statements  of  most  authors  on  the  condition  of 
the  tongue,  one  can  not  fail  to  notice  a lack  of  clearness  and  pre- 
cision, which  doubtless  indicates  that  the  relation  between  remote 
and  local  causes  is  not  well  understood  concerning  this  matter. 
A systematic  bacteriological  and  histological  study  of  coated 
tongues  is  very  much  needed  in  association  with  gastric  diseases. 
The  attempt  to  establish  a definite,  characteristic  condition  of  the 


SUBJECTIVE  SYMPTOMS. 


457 


tongue  for  every  gastric  disease  has  thus  far  failed.  The  exten- 
sion of  stomatitis  and  glossitis  to  the  stomach  by  the  deglutition 
of  infective  material  is  plausible.  But  the  various  forms  of  gas- 
tric diseases  may  also  extend  upward,  either  by  eructations  or 
direct  cellular  continuity.  Then,  again,  the  oral  and  gastric  cavi- 
ties are  in  intimate  correlation,  and  may  mutually  affect  each  other 
through  the  vascular  and  complex  nervous  channels.  Fleischer 
( loc . city  p.  820)  holds  that  the  importance  of  the  coating  of  the 
tongue  as  a sign  of  gastritis  has  been  much  overrated,  and  that 
the  tongue  may  be  clean  notwithstanding  very  evident  chronic 
gastritis,  and  may  be  coated  when  this  disease  is  absent.  Never- 
theless, he  considers  the  frequent  coincidence  of  coated  tongue 
and  gastritis  remarkable,  but  attributes  it  to  a concomitant 
stomatitis. 

General  Nutrition. — Chronic  gastritis  of  long  standing,  left  un- 
treated, will  inevitably  affect  the  general  nutrition.  As  von  Noor- 
den  repeatedly  emphasizes,  “ most  dyspeptics  do  not  eat  enough,” 
and  in  consequence  of  this  emaciation  ensues  to  such  a degree 
that  even  physicians  suspect  a grave  underlying  disease  (tubercu- 
losis or  carcinoma)  where  there  is  only  a chronic  gastritis.  The 
absence  of  appetite  is  most  frequently  caused  by  a suppression  of 
secretion  of  HC1. 

Feeling  of  pressure  and  fullness  in  the  epigastric  region  is,  in 
many  cases,  complained  of,  and  may  be  evident  on  awakening  or 
develop  after  ingestion  of  food.  The  epigastric  region  in  these 
cases  is  very  likely  to  be  arched  forward  and  outward,  and  very 
sensitive  to  pressure,  even  the  weight  of  the  clothes  being  annoy- 
ing. If  no  dilatation  exists,  the  lower  border  of  the  stomach  is 
found  in  its  natural  place.  It  must  not  be  forgotten  that  a stomach 
may  be  dilated  considerably  and  yet  the  lower  border  be  found  in 
normal  position,  for  the  organ  may  be  enlarged  upward  or  laterally, 
displacing  the  diaphragm.  Professor  J.  Schreiber,  of  Konigsberg, 
has  repeatedly  called  attention  to  the  fact  that  the  horizontal  um- 
bilical line  is  a misleading  landmark  by  which  to  judge  a dilatation, 
and  that  the  upper  border  should,  in  all  cases  of  suspected  dilatation, 
be  determined  (“  Archiv  f.  Verdauungskrankh.,”  Bd.  11,  Heft  4).  It 
may  be  possible  to  ascertain  by  palpation  whether  the  gastric  walls 
are  thickened  or  not.  If  a dilatation  be  present,  there  exists,  gen- 
erally, a stenosis  of  the  pylorus ; more  rarely  it  is  due  to  so-called 
atony.  The  feeling  of  pressure  may  increase  to  a constant  dull 
pain,  which  should,  if  it  becomes  intense,  lead  to  suspicion  of  car- 


458 


CHRONIC  GASTRITIS. 


cinoma  or  ulcer.  Some  patients  with  chronic  gastritis  suffer 
during  digestion  from  an  active  peristaltic  unrest  in  the  stomach 
and  intestines,  their  attention  being  directed  to  it  by  abdominal 
rumbling  and  gurgling  (borborygmus). 

Conditions  of  Gastric  Contents  ; Secretion. — The  results  of 
microscopical  and  chemical  analysis  after  test-meals,  or  of  lavage 
water  early  in  the  morning  before  any  food  has  been  taken,  will 
vary  according  to  the  particular  kind  of  chronic  gastritis  and  the 
present  state  of  the  disease.  Boas  recognizes,  with  regard  to  these 
points,  four  varieties  of  gastritis,  viz. : (i)  Acida  ; (2)  anacida  ; (3) 
mucosa ; (4)  atrophicans.  The  separation  of  these  four  types 
clinically  is  difficult  and  has  little  practical  value.  In  my  expe- 
rience it  is  sufficient  to  ascertain  whether  we  are  dealing  with  a 
simple  chronic  gastritis  or  one  that  has  already  advanced  to 
atrophy.  It  is  of  value  to  know  whether  the  mucosa  is  still  in  a 
condition  of  inflammatory  irritation,  or  whether  this  has  terminated 
in  a state  of  connective-tissue  degeneration. 

The  establishing  of  a separate  form  of  gastritis  mucipara,  for 
instance,  may  have  its  pathological  justification,  when  one  can 
demonstrate  extensive  mucoid  degeneration  of  the  mucosa,  and 
when  there  has  been  an  enormous  vomiting  of  mucus  in  the  history 
of  the  case. 

Simple  chronic  gastritis  and  chronic  gastritis  mucipara  simply 
denote  differences  of  degree  of  the  same  process.  Simple  chronic 
gastritis  is  also  a mucous  gastritis.  The  presence  of  large  amounts 
of  mucus  in  the  empty  stomach  in  the  morning  is  the  most  char- 
acteristic symptom  of  this  disease. 

Gastritis  Acida. — State  of  the  Secretions. — Prior  to  the  results  of 
recent  investigations,  it  had  been  uniformly  maintained  that  ab- 
sence or  great  diminution  of  HC1  was  a constant  symptom  of 
chronic  gastritis.  Boas  argues  that  there  is  a form  of  typical  in- 
flammation of  the  stomach — termed  by  him  “ Gastritis  Acida  ” — 
in  which  there  is  present  an  increased  amount  of  mucus,  together 
with  a normal  amount  of  acid,  or  even  superacidity  (Boas,  “ Ueber 
Gastritis  Acida,”  “ Mittheil.  d.  Naturforscher-Versamml.  in  Wien,” 
1894).  Even  the  mucus  from  the  fasting  stomach  may  turn  Congo- 
paper  blue. 

Gastritis  Anacida. — In  this  subdivision  free  HC1  is  diminished  or 
entirely  absent,  but  combined  HC1  is  still  present.  Egg-albumen 
discs  are  but  slowly  digested,  or  not  at  all,  in  the  filtrate,  even  after 
addition  of  HC1.  The  difference  between  this  and  the  atrophic  form 


TVPES  OF  CHRONIC  GASTRITIS.  459 

is  but  one  ot  degree,  as  in  the  latter  all  secretion  is  lost  com- 
pletely. 

Gastritis  Mucosa , or  Mucipara. — As  was  pointed  out  (page  131) 
before,  when  rhinitis,  laryngitis,  pharyngitis,  and  bronchitis  can  be 
eliminated,  large  quantities  of  mucus  in  the  gastric  contents,  as  a 
rule,  speak  for  chronic  gastritis  mucosa.  The  cases  not  forming 
much  mucus  represent  end  stages  of  the  disease — the  atrophy. 
The  mucus-formation  can  be  best  estimated  by  washing  out  the 
fasting  stomach.  There  should  be  no  difficulty  in  differentiating 
gastric  mucus  from  that  derived  from  the  respiratory  passages. 
The  former  is  generally  thin,  clear,  glassy,  stringy,  and  flowing; 
the  latter  thick,  opaque,  yellowish-gray,  and  lumpy.  In  the 
washing  from  the  fasting  organ  one  frequently  finds  the  organic, 
structural  form-elements  of  the  mucosa  minutely  described  in  the 
last  chapter  and  on  page  135.  If  these  bits  of  mucosa  are  found  at 
repeated  washings,  showing  these  elements  either  in  conglomera- 
tion or  singly,  there  can  be  no  doubt  of  the  existence  of  glandular 
chronic  gastritis.  Frequently  the  morning  contents  of  the  fasting 
organ  show  numerous  leukocytes.  The  contents  should  be  drawn 
by  expression ; if  possible,  without  using  water.  In  gastritis 
chronica  mucipara  the  contents  may  show  a normal  amount  of 
HC1,  or  may  be  either  neutral  or  alkaline. 

Gastritis  Atrophicans. — In  this  variety  both  free  and  combined 
HC1  are  absent,  and  the  tests  for  enzymes  and  proenzymes  are 
negative.  Milk  taken  or  poured  into  the  stomach  is  returned 
mostly  in  unchanged  condition.  Martius  and  Luttke  (Joe.  cit.)f  von 
Noorden,  and  others,  maintain  that  absolute  disappearance  of  pepsin 
and  rennin  is  never  seen.  From  large  clinical  experience  I am 
prepared  to  state  that  the  end  stages  of  atrophic  gastritis  give  no 
evidence  of  ferments  in  gastric  contents  by  any  of  the  known  tests. 
Nor  would  it  be  rational  to  suppose  that  in  hypertrophic  gastritis, 
in  which  the  stomach  is  converted  into  a hyperplastic,  dense,  hard 
mass  of  muscle  and  connective  tissue,  with  no  histological  remnant 
of  a glandular  layer,  there  should  be  any  possibility  of  the  forma- 
tion of  enzymes.  In  atrophic  gastritis,  more  than  in  the  other  forms, 
there  are  very  characteristic,  lancinating  pains. 

The  digestion  of  albumin  discs  or  fibrin  in  the  thermostat  is 
much  retarded,  or  may  be  wanting  entirely,  denoting  the  suppres- 
sion of  the  secretion  of  pepsin. 

Disappearance  of  rennin  and  its  zymogen  goes  on  simultaneously 
with  that  of  pepsin.  In  cases  with  loss  of  rennin  the  zymogen  of 


460 


CHRONIC  GASTRITIS. 


this  ferment  must  be  tested  for.  Among  other  observers,  Bouveret 
(“  La  pepsine  et  le  ferment  lab.,”  “ Gaz.  Med.  de  Paris,”  1 893,  No.  22) 
declares  that  the  absence  of  this  zymogen  is  an  important  criterion 
of  the  degree  to  which  the  destructive  process  has  advanced.  For 
the  same  purpose,  Jaworski  suggests  the  introduction  of  decinor- 
mal  solutions  of  hydrochloric  acid  into  the  stomach,  to  awaken 
any  slumbering  remnants  of  proenzyme  formation  and  convert 
them  into  perfect  enzymes.  In  no  case  that  shows  the  presence  of 
rennin  zymogen  need  hope  of  complete  or  partial  restitution  be 
resigned. 

Age. — This  is  preeminently  a disease  affecting  adults,  for  the 
young  are  not  so  liable  to  abuse  their  stomachs,  or  so  subject  to 
the  manifold  factors  composing  the  etiology ; besides,  their  recon- 
structive and  compensatory  powers  are  greater.  The  majority  of 
cases  are  over  forty  years  of  age,  but  Litten  (“  Zeitschr.  f.  klin. 
Med.,”  Bd.  xiv,  S.  573)  has  reported  a case  of  eighteen  years,  and 
Einhorn  one  of  twenty-one  years.  The  case  of  Westphalen  (“  St. 
Petersburger  med.  Wochenschr.,”  1890,  Nos.  37  and  38)  was,  how- 
ever, verified  by  autopsy  ; it  occurred  in  a young  man  twenty-eight 
years  old.  We  have  had  under  our  personal  observation  since 
1888  a young  printer,  at  that  time  in  his  twentieth  year,  whose, 
case  showed  absence  of  enzymes  and  HC1,  with  much  mucus. 
Numerous  leukocytes  were  evident  in  the  contents  before  food 
had  been  taken.  Although  we  have  frequently  since  analyzed  his 
stomach  contents,  no  hydrochloric  acid  or  proenzymes  have  ever 
been  detected.  But  on  several  occasions  there  appeared  fragments 
of  gastric  mucosa,  showing  glandular  atrophy  and  chronic  inflam- 
mation. 

The  condition  of  the  bowels  most  frequently  exhibits  constipation. 
Absence  of  the  antiseptic  action  of  hydrochloric  acid  favors  intes- 
tinal fermentation,  flatulence,  and  meteorism.  When  there  is  much 
decomposition  of  ingesta,  intestinal  irritation  will  eventually  set  in, 
accompanied  by  diarrhea. 

The  urine  is  rich  in  urates  and  phosphates  and  often  gives  a 
strong  indican  reaction.  The  total  acidity  of  the  urine  is  reduced. 

The  general  health  is  variable  ; the  body  weight  may  either  be 
reduced  or  remain  constant  for  years  : this  last  indicates  that  the 
intestinal  digestion  is  good.  Many  changes  of  the  general  condi- 
tion, from  good  to  bad  and  vice  versa,  may  occur,  but  as  the  chronic 
inflammation  progresses  there  are  marked  symptoms  of  general  dis- 
comfort and  indisposition  to  bodily  or  mental  exertion.  The  least 


MOTOR  FUNCTIONS  IN  CHRONIC  GASTRITIS.  46 1 

exertion  rapidly  tires,  bringing  on  pains  in  the  limbs,  and  despite 
this  exhaustion  there  may  be  insomnia.  This  leads  to  a depression 
of  spirit  which  may  control  the  entire  mentality,  and  brings  on  hy- 
pochondriasis and  melancholia.  This  leads  me  to  refer  to  the 
psychic  and  nervous  symptoms,  of  which  there  maybe  many,  begin- 
ning with  timidity  and  worry  at  every  new  symptom,  precordial 
fear,  oppression,  and  cardiac  palpitation  accompanied  by  occasional 
attacks  of  dyspnea.  The  so-called  stomach  vertigo,  first  described 
by  Trousseau,  I have  never  observed  in  chronic  gastritis,  nor  the 
agarophobia  (i.  e.,  terror  in  crossing  wide  and  empty  localities  alone) 
which  Fleischer  (loc.  cit.)  says  occurs  as  a psychic  accompaniment. 
From  practical  observation  I am  disposed  to  believe  that  these 
psychic  and  nervous  phenomena  have  been  exaggerated,  as  they 
•occur  only  in  very  protracted  cases,  and  then  even  inconstantly. 

Disturbances  of  Motility. — A great  number  of  cases  of  chronic 
gastritis  have  been  examined  at  the  University  of  Maryland  Hos- 
pital and  the  Maryland  General  Hospital,  with  regard  to  the  peris- 
talsis; and,  in  the  large  majority,  this  has  been  found  normal  or 
slightly  exaggerated.  We  use  the  method  described  on  pages  76- 
80.  Boas  declares  that  he  has  never  observed  a dilatation  arise 
from  a chronic  gastritis  (“  Diagnostik  u.Therap.  d.  Magenkrankh.,” 
2d  edition,  p.  21).  It  is  evident  that  stenosis  of  the  pylorus  can 
occur  which  is  not  caused  by  cicatricial  contraction  nor  by  neo- 
plasm, but  by  hyperplasia  of  the  muscular  sphincter  of  the  pyloric 
region.  If  a chronic  gastritis  lasts  long  enough,  it  is  a fair  pre- 
sumption that  it  may  result  in  a gastrectasia  due  either  to  atrophy 
of  the  muscularis  from  connective-tissue  invasion,  or  to  the 
muscular  hyperplasia,  producing  a stenosis.  Boas  has  also  con- 
clusively shown  that  lactic  acid  is  not,  as  a rule,  formed  in  glandular 
gastritis. 

Complications. — The  most  frequent  is  the  extension  of  the  in- 
flammation to  the  intestines.  The  frequent  association  of  chronic 
duodenitis  with  the  disease  explains  the  occurrence  of  catarrhal 
icterus,  which  is  an  extension  of  the  intestinal  inflammation  to  the 
gall-ducts.  The  results  of  chronic  gastritis  are,  in  protracted  cases 
(particularly  when  the  intestines  have  been  involved),  marked  dis- 
turbances of  nutrition  and  anemia,  which,  as  we  have  had  occasion 
to  observe,  may  assume  very  serious  forms. 

The  duration  may  vary  from  several  months  to  years,  particu- 
larly if  the  patients  have  not  the  means  nor  the  will-power  to  follow 
dietetic  regime. 


462 


CHRONIC  GASTRITIS. 


Atypical  forms  of  chronic  gastritis  are  by  no  means  rare 
occurrences,  and  sometimes  make  a clear  diagnosis  very  difficult. 
In  the  foregoing  description  of  the  disease  the  lack  of  very  charac- 
teristic and  peculiar  symptoms  is  evident.  In  addition  to  this,  the 
symptoms  of  loss  of  appetite,  pressure,  fullness,  eructation,  vomit- 
ing of  mucus,  may  be  absent  in  atypical  forms,  and  it  has  been 
observed  that  chronic  gastritis  may  run  its  course  in  a latent,  unde- 
tected manner.  Again,  it  may  exist  under  the  manifestations  of  a 
nervous  dyspepsia,  or  there  may  be  such  prominent  intestinal 
symptoms  as  to  disguise  the  gastritis. 

Diagnosis. — It  requires  careful  study  not  only  to  distinguish 
chronic  gastritis  from  other  diseases,  but  also  to  distinguish  the 
simple,  mucous,  atrophic,  and  chronic  gastritis  acida  (of  Boas) 
from  one  another.  As  a rule,  the  primary  and  secondary  forms 
can  be  distinguished  without  much  difficulty.  Generally  speaking, 
the  diagnosis  of  chronic  gastritis  can  only  be  satisfactorily  estab- 
lished after  the  possibility  of  the  existence  of  other  affections  of 
the  stomach  has  been  excluded.  This  disease  may  strikingly 
resemble  the  clinical  pictures  of  the  gastric  neuroses,  of  ulcer,  and 
even  carcinoma.  Dilatation  is  a very  rare  complication,  and 
therefore  not  a confusing  factor  in  diagnosis.  One  should  not 
make  the  diagnosis  definite  at  the  first  examination,  but  reserve 
opinion  until  the  patient  has  been  studied  during  three  or  four 
visits.  It  has,  in  some  cases,  taken  a much  longer  time  than  that 
to  obtain  satisfactory  evidence  of  the  disease.  The  best  evidence  is 
afforded  by  repeated  microscopical  and  chemical  examination  of  the 
wash-water  and  test-meals,  and  the  persistent  presence  of  much 
mucus  in  the  empty  stomach. 

It  will  be  necessary  to  dwell  upon  the  differential  diagnosis  be- 
tween chronic  gastritis  and  the  neuroses,  ulcer,  carcinoma,  and 
amyloid  degeneration  : The  neuroses  may  present  all  the  symptoms 
of  a chronic  gastritis,  particularly  the  absence  of  HC1;  but,  after 
patient  and  repeated  test-meal  analysis,  it  will  be  found  that  the 
neuroses  will  some  day  show  a normal  and  even  excessive  amount 
of  HC1.  The  course  to  pursue  is  to  wait  for  this  evidence.  The 
presence  of  much  mucus,  epithelial  cells,  and  leukocytes  in  the 
wash-water  from  the  jejune  stomach  indicates  chronic  gastritis. 
Demonstration  of  enzymes  and  proenzymes  is  very  valuable,  as 
a normal  amount  of  pepsin  and  rennin  (when  HC1  is  absent) 
speaks  for  neurosis  and  against  gastritis.  In  the  absence  of  HC1, 


DIFFERENTIAL  DIAGNOSIS.  463 

Jaworski’s  method  ot  pouring  in  decinormal  HC1  should  be  used 
to  stimulate  the  formation  of  enzymes. 

In  the  incipient  stage  of  chronic  gastritis  the  enzymes  may  be 
present,  even  in  normal  amount ; but  they  disappear  gradually  as 
the  disease  progresses.  By  the  time  the  physician  is  consulted,  the 
enzymes  are  very  much  diminished  or  entirely  absent;  this  is  an 
indication  of  an  inflammation  of  the  mucosa,  not  a neurosis. 

The  differential  diagnosis  between  idiopathic  chronic  gastritis  and 
ulcer  is  decided  by  the  symptom  of  pain,  which  is  always  present 
in  ulcer,  and  usually  absent  in  chronic  gastritis.  The  ulcer-pain  is 
localized,  well  circumscribed,  very  intense,  and  occurs  at  definite 
times  after  partaking  of  food.  Hematemesis,  of  course,  points  to 
ulcer.  The  vomit  of  ulcer  shows  hyperacidity,  which  is,  as  a rule, 
absent  in  gastritis.  In  atrophic  gastritis  there  may  be  lancinating 
pains,  but  they  are  diffuse  and  not  so  frequent  or  constant  as  in 
ulcer. 

From  carcinoma  the  differentiation  may  be  difficult  when  no 
palpable  tumor  can  be  detected.  This  is  intelligible  when  one  re- 
flects that  carcinoma  is  generally  complicated  with  chronic  gastritis. 
If  a pyloric  carcinoma  be  present,  the  most  noteworthy  symptoms 
are : stenosis,  motor  insufficiency,  and  stagnation  of  food  with 
large  amounts  of  lactic  acid.  A carcinoma  seems  to  strike  a 
stomach  suddenly  with  very  severe  symptoms  and  general  disturb- 
ances— pain,  emaciation,  and  vomiting;  whereas  chronic  gastritis 
is  characterized  by  slow  increase  of  the  gravity  of  symptoms,  with 
alternating  improvements  and  aggravations.  It  is  an  important 
fact  that  the  motility  is  not  disturbed  in  chronic  gastritis,  and, 
therefore,  the  stomach  rarely  contains  anything  but  mucus,  iso- 
lated cells,  and  leukocytes.  But  in  carcinoma  the  peristalsis  is 
seriously  impeded  from  the  onset,  and  therefore  there  must  be 
stagnation,  retention,  and  acid-fermentation.  These  products  of 
retained  ingesta  occur  even  when  there  is  no  stenosis  of  the  py- 
lorus, as  a result  of  carcinomatous  invasion  of  the  muscularis.  Gas- 
trectasia  is  an  exceedingly  rare  result  of  gastritis,  and  can  occur 
only  from  hyperplastic  thickening  of  the  pylorus,  a thing  seldom 
reported  in  the  literature  of  this  subject.  As  stated  before,  the 
presence  of  marked  amounts  of  lactic  acid  is  not  observed  in  gas- 
tritis, but  in  carcinoma  its  occurrence  is  very  frequent.  Organic  acids 
are  rare  in  the  test-meals  of  gastritis,  whereas  in  carcinoma  there 
is,  as  a rule,  an  excess  of  lactic  and  fatty  acids  early  in  the  disease 


464 


CHRONIC  GASTRITIS. 


(Boas.  loc.  cit.).  For  further  differentiation  see  article  on  Car- 
cinoma. 

Amyloid  degeneration  of  the  stomach  may  lead  to  complete 
suppression  of  the  gastric  secretion,  but  it  is  always  a secondary 
disease,  occurring  in  the  sequence  of  chronic  suppurative  pro- 
cesses and  pulmonary  tuberculosis.  If  the  existence  of  amyloid  de- 
generation can  be  established  in  the  spleen,  kidneys,  or  liver,  we 
are  justified  in  considering  a secondary  involvement  of  the  stomach 
when  HC1  secretion  has  been  proven  to  be  lost.  This  form  of 
degeneration  in  the  stomach  is,  in  my  experience,  extremely  rare. 

Synopsis  of  diagnostic  points  in  various  types  of  chronic  gastritis  : 


Contents  of  Fast- 
ing Stomach. 

Acidity. 

Ferments. 

(1)  Simple  Chronic 
Gastritis. 
Subacid  or  anacid. 

Limited  amount  of 
watery  mucus; 
leukocytes ; epi- 
thelial cells; 
round  cells. 

Variable^;  free  HCl 
rarely  present,  but 
if  present,  lessened 
in  amount ; com- 
bined HCl  present. 

Pepsin  and  rennin  pres- 
ent in  small  amount ; 
propeptone  formed  in 
the  stomach. 

(2)  Chronic  Mu- 
cous Gastritis. 

Much  mucus ; epi- 
thelial fragments. 

At  the  beginning 
there  may  be  a 
normal  amount  of 
combined  HCl; 
later  on  the  amount 
is  low;  HCl  ab- 
sent ; HCl  deficit. 

Pepsin  absent ; rennin 
absent;  both  proen- 
zymes present ; ex- 
perimental digestion 
occurs  on  supplying 
the  HCl  deficit. 

(3)  Chronic  Atro- 
phic Gastritis. 
Lancinating  pains 
present  in  this  form. 

Empty;  no  mucus. 

HCl  absent;  HCl 
deficit ; no  com- 
bined HCl. 

No  enzymes ; no  pro- 
enzymes ; no  curd- 
ling of  milk  on  add- 
ing HCl. 

(4)  Acid  Gastritis. 

Much  mucus ; giving 
HCl  reaction. 

Normal  amount  HCl, 
or  hyperacidity. 

Ferments  increased. 

Prognosis. — Chronic  gastritis  is  a tedious,  but  not  a very  seri- 
ous, affection,  as  many  cases  recover  under  suitable  treatment.  The 
prognosis  must  vary  with  the  stage  of  the  disease  as  presented, 
and  the  intelligence  and  will-power  of  the  patient.  Patients  who 
will  study  to  avoid  further  detrimental  influences,  and  who  have 
the  determination  to  carry  out  the  dietetic  and  hygienic  manage- 
ment, will  recover.  With  incorrigible  eaters  or  drinkers,  who  re- 
transgress against  their  stomachs  on  the  slightest  improvement, 
permanent  recovery  is  doubtful.  After  the  establishment  of  partial 
or  complete  atrophy  of  the  glandular  mucosa,  perfect  recovery 
is  impossible ; but  as  it  is  well  known  that  a good  state  of  general 


TREATMENT. 


465 


health  may  be  maintained  with  complete  suppression  of  the  gastric 
juice,  provided  the  intestines  still  function  normally,  atrophy  of  the 
mucosa  does  not  necessarily  imperil  vitality.  On  the  other  hand, 
there  are  numerous  well-authenticated  observations  (see  literature) 
that  demonstrate  severe  disturbances  of  nutrition,  particularly  per- 
nicious anemia,  as  a consequence  of  gastric  atrophy.  The  instances 
of  complete  extirpation  of  the  stomach — Brigham  in  this  country, 
whose  case  has  already  lived  longer  than  Schlatter’s  case  in  Zurich 
— show  that  metabolism  and  nutrition  may,  for  a time  at  least,  be 
apparently  normal  with  total  absence  of  the  stomach.  These  pa- 
tients remain  under  constant  medical  control,  however.  Fenwick 
(loc.  cit .)  suggests  that  this  pernicious  anemia  may  be  due  to  auto- 
intoxication from  the  stomach.  Other  authors,  again,  hold  that 
the  anemia  maybe  the  primary  factor,  and  bring  about  the  atrophy 
of  the  mucosa.  This  entire  question  still  partakes  of  a speculative 
nature,  since  exact  and  logical  experiments  and  deductions  are 
wanting. 

Treatment. — Prophylactic  Treatment. — The  prevention  of  the 
development  of  the  disease  implies  avoidance  of  the  causes  given 
under  the  head  of  etiology  of  acute  and  chronic  gastritis.  Special 
attention  should  be  directed  to  the  avoidance  of  continued  abuse 
of  alcohol.  Every  acute  gastritis,  be  it  an  independent,  idiopathic 
affection,  or  secondary  to  other  diseases,  must  be  carefully  treated 
in  order  to  prevent  its  transition  into  the  chronic  form.  Explicit 
directions  regarding  diet  and  mode  of  life  must  be  given  to  all 
sufferers  from  liver,  lung,  heart,  and  kidney  diseases ; also  to 
diabetics,  in  order  that  they  may  be  saved  from  secondary  gastritis, 
for  disturbances  of  appetite  and  impairment  of  digestive  powers 
must  inevitably  render  the  fundamental  disease  more  serious. 

The  chief  predisposing  factors  to  secondary  chronic  gastritis  are 
passive  congestion  and  accumulation  of  injurious  metabolic 
products  in  the  heart  muscle,  with  renal  insufficiency.  In  cases  of 
cardiac  insufficiency  with  threatened  passive  engorgement,  digitalis 
should  be  used  early.  One  should  not  hesitate  to  give  digitalis  on 
account  of  the  occasional  appetite-disturbing  effect  of  the  medicine, 
as  this  is  usually  transient ; an  improvement  of  the  appetite  and  of 
nutrition  in  general  will  be  observed  in  these  cases  if  the  treatment 
be  continued;  we  usually  combine  it  with  large  doses  of  strychnin. 
The  passive  engorgement  of  the  mucosa  is  more  harmful  than  the 
drug.  If  it  is  noticed  in  several  attacks  that  the  gastric  symptoms 
improve  on  administration  of  digitalis,  it  is  expedient  to  give  the 


466 


CHRONIC  GASTRITIS. 


remedy  at  the  outset  of  the  slightest  disturbance  of  appetite,  since 
our  experience  has  taught  us  that  this  will  unfailingly  become 
aggravated  by  delay  in  the  use  of  the  heart  tonic.  If  the  stomach 
rebels  against  the  remedy,  the  infusion  should  be  given  by  enema 
into  a rectum  previously  cleaned  by  warm  normal  salt  irrigation, 
or  digitalin  injected  hypodermically. 

Lavage. — When  it  is  no  longer  possible  to  remove  the  causes 
that  lead  to  a chronic  gastritis,  we  may  yet  be  able  to  remove 
those  that  maintain  or  aggravate  the  malady.  These  causes  are : 
the  accumulation  of  mucus,  and  the  mechanical  as  well  as  chemi- 
cal irritation  of  the  stagnating  contents,  particularly  when  atony 
and  hypertrophic  stenosis  exist.  To  accomplish  this,  emetics  are 
impracticable,  because  they  rarely  effect  a thorough  cleansing,  and 
may  increase  the  inflammation  by  the  convulsive  contractions  they 
excite  and  by  their  direct  irritation.  Purgatives  are  even  more 
deleterious,  for  several  reasons  : first,  they  also  increase  gastric 
irritation;  secondly,  they  can  not  be  used  habitually;  and, 
thirdly,  they  hurry  decomposing  masses  into  the  intestines,  there- 
by precipitating  an  involvement  of  this  tract  and  the  dangers  of 
intestinal  putrefaction  and  auto-intoxication.  Lavage  is  the  only 
correct  procedure  in  chronic  gastritis  whenever  increase  of  mucus, 
absence  of  HC1,  decomposition,  and  a protracted  stomach  diges- 
tion are  evident.  The  mucus  often  adheres  very  tightly  to  the 
gastric  walls,  since  it  only  appears,  as  a rule,  toward  the  close  of 
the  washing.  Its  evacuation  is  facilitated  by  allowing  the  water 
to  run  in  under  high  pressure,  and  directing  the  patient  to  change 
his  position — i.  e.f  lying  on  his  back,  rising  or  turning  on  his  side — 
during  the  lavage ; or  by  employment  of  gastric  massage.  The 
solution  of  the  mucus  is  effectually  accomplished  by  adding  one 
tablespoonful  of  salt  and  two  tablespoonfuls  of  sodium  bicarbonate 
or  biborate  to  a liter  of  warm  water.  To  disinfect  the  stomach 
after  the  removal  of  mucus  and  fermenting  ingesta,  the  following 
remedies  are  approved  aids  : Salicylic  acid,  1 : 1000;  thymol,  0.5  : 
1000;  boric  acid,  10:  1000;  chloroform  water,  5 to  10  : 1000; 
shake  the  chloroform  with  the  water,  and,  after  settling,  pour  off 
the  water,  using  only  the  latter;  hydrochloric  acid,  6 : IOOO;  re- 
sorcin resublimate,  10  : 1000;  benzol,  5 : 1000.  The  solution  must 
be  prepared  immediately  before  the  washing. 

The  frequency  of  the  lavage  depends  upon  the  state  of  the 
stomach.  There  may  be  cases  that  do  not  require  it  oftener  than 
once  in  two  or  three  days  ; others  require  it  twice  in  twenty-four 


D I ETETIC  TREATM  ENT. 


467 


hours;  usually,  once  a day  is  sufficient.  The  time  of  the  washing 
should  be  so  selected  that  the  exhausted  stomach  may  enjoy  the 
longest  possible  rest.  For  this  purpose  six  o’clock  in  the  evening 
is  most  suitable,  as  it  is  then  about  six  hours  after  the  main  meal 
of  the  day,  and  no  food  or  only  very  light  diet  is  taken  after  the 
lavage  and  before  bedtime.  In  other  cases  this  hour  may  be  in- 
convenient, and  an  early  hour  before  breakfast  must  be  chosen.  A 
plan  useful  in  many  instances  in  which  the  stomach  requires  rest 
is  to  give  a fair  breakfast  at  9 A.  m.,  dinner  at  3 p.  m.,  no  supper, 
and  lavage  at  9 p.  m.  Washing  out  the  stomach  is  advisable  only 
when  there  is  much  formation  of  mucus  and  when  there  may  be 
stagnation  of  food.  In  atrophic  or  chronic  gastritis  without  much 
mucus,  frequent  lavage  is  not  necessary.  In  these  cases  the 
stomach-tube  is  recommended,  not  to  remove  fermenting  ingesta 
or  mucus,  but  to  treat  the  mucosa  directly,  to  stimulate  its  slug- 
gish secretion  by  irrigating  with  decinormal  solution  of  HC1;  if 
enzymes  are  still  to  be  detected,  common  salt  solutions  are  useful 
for  this  purpose  (about  one  tablespoonful  to  the  quart).  Solutions 
of  NaCl  must  not  exceed  the  strength  of  one  per  cent.,  as  solu- 
tions of  four  per  cent.  NaCl  check  the  HC1  secretion  and  are  avail- 
able in  the  treatment  of  hyperacidity.  (See  “Achylia  Gastrica.”) 
Dietetic  Treatment . — In  each  case  it  is  advisable  to  give  the 
patient  a written  diet-list,  based  upon  a chemical  study  of  the  indi- 
vidual’s digestive  power.  Sometimes  it  will  be  impossible  to  give 
a diet  at  first  that  will  at  the  same  time  suit  the  patient’s  palate  and 
digestive  power.  The  most  digestible  food  will  at  times  disagree 
with  chronic  gastritics,  and  food  which  would  seem  a priori  very 
indigestible,  agrees  well.  A good  plan  is  to  inquire  minutely  into 
each  patient’s  accustomed  diet  and  ascertain  what  food  especially 
disagrees.  At  the  beginning,  the  diet  should  be  of  a light  kind  : 
one  that  makes  but  slight  demands  upon  the  working  capacity  of 
the  stomach.  As  the  motility  is  good  in  this  trouble,  the  diet,  as 
far  as  possible,  should  be  liquid  or  semiliquid,  and  in  some  cases 
four  to  six  small  meals  a day  are  preferable  to  three  large  ones. 
In  others  it  will  be  insuring  rest  to  the  stomach  to  give  only 
two  meals  a day,  excluding  the  supper.  Nutritious  soups,  such 
as  beef  bouillon  enriched  by  the  addition  of  butter,  eggs,  beef- 
meal  or  jelly,  somatose,  or  nutrose,  are  generally  well  borne,  but 
as  a rule  do  not  suffice  to  maintain  strength  and  body  weight.  It 
is  well  to  insist  on  slow  eating,  thorough  chewing,  and  insalivation 
as  important.  The  teeth  should  be  looked  after,  and,  if  necessary, 


468 


CHRONIC  GASTRITIS. 


repaired,  or  artificial  ones  provided.  Should  there  be  a normal 
amount  of  HC1  and  pepsin  secreted,  then  a diet  rich  in  proteid 
will  be  advisable.  Suitable  articles  of  diet  are  all  white  meats,  fish, 
and  eggs,  properly  prepared  ; which  means  that  the  roast  or  broiled 
meats,  even  after  they  are  on  the  table,  must  be  very  finely  divided 
on  the  plate  before  placing  in  the  mouth.  Light  vegetables  are 
permissible  in  form  of  purees,  viz. : potatoes  mashed  in  milk,  peas 
or  beans  driven  through  a sieve,  spinach,  etc.  When  the  HC1, 
although  present,  is  considerably  reduced,  the  diet  will  be  similar; 
but  spices  and  well-salted  food  are  more  adapted.  If  the  secretion 
is  completely  suppressed,  it  is  not  expedient  to  greatly  restrict  the 
diet,  as  these  patients  are  more  liable  to  suffer  from  inanition.  The 
greatest  care  is  to  be  employed  in  the  preparation  of  the  food, 
which  must  be  presented  in  an  appetizing  and  finely  divided  form. 
All  meats  and  fish  must  be  prepared  in  the  steam  broiler,  and,  if 
needed,  they  should  be  previously  minced  and  then  reformed  into 
any  desirable  shape,  held  by  a supporting  substance  such  as  ex- 
perienced cooks  are  familiar  with,  generally  consisting  of  bread- 
crumbs, eggs,  salt,  and  butter.  Milk,  if  it  agrees  well,  is  a valuable 
adjunct  to  the  diet,  and  even  if  not  well  digested,  or  if  there  is  an 
aversion  to  it,  should  be  surreptitiously  added  to  soups,  chocolate, 
rice,  sago,  gelatins,  and  farinaceous  foods.  When  it  is  thus  mixed 
with  other  foods  it  is  generally  very  well  digested,  and  adds  to 
their  nourishing  quality.  Von  Mehring  has  recommended  a choco- 
late (Kraftchocolade)  which  contains  20  per  cent,  of  fat ; it  is  very 
palatable  and  usually  causes  no  digestive  distress.  When  there 
is  emaciation,  we  give  small  amounts  of  alcohol,  upon  the  authority 
of  Chittenden’s  experiments  that  alcohol  up  to  three  per  cent,  favors 
proteolysis  and  amylolysis,  and  is  a fat-sparer.  If  we  are  sure,  from 
test-meals,  that  there  is  no  gastric  fermentation, — and  according 
'to  our  experience  there  rarely  is  in  chronic  gastritis, — we  recom- 
mend the  genuine  Oporto,  Malaga,  or  imported  Hungarian  Tokay 
wines.*  When  it  is  evident  that  the  gastritis  was  caused  by 
bacchanalian  excess,  it  is,  naturally,  a good  plan  to  exclude 
alcohol  as  far  as  possible.  Indeed,  when  the  emaciation  is  not 
marked,  or  when,  after  a trial,  the  collective  symptoms  appear 
to  become  worse,  alcohol  is  best  avoided.  There  are,  how- 
ever, cases  of  distinct  alcoholic  gastritis  in  which,  after  well- 
observed  test-meals,  the  proteolysis  is  carried  on  better  when 


J.  Palugyay  & Sons,  Pressburg. 


DIETETIC  TREATMENT. 


469 


wine  is  taken.*  The  wines  we  have  recommended  have  not 
only  a stimulating,  but,  on  account  of  their  large  percentage  of 
grape-sugar,  a nutritive,  value.  This  grape-sugar  will,  however, 
increase  the  lactic  acid  formation  if  it  be  already  present.  In  this 
last  case  a standard  champagne — Mumm’s  Extra  Dry,  “ Roederer,” 
Piper-Heidseick — is  preferable.  Beer  and  claret  are,  according  to 
our  experience,  rarely  well  borne,  and  frequently  augment  gastric 
distress.  In  cases  of  marked  anorexia  a palatable  dilution  of  brandy 
or  whisky,  taken  half  an  hour  before  meal-times,  very  often  pro- 
duces an  appetite.  The  so-called  “ Angostura  Cocktail  ” is  some- 
times useful  to  sufferers  from  anorexia,  but  must  not  be  allowed  to 
alcoholic  cases.  The  physiological  reasons  for  the  administration 
of  alcohol  are  explained  in  the  chapter  on  The  Dietetics  of  Alcoholic 
Beverages  (also  in  the  “ Dietetic  and  Hygienic  Gazette,”  May,  1896, 
p.  289;  and  R.  H.  Chittenden,  “ Amer.  Jour.  Med.  Sciences,”  Jan. 
to  April,  1896,  “Influences  of  Alcohol  on  the  Chemical  Processes 
of  Digestion”). 

Constipation  in  chronic  gastritis  should  always  be  treated  diet- 
etically,  never  by  medicines  per  os.  A glass  of  cold  water,  or, 
preferably,  of  Bedford  Magnesia  Spring  water,  before  breakfast,  is 
a simple  thing,  and  yet,  if  persisted  in,  very  often  gives  an  evacua- 
tion. The  breakfast  should  contain  honey,  milk-sugar  or  levulose, 
some  plum,  fig,  or  prune  preserves,  and  Graham  bread.  Twice 
daily  a glass  of  buttermilk  or  kefyr  may  be  administered,  if  agree- 
able to  the  patient.  When  the  constipation  resists  this  diet  at  the 
beginning,  a trial  for  the  first  week  should  be  made  with  large  colon 
irrigations,  with  one  liter  of  normal  salt  solution  introduced  in  the 
knee-elbow  position.  Fleiner’s  enemata  of  250  c.c.  ( y2  pint)  of  pure 
olive  oil  are  more  lasting  in  their  effects,  one  enema  sometimes 
keeping  the  bowels  regular  for  a week.  When  diarrhea  is  present, 
large  irrigations  of  warm  water,  by  removing  fermenting  and  putre- 
factive colon  contents,  frequently  cure  it  without  other  medication. 
But  strict  dieting  for  a few  days  is  always  advisable  in  exhaustive 
diarrheas,  as  it  shortens  the  attack.  In  diarrheas,  as  well  as  in  con- 
stipation, the  state  of  the  gastric  secretion  must  be  regarded,  and 
HC1  or  alkalies  must  be  supplied,  as  the  case  may  be.  Excess  of 
HC1  secretion  may  provoke  diarrhea  by  causing  carbohydrate  indi- 


* The  “rationale”  of  the  administration  of  alcohol  is  governed  by  its  effects  on  the 
gastric  digestion  as  observed  in  test-meal  analysis — if  it  impedes  digestion  it  must  be 
forbidden. 


31 


470 


CHRONIC  GASTRITIS. 


gestion.  A diet  of  Pasteurized  milk  and  some  stimulant,  as  brandy, 
and,  perhaps,  albumin  water  for  forty-eight  hours,  to  the  exclusion 
of  everything  else,  is  most  effective.  Soup  made  of  bouillon  and 
thickened  with  wheat-flour  toasted  brown  in  hot  butter,  is  quite 
binding.  “ Eichelcacao,”  a palatable  German  preparation  of  choc- 
olate, can  be  recommended  for  its  constipating  effect,  as  it  contains 
much  tannin. 

For  special  full  diet-lists  and  further  dietetic  directions  concern- 
ing this  disease,  as  well  as  other  recipes,  we  refer  to  the  section 
especially  devoted  to  this  subject — the  chapter  on  Dietetics  (pp. 
223-226). 

As  Gilman  Thompson  points  out,  there  are  some  persons  in 
whom  the  digestion  of  salt  and  smoked  meats  seems  to  be  more 
easily  accomplished  than  that  of  prepared  fresh  meat.  Nicmeyer 
offers  the  explanation  that  these  preparations  are  less  likely  to  de- 
compose in  the  stomach.  As  a rule,  there  is  very  little  fermenta- 
tion and  formation  of  organic  acids  in  chronic  gastritis.  After 
carefully  observing  this  point,  we  maintain  that  it  is  not  necessary 
to  withhold  the  saccharine  and  farinaceous  foods,  as  Gilman 
Thompson  suggests  ( loc . cit.,  p.  508).  On  the  contrary,  they  should 
be  liberally  supplied,  as  amylolysis  progresses  rapidly  in  stomachs 
that  secrete  no  HC1,  and  test-meals  in  my  experience  do  not,  as  a 
rule,  show  the  excess  of  organic  acids  asserted  by  von  Leube,  Ewald, 
and  Rosenheim. 

Balneological. — There  is  much  truth  in  what  Prof.  Ira  Remsen 
said  when  he  opined  that  the  effect  of  the  use  of  natural  or  mineral 
spring  waters  was  not  attributable  to  the  chemical  constituents  or 
salts  of  these  waters,  but  more  to  the  favorable  mode  of  life,  the 
better  diet,  the  greater  introduction  of  plain  water  into  organisms 
which  previously  received  very  little  of  it,  and,  lastly,  to  important 
psychic  influences.  To  these  may  be  added  the  perfect  rest,  com- 
fort, and  auxiliary  methods  of  treatment  employed  at  the  springs. 
Thousands  of  Americans  visit  the  German,  Austrian,  and  French 
spas  annually,  when  they  might  have  almost  the  same  waters — 
and  sometimes  much  better  ones — in  their  own  country.*  Obser- 
vations are  very  numerous  on  the  treatment  of  chronic  gastritis  by 
mineral  waters,  but  are  rather  inexact  and  based  upon  imperfect 


* In  extended  travels  through  our  Eastern  States,  I have  visited  20  mineral  springs 
discharging  very  palatable — sometimes  carbonated — waters  that  are  not  at  all  known 
except  to  people  living  in  the  immediate  vicinity. 


MINERAL  WATERS,  BATHS,  GYMNASTICS.  47 1 

histories,  as  many  cases  are  called  chronic  gastritis  which,  in  fact, 
do  not  deserve  the  name.  One  can  not  well  judge  of  the  effect  of 
the  waters  alone,  as  they  are  always  combined  with  dieting.  The 
systematic  drinking  of  alkaline  waters  must  not  be  estimated  to  be 
worth  more  than  that  of  a poor  substitute  for  lavage.  As  the  ob- 
ject is  to  promote  the  solution  and  evacuation  of  mucus,  all  waters 
will  be  equally  serviceable,  even  ordinary  spring  or  hydrant  water. 
The  salts  can  be  added  to  imitate  the  real  composition  of  the  famous 
springs,  and  are  made  by  several  wholesale  manufacturers  of  effer- 
vescent salts  for  this  purpose,  so  that  the  poorer  patients  may  have 
the  effect  of  mineral  springs  at  home. 

(For  the  effects  and  contraindications  of  mineral  waters  the 
reader  is  referred  to  the  section  on  Mineral  Springs.  The  compo- 
sition of  artificial  Carlsbad  salts  is  given  on  pp.  335  to  336.) 

In  the  use  of  alkaline  chlorids  it  is  expected  to  stimulate  the 
secretion  of  HC1.  Hot  spring  waters  must  be  cooled,  and  the  cold 
water  warmed ; and  in  dilatation  and  atony,  the  patient  had  best 
abandon  the  use  of  water  in  this  manner  entirely. 

Baths . — As  in  chronic  gastritis  the  general  metabolic  processes 
are  much  depressed,  a cold  sponge-bath  taken  before  breakfast 
will  gradually  make  the  dyspeptic  more  resistant  by  its  stimulation 
of  cellular  oxidation  and  its  hardening  effect.  Warm  baths  we 
advise,  for  purposes  of  cleanliness  only,  once  or  twice  a week. 

Gymnastics. — All  patients  with  chronic  gastritis  should  be  en- 
couraged to  take  moderate  exercise  : walking,  bicycle  riding,  horse- 
back riding;  also  rowing  and  swimming.  A pair  of  four-pound 
dumb-bells  for  men  and  two-pounders  for  women  should  be  used 
three  times  daily,  each  time  for  five  minutes,  with  three  minutes  of 
rest  intervening  between  the  five  minutes  of  exercise.  This  will 
make  fifteen  minutes  of  training,  and  should  be  done  before  dressing, 
in  the  undergarments,  immediately  after  the  cold  sponge  bath. 
Great  care  should  be  bestowed  upon  the  tonicity  of  the  abdominal 
muscles.  Loss  of  the  unconsciously  and  continuously  acting  tonus 
of  these  muscles  is  a most  potent  factor  in  the  etiology  of  dilata- 
tion, gastroptosis,  and  floating  kidney.  There  are,  of  course, 
other  causes ; but  even  if  the  attachments  of  an  organ  are 
loosened,  it  can  not  wander  far  from  its  normal  location  with  a 
vigorous,  unrelenting,  external  abdominal  wall.  Therefore,  all 
patients  subject  to  digestive  diseases,  except  ulcer  and  carcinoma, 
should  train  their  abdominal  muscles  and  keep  them  active.  San- 


472 


CHRONIC  GASTRITIS. 


dow’s  directions  for  accomplishing  this,  as  described  in  his  book, 
are  excellent. 

Rest. — When  the  patient  has  lost  weight  and  becomes  emaci- 
ated, gymnastics  are  out  of  place ; then  an  absolute  rest  cure  is 
peremptory. 

Electricity . — The  faradic  and  galvanic  currents  are  useful  in  the 
treatment  of  chronic  gastritis.  The  former  may  be  used  as  general 
external  faradism,  which  is  one  variety  of  a general  massage.  One 
pole,  in  shape  of  a broad,  flat  electrode,  is  moved  slowly  up  and 
down  over  the  spinal  column,  while  the  other  is  moved  over  both 
arms  and  limbs,  and  particularly  over  the  abdominal  muscles. 
With  one  pole  over  the  spine,  and  the  other  over  the  epigastrium, 
the  current  appears  to  go  directly  through  the  stomach,  and  yet 
there  is  no  evidence  that  the  organ  does  contract.  In  this  case  it 
is  doubtful  whether  any  current  reachess  the  stomach  at  all.  There 
is  as  yet  no  satisfactory  explanation  of  how  the  good  effects  ob- 
served after  this  method  are  brought  about.  However,  they  may, 
perhaps,  be  largely  attributable  to  the  abdominal  massage  and  the 
psychic  influence.  For  the  intragastric  application  of  both  the 
faradic  and  galvanic  currents,  the  practical  intragastric  electrode  of 
Einhorn  is  possibly  the  most  convenient.  The  secretion  of  gastric 
juice  can  not  be  influenced  by  either  the  faradic  or  galvanic  cur- 
rent, nor  can  the  motility  be  enhanced  (J.  C.  Hemmeter,  “ New 
York  Med.  Journal,”  June  22,  1895,  p.  769).  As  the  currents 
usually  employed  for  this  purpose  are  too  weak  to  effect  a con- 
traction of  the  muscularis,  Meltzer  (“New  York  Med.  Journal,” 
June  15,  1895)  holds  that  percutaneous  and  direct  faradization  of 
the  stomach  and  intestines  can  not  produce  any  contraction  of 
these  parts.  Max  Einhorn  (“  Archiv  f.  Verdauungskrankheiten,” 
Bd.  11,  S.  454),  in  his  recent  contributions  to  the  subject,  is  of 
entirely  opposite  opinion  (see  part  1,  p.  60).  As  Ziemssen  (“  Elec- 
trizitat  i.  d.  Medizin,”  1887,  p.  445)  has  emphasized,  it  is  not  neces- 
sary to  effect  gastric  contraction  in  order  that  electricity  should 
prove  beneficial.  In  fact,  it  would  appear  that  a neurometabolic  or 
neurotrophic  effect  of  electricity  is  becoming  more  and  more  under- 
stood, so  that  the  faradic  and  galvanic  current  should  be  employed, 
both  externally  over  the  spine  and  epigastrium,  and  internally  with 
the  intragastric  electrode  ; not  because  of  any  undeniable  evidence 
that  it  can  influence  secretion,  motility,  or  absorption,  but  because 
of  the  general  uniformity  of  opinion  among  experienced  clinicians 
that  chronic  gastritis  is  undoubtedly  benefited  by  electrical  treat- 


MEDICINAL  TREATMENT. 


473 


ment.  Even  Goldschmidt  (, loc . cit),  whose  results  regarding  the 
effect  of  the  faradic  and  galvanic  currents  on  secretion  and  motility- 
are  entirely  negative,  admits  that  these  are  useful  agents  in  the 
treatment,  even  benefiting  stomach  diseases  depending  upon 
organic  changes.  It  is  evident  that  while  experimental  evidence 
of  the  manner  in  which  electricity  acts  on  the  stomach  is  neces- 
sary, the  clinical  approval  of  its  therapeutic  utility  is  more 
important. 

Medicinal  Treatment. — Two  chemicals  seem  to  have  maintained 
their  reputation  as  being  able  to  benefit  the  disease;  these  are  ar- 


Fig.  34A. — Connective-tissue  Hyperplasia  Separating  Remnants  of  Glands  which  Show 
a Small  Nucleus  Surrounded  by  a Thin  Shell  of  Protoplasm.— {From  the  Author's 
Clinic , University  of  Maryland .)  X 70  diameters. 


gentic  nitrate,  either  in  form  of  gastric  spray  (i  : 1000)  or  lavage 
(1  : 2000),  or  in  form  of  solution,  0.3  to  120  of  peppermint  water; 
of  this,  one  tablespoonful  three  times  daily,  on  an  empty  stomach. 
The  second  drug  is  bismuth  subnitrate,  recommended  by  Penzoldt 
(loc.  cit.)y  Fleiner  (loc.  cit),  and  Pick  (loc.  cit.)  in  large  doses,  4 to  6 
gm.,  in  wafers.  With  both  remedies  we  have  had  experience,  and 
prefer  the  latter,  together  with  bismuth  subgallate,  because  it 
certainly  diminishes  the  amount  of  mucus  formed  in  alcoholic 
gastritis : 


474 


CHRONIC  GASTRITIS. 


R . Bismuth  subnitratis, 

Bismuth  subgallatis, 

Fiant  pulv.  No.  xxiv. 

SiG. — One  powder  in  a wafer  four  times  daily 

Unfortunately,  this  treatment  is  constipating,  and  must,  there- 
fore, be  combined  with  a diet  promoting  evacuation  and  the  use 
of  Saratoga  Congress  water.  Argentic  nitrate  is  best  employed 
in  form  of  the  intragastric  spray  or  in  the  lavage.  These  drugs 
are  permissible,  particularly  when  diet  and  massage  can  not  be 
properly  carried  out.  They  were  originally  suggested  for  the 
treatment  of  ulcer ; their  efficacy  in  some  cases  of  chronic  gastritis 


48  gm.  3 xij 

16  gm.  giv.  M. 


Fig.  34B. — Detachment  of  Remnants  of  Secretory  Cells  Containing  Vacuoles  from 
Lumen  of  Peptic  Duct.— {From  the  Author's  Clinic , University  of  Maryland.)  X 325 
diameters. 


is,  however,  undoubted.  The  bismuth  subnitrate  and  subgallate 
may  be  applied  by  means  of  an  intragastric  powder-blower.  By  the 
use  of  the  fluoroscope  and  X-rays  it  is  demonstrable  that  the  entire 
stomach  can  be  coated  in  this  way. 

The  Hygiene  of  the  Mouth . — The  frequent  association  of  stomati- 
tis, gingivitis,  and  glossitis  with  this  disease  make  it  all-important 
that  the  mouth  should  be  in  a healthy  condition.  Dental  defects 
and  their  repairs  have  already  been  referred  to;  but,  in  addition, 
the  mouth  should  be  disinfected  after  each  meal.  After  removing 


TREATMENT  OF  SPECIAL  SYMPTOMS. 


475 


the  food  debris  by  toothpick  and  brush,  one  of  the  following  anti- 
septic lotions  should  be  used,  both  on  the  brush,  applied  to  the 
teeth  and  the  root  of  tongue,  and  as  a mouth-wash  : 


R.  Acid,  thymol, 0.25  gr.  iv 

Acid,  benzoic., 3.0  gr.  xlv 

Tinct.  eucalypt., 15-0  f^iiiss 

Alcohol, 100.0  f^iiiss 

01.  menth.  pip., 0.75  ffbxij.  M. 

SiG. — Pour  sufficient  into  ]/2  of  a glass  of  water  until  turbidity  results. 

If  much  decomposition  be  present,  0.8  hydrarg.  bichlorid.  corrosiv.  may  be  added. 


R . Spirit,  lavandul. , 


Spirit,  myrciae, aa  50.0  f g xiiss 

Tinct.  myrrh. 5.0  f^j 

Saccharin, 1.0  gr.  xv 

Menthol 1.0  gr.  xv.  M. 


SiG. — One-half  to  one  teaspoonful  to  a glass  of  water. 


Treatment  of  the  Symptoms. — This  is  of  subsidiary  importance  to 
systematic  treatment  by  diet,  hygiene,  and  lavage ; but  in  cases 
that  have  progressed  too  far,  or  in  secondary  forms  that  are  incura- 
ble (albuminuria,  diabetes,  etc.),  a special  therapy  for  symptoms 
may  be  indispensable. 

The  treatment  of  loss  of  appetite  which  we  advocate  is  the  follow- 
ing : Lavage  with  chlorid  of  sodium,  §ss  to  the  quart  or  a decinor- 
mal  solution  of  HC1 ; fluid  extract  of  condurango  in  doses  of  5j ; 
tincture  or  elixir  of  gentian.  Lavage  with  quassia,  Colombo,  or 
calisaya  solutions  will  often  produce  appetite.  Orexin,  a stimulant 
to  the  appetite  and  HC1  secretion  (first  recommended  by  Penzoldt), 
is  best  given  in  the  following  form  : 

R.  Orexin,  basic, 0.2  gr.  iiiss. 

SiG. — Make  one  wafer.  Take  one  wafer  in  a cup  of  bouillon  half  an  hour  before 
meals,  t.  i.  d. 


Our  favorite  tonic  for  anorexia  in  chronic  gastritis  contains 
strychnin  and  hydrochloric  acid  in  the  following  proportion  for 
adults : 


R . Strych.  sulphatis, 0.02  gr. 

Acid,  hydrochlorici  dilut., 19.4  f^v 

Elixir  gentianse, q.  s.  180.0  f^jvj.  M. 

SiG. — f.^ss  in  ij  aquae  after  meals,  through  a glass  tube. 

Fluid  extract  condurango  f^xij  may,  if  desired,  be  added. 

Some  old  gastritics  can  not  tolerate  so  much  hydrochloric  acid.  Then  the  dose  must 
be  reduced  to  five  drops,  t.  i.  d.  Always  precede  the  administration  of  H Cl  by  a test- 
meal  analysis,  so  as  to  find  out  the  degree  of  HC1  deficiency. 

Pyrosis  and  eructation  are  best  treated  with  magnesia  and  sodium 


476 


CHRONIC  GASTRITIS. 


bicarbonate,  according  to  the  principles  laid  down  in  the  manage- 
ment of  hyperacidity. 

Pain. — If  diet  and  lavage  do  not  relieve  this,  it  is  best  to  subject 
the  patient  to  a rest  cure  of  eight  days,  with  hot  external  fomenta- 
tions to  epigastrium.  The  galvanic  current  has  been  a very 
reliable  means  of  easing  pain  in  this  affection.  Opiates  and  other 
narcotics  must  be  avoided ; but,  in  the  very  rare  cases  where  this 
is  impossible,  they  should  be  given  by  the  rectum  or  (morphin) 
hypodermically. 

The  same  treatment  applies  also  to  vomiting,  which  is,  as  a rule, 
relieved  by  diet,  lavage,  small  pieces  of  ice,  or  champagne ; very 
rarely  does  it  become  so  distressing  a symptom  as  to  require  a 
hypodermic  injection  of  morphin.  Spraying  the  stomach  with 
menthol  and  cocain  in  weak  solutions  relieves  vomiting  when 
lavage  has  failed. 

Deficiency  of  gastric  juice  and  ferments  may  be  supplanted  by 
the  use  of  HC1  internally,  as  per  formula  stated  above.  If  HC1  is 
no  longer  tolerated,  it  is  well  to  convert  the  entire  gastric  chemistry 
into  an  alkaline  proteolysis  by  pancreatin  and  bicarbonate  of 
sodium.  In  long-standing  cases  the  mucosa  acquires  a strange 
hypersensitiveness  to  all  acids,  which  points  the  way  to  this  plan 
of  treatment.  Reliable  pancreatin  and  sodium  bicarbonate,  of  each 
five  grs.,  are  recommended  by  Boas,  Witte,  Simon,  Schering,  and 
Penzoldt.  In  our  private  sanitarium  we  have,  by  a study  of  test- 
meals,  found  Reichmann’s  preparation  of  fresh  ox  pancreas  an 
effective  digestant.  It  is  made  by  finely  mincing  one  ox  pancreas 
and  extracting  it  with  15  per  cent,  alcohol  or  brandy  for  forty-eight 
hours,  and  straining.  The  dose  is  a wineglassful  after  meals.  We 
very  rarely  found  it  necessary  to  give  pepsin ; for  if  HC1  is  still 
secreted,  pepsin  will  be  found  also,  and  if  HC1  be  absent,  although 
the  ferments  may  be  wanting,  it  is  expedient  to  give  only  the  acid, 
as  proteolysis  is  sufficiently  effective  in  the  intestine,  and  the  effect 
of  the  HC1  is  to  improve  the  appetite  and  prevent  intestinal  fer- 
mentations. 

Motor  insufficiency  is,  fortunately,  a very  rare  occurrence  in  the 
disease,  but,  if  present,  may  be  met  with  use  of  lavage,  electricity, 
hydrotherapy,  massage,  and  strychnin.  This  will  be  more  fully 
treated  in  the  section  on  this  defect. 

Psychic  depression  may,  according  to  the  most  prominent  under- 
lying cause,  require  one  or  several  of  the  methods  of  treatment 
mentioned.  But  regular  bowel  movements,  electricity,  a daily 


ADVANCED  CHEMICAL  AND  MECHANICAL  DEFECTS.  477 

tepid  or  cold  sponge  bath,  moderate  exercise,  massage,  surf  baths, 
and  climatic  changes  are  the  most  reliable  means  to  be  employed. 
Some  of  these  cases  will  not  recover  until  brought  to  a properly 
managed  sanitarium  for  digestive  sufferers. 

Advanced  Chemical  and  Mechanical  Defects . — When  the  glandular 
elements  have  been  completely  destroyed  as  a result  of  hypertro- 
phic or  atrophic  metamorphosis  of  the  mucosa  and  degenerative 
processes  in  the  muscularis,  and  also  of  cirrhotic  contraction  of  the 
stomach,  secretion,  absorption,  and  motility  no  longer  exist.  The 
gravest  defect  is  the  loss  of  motility.  For,  in  the  total  absence 
of  all  gastric  digestion,  no  food  except  a small  fraction  of  the  car- 
bohydrates (ptyalin)  enters  into  solution.  The  ingesta  are  not  re- 
duced sufficiently  in  size,  because  there  is  no  churning  peristalsis 
and  no  secretion  ; they  are  not  evacuated  into  the  duodenum,  be- 
cause the  propelling  peristalsis  is  missing.  Now,  although  there  is 
no  stenosis  of  the  pylorus  from  cicatricial  contraction  or  neoplasm, 
we  have  seen  such  cases  in  which  there  was  not  even  a pyloric 
hyperplasia.  Under  these  conditions  there  is  what  we  may  term 
a “ relative  pyloric  stenosis  that  is,  the  pylorus  is  relatively  too 
small  and  peristalsis  too  defective  for  the  passage  of  the  insufficiently 
macerated  ingesta.  This  combination  of  things  may  occur  in  the 
last  stages  of  chronic  gastritis  accompanied  by  the  clinical  aspects 
of  progressive  anemia,  due  to  inevitable  malnutrition,  and  may  sim- 
ulate carcinoma.  Operations  have  been  undertaken,  in  the  author’s 
experience,  where  the  markedly  thickened,  hyperplastic  muscularis 
gave  the  impression  of  a gastric  neoplasm,  and  the  exploratory  in- 
cision revealed  the  effects  of  a chronic  hyperplastic  gastritis. 

The  intestine,  although  it  may  be  healthy,  can  not  supplant  the 
absent  digestion  of  the  stomach  by  its  vicarious  action,  since  it  gets 
no  chance  to  do  so,  the  gastric  contents  fermenting,  and  eventually 
being  expelled  by  emesis,  rather  than  propelled  into  the  duodenum. 
This  state  should  be  treated  exactly  as  if  there  were  a real  pyloric 
stenosis,  namely,  by  operation, — either  by  gastro-enterostomy  or  by 
dilatation  of  the  pylorus ; or,  if  an  excessive  atonic  gastrectasia 
with  immense  enlargement  of  the  stomach  and  normal  pylorus  be 
present,  by  gastroplication  (Bircher).  So  far  it  appears  that  gastro- 
enterostomy has  been  done  but  once  under  these  conditions  for 
typical  gastric  atrophy (Westphalen,  “Petersburger  med.  Wochen- 
schr.,’’  1890,  37,  38)  occurring  in  a tuberculous  patient.  As  the 
expelling  force  of  the  peristalsis  is  much  reduced,  gastro-enteros- 
tomy will  probably  be  preferable  to  dilatation  of  the  pylorus.  The 


478 


CHRONIC  GASTRITIS. 


indications  for  surgical  operations  upon  the  stomach  have  been 
separately  considered  (p.  348). 

LITERATURE 

ON  ACUTE  AND  CHRONIC  GASTRITIS. 

In  addition  to  the  text-books  of — 


Debove  and  Remond, 

Eichhorst, 

Niemeyer, 

Einhorn, 

Ewald, 

Orth, 

Fleiner, 

Fleischer, 

Oser, 

Martin,  Sidney, 

Forster, 

Penzoldt, 

Bamberger, 

Henoch, 

Pick, 

Birch-Hirschfeld, 

Jiirgensen, 

Riegel, 

Boas, 

Kunze, 

Rokitansky, 

Bouveret, 

Lebert, 

Rosenheim, 

Brinton, 

Leo, 

Striimpell, 

Cohnheim, 

Leube, 

Trousseau, 

Cruveilhier, 

Liebermeister, 

Wegele, 

Dujardin-Beaumetz, 

Hayem, 

Ziegler,  and  others. 

1.  Aaron,  C.  D.,  “Chronic  Dyspepsia,”  “Trans.  Mich.  Med.  Soc.,”  Grand 
Rapids,  1898,  281-291. 

2.  Beaumont,  “Experiments  and  Observations  of  the  Gastric  Juice  and  the 
Physiology  of  Digestion,”  Combe’s  edition,  1833. 

3.  Benedict,  A.  L.,  “ Some  Thoughts  on  Subacute  and  Chronic  Gastritis,” 
“Medicine,”  Detroit,  1897,111,  353-359. 

4.  Boas,  J.,  “ Ueber  Schwefelwasserstoff bildung  bei  Magenkrankheiten,” 
“ Centralblatt  f.  klin.  Med.,”  1895. 

5.  Cahn,  A.,  “ Die  Verwendung  der  Peptone  als  Nahrungsmittel,”  “ Berlin, 
klin.  Wochenschr.,”  1893. 

6.  Cagigal,  A.  O.,  “Um  caso'de  gastrite  chronica  e arterio  esclerose  com- 
modificacoes  nervosas  perephericas,”  “Coimbra  med.,”  1898,  xviii,  87,  88. 

7.  Chaffee,  F.  F.,  “ Chronic  Gastritis,”  “ Trans.  Vermont  Med.  Soc.,”  1895- 
’96;  Burlington,  1897,  47-65. 

8.  Charles,  “ On  a Case  of  Cirrhosis,  or  Fibroid  Infiltration  of  the  Stomach,’ 
“ Dublin  Jour,  of  Med.  Science,”  1878. 

9.  Curschmann,  “ Sitzung  des  Aertzlichen  Vereins  zu  Hamburg  vom  19. 
Mai,  1885,”  “ Deutsche  Med.  Wochenschr.,”  1885. 

10.  Cutler,  E.  G.,  “General  Remarks  on  Gastric  Dyspepsia,”  “Boston  Med. 
and  Surg.  Jour.,”  1897,  cxxxvil. 

11.  Deekens,  A.  H.,  “Chronic  Catarrhal  Gastritis:  Its  Pathology,  Sympto- 
matology, and  Treatment,”  “Med.  Sentinel,”  Portland,  Oregon,  1898,  vi,  123- 
134- 

12.  Deininger,  “ Zwei  Falle  von  Idiopathischer  Gastritis  Phlegmonosa,” 
“ Deutsches  Archiv  fur  klin.  Med.,”  xxiii. 

13.  Ebstein,  “ Ueber  die  Veranderungen  welche  die  Magenschleimhaut 
durch  Einverleibung  von  Alcohol  und  Phosphor  erleidet,”  “ Virchow’s  Arch.,” 
Bd.  lv. 


LITERATURE  ON  ACUTE  AND  CHRONIC  GASTRITIS.  479 

14.  Edinger,  “Zur  Kenntniss  der  Driissenzellen  des  Magens,  besonders 
beim  Menschen,”  “ M.  Schultzer’s  Archiv,”  Bd.  xvii,  S.  209. 

15.  Eisenlohr,  “ Ueber  primare  Atrophie  der  Magen-  und  Darmschleimhaut 
und  deren  Beziehung  zu  schwerer  Anamie  und  Riickenmarkserkrankungen,” 
“ Deutsche  med.  Wochenschr.,”  1892. 

16.  Ewald,  “ Zur  Diagnose  und  Therapie  der  Magenkrankheiten,”  “ Berlin, 
klin.  Wochenschr.,”  1886. 

17.  Fenwick,  Lecture  on  “Atrophy  of  the  Stomach,”  “ Lancet,”  1877. 

18.  Fenwick,  “On  Atrophy  of  the  Stomach,”  London,  1880. 

19.  Fenwick,  “ Ueber  den  Zusammenhang  einiger  krankhafter  Zustande 
des  Magens  mit  anderen  Organerkrankungen,”  “Virchow’s  Archiv,”  Bd. 
CVIII. 

20.  Fleiner,  “ Erfahrungen  iiber  die  Therapie  der  Magenkrankheiten,” 
“ Volkmann’s  Sammlung  klinischer  Vortrage,”  Nr.  103,  1894. 

21.  Fleiner,  “Ueber  die  Behandlung  der  Constipation,  etc.,  mit  grossen 
Oelklystieren,”  “Berlin,  klin.  Wochenschr.,”  1893,  Nr.  3 und  4. 

22.  Gerhardt,  “ Magenkatarrh  durch  lebende  Dipterenlarven,”  “ Jenaer 
med.  Zeitschr.,”  ill. 

23.  Glax,  “ Die  Magenentziindung,”  “ Deutsche  med.  Zeitung,”  1894. 

24.  Gluzinski,  “Ueber  das  Verhalten  des  Magensaftes  in  fieberhaften 
Krankheiten,”  “ Deutsches  Archiv  f.  klin.  Med.,”  Bd.  xlii. 

25.  Gostkowski,  “ Ein  Fall  von  NH3  Vergiftung  mit  totaler  Abstossung  des 
Magenschleimhaut,”  Dissert.,  Leipzig,  i895~’96. 

26.  Griitzner,  P.,  “ Neue  Untersuchungen  iiber  Bildung  und  Ausscheidung 
des  Pepsins  im  Magen,”  Breslau,  1875. 

27.  Hanot  et  Gombault,  “ Etude  sur  la  Gastrite  chronique  avec  sclerose  sous- 
muqueuse  hypertrophiqueet  retroperitonite  calleuse,”  “Archiv.  de  Physiologie,” 
1882, IX. 

28.  Harnack,  E.,  “Ueber  die  Verschiedenheit  gewisser  Aetzwirkungen  auf 
lebendes  und  todtes  Magengewebe,”  “Berlin,  klin.  Wochenschr.,”  1892. 

29.  Hayem,  “ Sur  l’anatomie  pathologique  de  la  gastrite  parenchymateuse 
hyperpeptique,”  Paris,  1893. 

30.  Hayem,  “ Classement  des  varietes  anatomiques  des  gastrites,”  “ Soc. 
Med.  des  hop.  de  Paris,”  24,  vii,  1896. 

31.  Hayem,  “ Gastrite  degenerative,”  “ Soc.  Med.  des  hop.  de  Paris,”  28,  x, 
1896. 

32.  Hayem,  G.,  et  G.  Lion,  “ Traitement  des  gastrites”  (Abstr.),  “ Rev.  de 
therap,  med.-chir.,”  Par.,  1897,  lxiv,  429-433. 

33.  Henne,  “ Experimentelle  Beitragezur  Therapie  der  Magenkrankheiten,” 
“ Deutsche  Zeitschr.  f.  klin.  Med.,”  xix,  Supplement. 

34.  Honigmann,  “ Epikritische  Bemerkungen  zur  Deutung  des  Salzsaure- 
befundes  im  Mageninhalt,”  “ Berlin,  klin.  Wochenschr.,”  1893. 

35.  Honigmann,  “ Ueber  einige  wesentliche  Punkte  aus  der  Diatetik  fur 
Magenkranke,”  Sep.-Abdr.  aus  der  “ Zeitschrift  fur  Krankenpflege,”  1894. 

36.  Immermann,  “Ueber  die  Functionen  des  Magens  bei  Phthisis  tuber- 
culosa,” “ Verhandlungen  des  Congresses  fur  innere  Medicin,”  Wiesbaden, 
1889. 

37.  Jaworski,  “ Zur  Diagnose  des  Atrophischen  Magenkatarrhs,”  “Verhand- 
lungen des  Congresses  fur  innere  Medicin,”  Wiesbaden,  1888. 


480 


CHRONIC  GASTRITIS. 


38.  v.  Kahlden,  “Ueber  chronisch  sclerosirende  Gastritis,”  “ Centralblatt 
f.  klin.  Med.,”  1887,  Nr.  16. 

39.  Kalnin,  K.  K.,  “ Apropos  of  Application  of  Tincture  of  Iodine  in  the 
Treatment  of  Chronic  Gastric  Catarrh.” 

40.  Kaufmann,  “ Zwie  Falle  geheilter  pernicioser  Anamie,”  etc.,  “Berlin, 
klin.  Wochenschr.,”  1891. 

41.  King,  C.,  “ Dyspepsia,”  “N.  Y.  Lancet,”  1898,  297-300. 

42.  Klebs,  “ Handbuch  d.  patholog.  Anatomie,”  1868,  S.  174. 

43.  Kiihnau,  “Berlin,  klin.  Wochenschr.,”  1897,  No.  19. 

44.  Kulneff,  “Ueber  basiche  Zersetzungsproducte  in  Magen-  und  Darm- 
inhalt,”  “ Berlin,  klin.  Wochenschr.,”  1891. 

45.  Kupffer,  C.,  “ Epithel  und  Driisen  des  menschl.  Magens,”  Miinchen, 
1883. 

46.  Leary,  F.,  “Diphtheric  Gastritis,”  “Jour.  Boston  Soc.  Med.  Sc.,” 
1897,  No.  16,  8-12. 

47.  Lesser,  “ Cirrhosis  ventriculi,”  Inaug.  Diss.,  Berlin,  1876. 

48.  Leube,  “Ueber  die  Therapie  der  Magenkrankheiten,’’  “Volkmann’s 
Sammlung  klin.  Vortrage,”  1873,  Nr.  62. 

49.  Leube,  “ Beitrage  zur  Diagnostik  der  Magenerkrankungen,”  “ Deutsches 
Archiv  f.  klin.  Med.,”  1883,  xxxm. 

50.  Leube,  “ Ueber  eine  neue  Art  von  Fleisch-solution  als  Nahrungs-  und 
Heilmittel  bei  Erkrankungen  des  Magens,”  “Berlin,  klin.  Wochenschr.,” 

1873. 

51.  Litten  und  Rosengart,  “ Ein  Fall  von  fast  volligem  Erloschen  der  Secre- 
tion des  Magensaftes  (Atrophie  der  Magenschleimhaut),”  “ Zeitschr.  f.  klin. 
Med.,”  xiv. 

52.  Losch,  “Ueber  die  nach  Einwirkung  abnormer  Reize  auf  die  Magen- 
schleimhaut auftretenden  pathologisch-anatomischen  Veranderungen,”  “All- 
gem. Wien.  med.  Zeitung,”  1881,  Nr.  50. 

53.  Lyon,  G.,  “ Traitement  de  la  gastrite  hyperpeptique  ” (Abstr.),  “Rev. 
de  therap.  med.  chir.,”  Par.,  1898,  LXV,  757-766. 

54.  Marfan,  “ Troubles  et  lesions  gastriques  dans  la  phthisie  pulmonaire,” 
Paris,  1889. 

55.  Manassein,  “ Chemische  Beitrage  zur  Fieberlehre,”  “Virchow’s  Archiv,” 
Bd.  lv. 

56.  Mathieu,  A.,  “Un  cas  d’uremie  gastrique  chronique,”  “Bull.  gen.  d. 
therap.,”  etc.,  Par.,  1898,  cxxxvi,  743-750. 

57.  Mester,  B.,  “Ueber  Magensaft  und  Darmfaulniss,”  “Zeitschr.  fiir  klin. 
Med.,”  xxiv. 

58.  Meyer,  G.,  “ Zur  Kenntniss  der  sogenannten  Magenatrophie,”  “ Zeitschr. 
f.  klin.  Med.,”  Bd.  xvi. 

59.  Mintz,  “ Ein  Fall  von  Gastritis  phlegmonosa  diffusa  im  Verlaufe  eines 
“ Magenkrebses,”  “ Deutsches  Archiv  f.  klin.  Med.,”  Bd.  xlix. 

60.  Murdoch,  F.  H.,  “The  Diagnosis  and  Treatment  of  Gastric  Catarrh,” 
“N.  Y.  Med.  Jour.,”  1897,  lxvii,  289. 

61.  v.  Noorden,  “ Ueber  die  Ausniitzung  der  Nahrung  bei  Magenkrank- 
heiten,” “ Zeitschrift  f.  klin.  Med.,”  Bd.  xvii. 

62.  v.  Noorden,  “ Der  Stoffwechsel  der  Magenkranken  und  seine  anspriiche 
an  die  Therapie,”  “ Berliner  Klinik,”  1893. 


LITERATURE  ON  ACUTE  AND  CHRONIC  GASTRITIS.  48 1 

63.  Nothnagel,  “ Cirrhotische  Verkleinerung  des  Magens  und  Schwund  der 
Labdriisen  unter  dem  klinischen  Bilde  der  perniciosen  Anamie,”  “Deutsches 
Archiv  f.  klin.  Med.,”  xxiv. 

64.  Oppler,  B.,  “Der  chronische  Magenkatarrh  und  seine  Behandlung,” 
“Berliner  Klinik,”  1898,  Heft  cxxm,  1-25. 

65.  Oppolzer,  “ Erfahrungen  iiber  die  Therapie  der  Magenkrankheiten,” 
< ' Zeitschr.  d.  k.  k.  Ges.  d.  Aerzte  zu  Wien,”  Wien,  1857,  xm. 

66.  Penzoldt,  “ Beitrag  zur  Lehre  von  der  menschlichen  Magenverdauung,” 
“ Deutsches  Archiv  f.  klin.  Med.,”  Bd.  Li  u.  LIU. 

67.  Penzoldt,  “ Salzsaures  Orexin,  ein  echtes  Stomachicum,”  “ Therapeu- 
tische  Monatshefte,”  Februar,  1890. 

68.  v.  Pfungen,  “ Ueber  Atonie  des  Magens,”  Wien,  1887. 

69.  Pick  (Coblenz),  “ Die  Behandlung  des  chronischen  Magenkatarrhs  mit 
grossen  Bismuthdosen,”  “ Berlin,  klin.  Wochenschr.,”  1893. 

70.  Popoff,  P.  M.,  “ Ueber  Magenkatarrh,”  “ Zeitschr.  f.  kl.  Med.,”  Bd.  xxxn, 
XXII. 

71.  Quincke,  “Luftschlucken,”  “ Verhandlungen  des  VIII.  Congresses  fur 
innere  Medicin,”  Wiesbaden,  1889. 

72.  Quincke,  “ Ueber  perniciose  Anamie,”  “ Volkmann’s  Sammlung  klin. 
Vortrage.” 

73.  Reed,  B.,  “ Diet  in  the  Chronic  Catarrh  of  the  Gastrointestinal  Tract,” 
“ Jour,  of  Am.  Med.  Assn.,”  Feb.  19,  1898. 

74.  Reichmann,  “ Ueber  die  Anwendung  der  Pankreaspraparate  beim  atro- 
phischen  Magenkatarrh,”  “ Deutsch.  med.  Wochenschr.,”  1889. 

75.  Reichmann,  N.,  “Zur  Diagnose  der  Gastritis  atrophicans,”  “ Gazetta 
lekanka  (Polnisch)  ; “ Berlin,  klin.  Wochenschr.,”  1898,  xxxv,  1015. 

76.  Riegel,  “ Beitrage  zur  Pathologie  und  Diagnostik  der  Magenkrankheiten,” 
“ Deutsche  Archiv  f.  klin.  Med.,”  xxxvi ; “ Zeitschr.  f.  klin.  Med.,”  xi. 

77.  Riegel,  “Ueber  Diagnostik  und  Therapie  der  Magenkrankheiten,” 
“ Volkmann’s  Sammlung  klin.  Vortrage,”  1886,  Nr.  289. 

78.  Rodrigues,  d’Oliveira  J.,  “ Nota  sobre  um  caso  de  gastrite  chronica 
glandular  hyperpeptica,”  “ Coimbra  med.,”  1897,  xvii,  458,  474,494. 

79.  Rosenheim,  “ Ueber  atrophische  Processe  an  der  Magenschleimhaut  in 
ihrer  Beziehung  zum  Carcinom  und  als  selbststandige  Erkrankung,”  “ Berlin, 
klin.  Wochenschr.,”  1888. 

80.  Rosenheim,  “Ueber  die  Magendusche,”  “ Therapeut.  Monatshefte,” 
1892. 

81.  Sachs,  “Die  Kenntniss  der  Magenschleimhaut  in  krankhaften  Zu- 
standen,”  “ Archiv  fiir  exp.  Patholog.  u.  Pharm.,”  xxn  u.  xxiv. 

82.  Schwalbe,  “ Die  Gastritis  der  Phthisiker  vom  patholog.-anatomischen 
Standpunkte,”  “Virchow’s  Archiv,”  Bd.  cxvii. 

83.  Senator,  “ Ueber  ein  Fall  von  Hydrothionanamie  und  iiber  Selbst- 
infection  durch  abnorme  Verdauungsvorgange,”  “Berlin,  klin.  Wochenschr.,” 
1868. 

84.  Stintzing,  “Zur  Structur  der  enkrankten  Magenschleimhaut,”  “Miinch- 
ener  med.  Wochenschr.,”  1889,  Nr.  48. 

85.  Stintzing,  “ Miinchener  med.  Wochenschr.,”  1890. 

86.  Symes,  L.,  “ Dyspeptic  Conditions,”  “ Dublin  Jour.  Med.  Sc.,”  1897,  civ, 
115-121. 


482 


CHRONIC  GASTRITIS. 


87.  Tawitzki,  “ Ueber  den  Einfluss  der  Bitterstoffe  auf  die  Mengen  der  Salz- 
saure  im  Magensaft  bei  gewissen  Formen  von  Magen-  und  Darmkatarrhen,” 
“ Deutsches  Archivf.  klin.  Med.,”  Bd.  xlviii. 

88.  Tournier,  C.,  “ D’un  type  de  catarrhe  gastrique  avec  hyperesthesie  dela 
muqueuse  et  colite  muco-membraneuse  ; difficultes  diagnostiques  avec  l’ulcere,” 
“ Prov.  medicale,”  21,  22,  1897. 

89.  Uffelmann,  “ Beobachtungen  und  Untersuchungen  an  einem  gastroto- 
mirten  fiebernden  Knaben,”  “ Deutsches  Archiv  f.  klin.  Med.,”  xx,  1877. 

90.  Virchow,  R.,  “ Der  Zustand  des  Magens  bei  Phosphorvergiftung,”  “ Vir- 
chow’s Archiv,”  Bd.  xxxi,  S.  388. 

91.  Wasbutzki  “Ueber  den  Einfluss  von  Magengahrungen  auf  die  Faulniss- 
vorgange  im  Darmkanal,’’  “Archiv  f.  exp.  Patholog.,”  etc.,  Bd.  xxvi. 

92.  Werther,  “ Ueber  den  therapeutischen  Werth  der  Pepsinweine,”  “ Berlin, 
klin.  Wochenschr.,”  1892. 

93.  Widal,  “ Le  Bulletin  Medicale,”  1896,  Nos.  59,  61,  64,  78,  83,  and  1897, 
No.  4. 

94.  Will,  F.  J.,  “ Gastric  Catarrh,”  “Trans.  Iowa  Med.  Soc.,”  Cedar  Rapids, 
1897,  xv,  299-305. 

95.  Wolf-Gothenberg,  “ Beitrage  zur  Kenntniss  der  Einwirkung  verschie- 
dener  Genuss  und  Arzneimittel  auf  den  menschlichen  Magensaft,”  “ Zeitschr. 
f.  klin.  Med.,”  Bd.  xvi. 

BIBLIOGRAPHY  OF  PHLEGMONOUS  GASTRITIS. 

A. 

1.  Ackermann,  “ Ein  Fall  von  phlegmonoser  Gastritis  mit  Thrombose  zahl- 
reicher  Magenvenen  und  embolischen  Heerden  in  der  Leber  und  in  den 
Lungen,”  “Virchow’s  Archiv,”  1869,  Bd.  xlv,  S.  39. 

2.  Albers,  “ Rheinisch-Westph.  med.  Correspondenzblatt,”  1884,  No.  5,  re- 
ported by  “Tillmann’s  Archiv  f.  klin.  Chir.,”  Berlin,  1882,  Bd.  xxvil,  S.  155. 

3.  Andral,  G.,  “ Maladies  de  l’abdomen,”  “ Clinique  medicale,”  1839, 
tome  11. 

4.  Asverus,  “Ein  Fall  von  Gastritis  phlegmonosa,”  “Jenaische  Zeitschr.  f. 
med.  Natur.,”  Jena,  1866,  Bd.  11,  S.  476-482. 

5.  Auvray,  “ Etude  sur  la  Gastrite  phlegmoneuse,”  “ These  de  Paris,”  1866. 

B. 

6.  Baerecke,  V.  Z.,  “Was  it  a Case  of  Phlegmonous  Gastritis?”  “ N.  Y. 
Med.  Record,”  1898,  liv. 

7.  Bamberger,  “ Henoch’s  Klinik  der  Unterleibskrankheiten,”  Berlin,  1 85 5 ^ 
Bd.  11,  S.  196. 

8.  Beckler,  “Ein  Fall  von  idiopathischer  phlegmonoser  Gastritis,”  “Bayer, 
Aerztl.  Int.  Int-Bl.,”  Munchen,  1880,  Bd.  xxvn,  Nr.  37,  S.  403. 

9.  Belfrage  and  Bedenius,  “ Schmidt’s  Jahrb.,”  Leipzig,  1872,  Bd.  cliv,  S.  298. 

10.  Bianchette,  “ Sopra  un  laso  bi  Gastrite  Flemonosa,”  “ Gaz.  Med.  Ital.,” 
Prove.  Venete.  Padova,  1875,  vol.  xvn,  p.  217. 

1 1.  Bonetes,  “ Sepulchretum  sive  Anatomia  Practica,”  Lib.  ill,  Geneva,  1700. 

12.  Bouveret,  “ Traite  de  pathologia  Generale,”  1895,  tome  1,  p.  781. 

13.  Bret  and  Paviot,  “ Rev.  de  med.,”  Paris,  May  10,  1894,  p.  384. 

14.  Brinton,  “ Diseases  of  the  Stomach.” 

15.  Budd,  “ Organic  and  Functional  Diseases  of  the  Stomach,”  1855. 


LITERATURE  ON  PHLEGMONOUS  GASTRITIS. 


483 


c. 

16.  Cahn,  “Gastritis  diphtheritica  mit  acuter  gelber  Leberatrophie,” 
“ Deutsches  Archiv  f.  klin.  Med.,”  Leipzig,  1883,  Bd.  xxxiv,  S.  113-121. 

17.  Callow,  vide  Auvray  ( loc . ci/.). 

18.  Caudmont,  “ Bull.  Sec.  Anat.  de  Paris,”  1848,  tome  xxxm,  p.  273. 

19.  Chvostek,  “Zwei  Falle  von  primarer  diffuser  phlegmonbser  Gastritis,” 
“ Wien.  med.  Presse,”  1877,  Nr.  22,  29,  Bd.  xvii,  S.  693. 

20.  Chvostek,  “ Ein  weiterer  Beitrag  zur  primaren  diffusen  phlegmonosen 
Gastritis,  “ Wien.  med.  Bl.,”  1881,  Nr.  28,  Bd.  iv,  S.  831,  861,  891, 924,  962. 

21.  Cornil,  vide  Auvray  {loc.  cit.,  p.  20). 

22.  Cruveilhier,  vide  Raynaud,  p.  526. 


D. 

23.  Deininger,  “Zwei  Falle  von  idiopathischer  Gastritis  phlegmonosa,” 
“ Deutsches  Archiv  f.  klin.  Med.,”  Leipzig,  1 878— ’79,  Bd.  xxn,  S.  624-632. 

24.  Dirner,  “Gastritis  phlegmonosa,”  “ Orbosi  hetila,”  Budapest,  1881,  vol. 
xxv,  page  793. 

25.  Dumesnil,  vide  Auvray  {loc.  ci/.). 

E. 

26.  Ewald,  “Lectures  on  Diseases  of  the  Stomach,”  “ N.  Sydenham  Soc. 
Trans.,”  1892,  p.  504.  (Cases  reported  from  clinic  of  Frerichs.) 


27.  Fagge,  “ A Case  of  Diffused  Suppurative  Inflammation  of  the  Stomach,” 
“ Trans.  Path.  Soc.,”  London,  1874-75,  vol.  xxvi,  p.  81. 

28.  Feroci,  “ Ann.  univ.  di  med.  e chir.,”  Milano,  1873. 

29.  Ferraresi,  “ Sulla  Gastrite  Flemmonoso,”  “ Atti  Accad.  med.  di  Roma,” 
1887,  series  xi,  vol.  cxi,  p.  267. 

30.  Flint,  quoted  by  Reinking  {loc.  cit.),  S.  16,  “ Phila.  Med.  Times,”  Aug.  8, 
1878. 

31.  Fontain,  “ Gastrite  Phlegmoneuse,”  “ Bull,  et  mem.  Soc.  med.  d.  hop.  de 
Paris,”  1866,  tome  xi,  p.  131. 

32.  Frankel,  “ Ueber  einen  Fall  von  Gastritis  acuta  emphysematosa, 
wahrscheinlich  mykotischen  Ursprungs,”  “Virchow’s  Archiv,”  1889,  Bd. 
cxviil,  S.  526. 

G. 

34.  Garel,  cited  by  Reinking,  1879  {loc.  cit.),  S.  17,  “ Lyon  med.,”  Oct.,  1871. 

35.  Gaudy,  “Observation  de  Gastrite  Phlegmoneuse,”  “Archiv  Med.  Beige,” 
Bruxelles,  1863,  tome  xxxi,  pp.  459-464. 

36.  Gilbert  and  Dominici,  “ Med.  Jour.,”  New  York,  May,  1894;  cited  from 
Leith’s  article  {loc.  cit.). 

37.  Glaser,  “ Zwei  Falle  von  Gastritis  phlegmonosa  idiopathica,”  “ Berl.  klin. 
Wochenschr.,”  1883,  Bd.  xx,  S.  790.  (Two  cases.) 

38.  Glax,  “Ueber  Gastritis  phlegmonosa,”  “ Berl.  klin.  Wochenschr.,”  1879, 
Bd.  xvi,  S.  565. 

39.  Glax,  “Die  Magenentziindung,”  “Deutsche  med.  Ztg.,”  Beilin,  1884, 
Nr.  3. 

40.  Guyot,  “Gastrite  Phlegmoneuse,”  “Union  med.,”  Paris,  1865,  N.  S., 
tome  xxvii,  pp.  184,  185. 


484 


CHRONIC  GASTRITIS. 


H. 

41  (a).  Habershon,  “ Case  of  Suppuration  in  the  Coats  of  the  Stomach,” 
*'  Guy’s  Hosp.  Rep.,”  London,  1855,  p.  1 1 5. 

41  ( b ).  Hemmeter,  John  C.  “ A case  of  phlegmonous  Gastritis,”  etc.,  “New 
York  Med.  Rec.,”  Sept.,  1897. 

42.  Herzog,  “ Kaspar’s  Wochenschr.,”  1839,  S.  813;  quoted  by  Reinking 
{loc.  cit .,  S.  11). 

43.  Heyfelder,  “ Sanitatsbericht  liber  das  Fiirstenthum  Hohenzollern  Sig- 
maringen  wahrend  des  Jahres  1836,”  “ Schmidt’s  Jahrb.,”  Leipzig,  1837,  Bd. 
xvi,  S.  192. 

44.  Hun,  “Idiopathic  Phlegmonous  Inflammation  of  the  Submucous  Cellu- 
lar Tissue  of  the  Stomach,”  “ N.  Y.  Med.  Jour.,”  1868,  vol.  vm,  p.  18. 


45.  Kelynack,  “A  Case  of  Diffuse  Phlegmonous  Gastritis,”  “Lancet,” 
London,  1896,  March  14th. 

46.  Klaus,  “ Beitrag  zur  Kenntniss  d.  Magenkrankheiten,”  Inaug.-Diss., 
Erlangen,  1857. 

47.  Klebs,  “ Ueber  infectiose  Magenaffectionen,”  “ Allg.  Wien.  med.  Ztg.,” 
1881,  Nos.  29,  30,  31,  32,  34,  35. 

48.  Krabbe,  “ Tidsker.  f.  Vet.,”  Kjobenhaven,  1872;  and  “Deutsche 
Zeitschr.  f.  Thiermedicin,”  Leipzig,  Bd.  1. 

49.  Krause,  “Ueber  submucose  phlegmonose  eitrige  Magenentziindungen,’ 
Berlin,  1872,  Inaug.-Diss.,  Kiel,  1874. 

50.  Kurschmann,  “ Magenabscess,”  “Wien.  med.  Wochenschr.,”  1880, 
No.  14. 

L. 

51.  Lasege,  vide  Auvray  {loc.  cit.). 

52.  Leith,  “Phlegmonous  Gastritis:  Its  Pathology,  Etiology,  Symptoms,  and 
Treatment,”  “Edinburgh  Hospital  Reports,”  vol.  iv,  pp.  51-114. 

53.  Leube,  “ Ziemssen’s  Cyclopaedia  of  the  Practice  of  Medicine,”  1877,  vol. 
vii,  p.  154. 

54.  Lewandowski,  “Zur  Casuistik  der  idiopathischen  Gastritis  phlegmo- 
nosa,”  “ Berlin,  klin.  Wochenschr.,”  1879,  Bd.  xvi,  S.  568. 

55.  Lewin,  “ Zur  Casuistik  der  Gastritis  phlegmonosa  idiopathica,”  “ Berlin, 
klin.  Wochenschr.,”  1884,  Bd.  XXI,  S.  83. 

56.  Lieutaud,  “ Historia  Anatomica-medica  ” (includes  observations  by 
Riolanus,  Baunimus,  and  others),  1767,  tome  1,  p.  2. 

57.  Lindemann,  “ Fall  von  Gastritis  phlegmonosa  diffusa,”  “ Munch,  med. 
Wochenschr.,”  1887,  Nr.  25. 

58.  Lowenstein,  “Ueber  Gastritis  phlegmonosa,”  Inaug.-Diss.,  Kiel,  1874. 

59.  Loomis,  “Med.  Rec.,”  N.  Y.,  Feb.  15,  1869. 

M. 

60.  Macleod,  “Suppurative  Gastritis,”  “ Lancet,”  London,  1887,  vol.  xi,  p. 
1116. 

61.  Malmsten  and  Key,  “ Fall  af  Flegmonos  Gastritis,  Hygeia,”  Stockholm, 
1871,  p.  69. 

62.  Manoury,  “Infiltration  Purulente  Puerperale  de  l’Estomac,”  “Bull.  Soc. 
Anat.  de  Paris,”  1842,  tome  xvii,  p.  175. 


LITERATURE  ON  PHLEGMONOUS  GASTRITIS. 


485 


63.  Martin,  “ Diseases  of  the  Stomach,”  1895,  p.  277. 

64.  Mascaral,  “Bull.  Soc.  Anat.  cle  Paris,”  1830,  tome  xv,  p.  176. 

65.  Mayor,  “ Absces  Sous-muquex  de  l’Estomac,”  “Bull.  Soc.  Anat.  de 
Paris,”  1840,  tome  xvn,  p.  298. 

66.  Mazet,  “Phlegmon.  Diffuse  de  l'Estomac,’’  “ Bull.  Soc.  Anat.  de  Paris,” 
1840,  tome  xv,  p.  174. 

67.  Meyer,  “St.  Petersb.  med.  Wochenschr.,”  1892,  No.  40. 

68.  Mintz,  “ Ein  Fall  von  Gastritis  phlegmonosa  diffusa  im  Verlaufe  eines 
Magenkrebses,”  “ Deutsches  Archiv  f.  klin.  Med.,”  Leipzig,  1892,  Bd.  xlix, 
S.  487. 

69.  Morel,  “ Gastrite  Phlegmoneuse,”  “ Bull.  Soc.  Anat.  de  Paris,”  1865. 

N. 

70.  Nasse  and  Orth,  “Virchow’s  Archiv,”  Bd.  civ,  S.  584. 

71.  Nielsen,  “ Bradsot  hos  Faaret  (Gastromycosis  ovis),”  “ Tidsker.  f.  Vet.,” 
Kjobenhaven,  1887,  pp.  1-2 1. 

O. 

72.  Odmanson,  “Gastritis  phlegmonosa  diffusa,”  “ Forh.  v.  Svens  Lak. 
Sallsk.  Sammank,”  Stockholm,  1865,  p.  265. 

73.  Oser,  “ Realencyclopadie  ” : “ Magenentziindung,”  1887,  Bd.  xi,  S.  412. 

P. 

74.  Page,  “A  Case  of  Gastrostomy  Fatal  on  the  Twenty-third  Day,  from 
Acute  Parenchymatous  Gastritis,”  “Lancet,”  London,  1833,  vol.  11,  p.  53. 

75.  Petersen,  “Ein  Fall  von  Gastritis  phlegmonosa,”  “St.  Petersb.  med. 
Wochenschr.,”  1879,  Bd.  iv,  S.  288. 

76.  Pilliet,  “ Bull.  Soc.  Anat.  de  Paris,  1893,  No.  12. 


77.  Rakowak,  “ Duchek’s  Klinik;  “Wien.  med.  Presse,”  1873,  No.  25. 

78.  Raynaud,  “ De  l’lnfiltration  Purulence  de  l’Estomac,”  “ Bull.  Soc.  Anat. 
de  Paris,”  1861,  tome  vi,  pp.  62-93. 

79.  Reinking,  “ Beitrag  zur  Kenntniss  der  phlegmonosen  Gastritis,”  Inaug.- 
Diss.,  Kiel,  1890,  S.  26. 

80.  Robel,  P.,  Opera,  1656. 

S. 

81.  Sand,  “ Dissertatio  de  raro  Ventriculi  Abscessu  Regiomont,”  1701. 

82.  Sebillon,  “ De  la  Gastrite  phlegmonosa,”  “These  de  Paris,”  1885. 

83.  Sestier,  “ Abscess  Metastatique  des  Parois  de  l’Estomac,”  “Bull.  Soc. 
Anat.  de  Paris,”  1883,  tome  vm,  p.  130. 

84.  Silcock,  “ Stomach  Exhibiting  the  Condition  known  as  Phlegmonous 
Gastritis,”  “ Trans.  Path.  Soc.,”  London,  i882-’83,  vol.  xxxiv,  p.  90. 

85.  Smirnow,  “ Ueber  Gastritis  membranacea  und  diphtheritica,”  “ Virchow’s 
Archiv,”  1889,  Bd.  cxm,  S.  333. 

86.  Smith,  “ Med.  Rec.,”  New  York,  Oct.  12,  1889. 

87.  Stewart,  “A  Case  of  Gastritis  Phlegmonosa,  with  Inflammation  and 
Gangrene  of  the  Gall-bladder,”  “ Edin.  Med.  Jour.,”  1868,  N.  S.,  vol.  xn, 
P-  732. 

88.  Strieker  und  Kooslakoff,  “ Experimente  iiber  Entziindungen  des  Magens," 
“ Sitzungsb.  d.  k.  Akad.  d.  Wissensch.,”  Wien,  1866,  Bd.  liii. 

32 


486 


ULCER  OF  THE  STOMACH. 


T. 

89.  Testi,  Alberico,  “Un  raro  caso  di  ascesso  dello  stomaco,”  “ Annal  univ. 
di  med.  e chir.,”  Milano,  Dec.,  1883,  pp.  523-547. 

90.  Thoman,  “Allgem.  Wiener  Zeitung,”  1891,  Nr.  10. 

91.  Thungel,  “ Ein  Fall  von  Vereiterung  des  submucosen  Zellgewebes  des 
Magens,”  “ Virchow’s  Archiv,”  1865,  Bd.  xxxm,  S.  406-408. 

92.  Treuberg,  “Primary  Phlegmonous  Inflammation  of  the  Stomach,” 
“ Vrach,”  St.  Petersb.,  1883,  vol.  lv,  p.  355. 


93.  Varandaeus,  “ Tractatus  de  Morbis  Ventriculi,”  1620. 

94.  Vorwaltner,  “ Eph.  Nat.  cur.,”  Dec.  3,  Obs.  142. 


95.  Wallmann,  “Wiener  med.  Wochenschr.,”  1857,  Bd.  xm,  S.  733. 

96.  Whipham,  “ Remarks  on  a Case  of  Phlegmonous  Gastritis,”  “ Brit.  Med. 
Jour.,”  London,  1884,  vol.  1,  p.  896. 

97.  Wilks  and  Mokon,  “ Pathological  Anatomy,”  3d  edition,  1889,  p.  399. 


98.  Ziegler,  “ Pathologische  Anatomie,”  Bd.  11,  S.  513. 


CHAPTER  III. 

ULCER  OF  THE  STOMACH. 

Ulcus  Ventriculi , Pepticum , Rotundum , Perforans , Rodens , Corrosivum , 
e Digestione. 

Ulcer  of  the  stomach  is  a loss  of  substance  of  the  gastric 
mucosa,  characterized  by  very  little  tendency  toward  healing,  but 
rather  by  destructive  progression  both  in  a lateral  direction — i.  e.y 
in  a plane  with  the  surface — and  toward  the  depth  of  the  mucosa. 
It  may  occur  in  two  forms,  (1)  the  acute  and  (2)  the  chronic.  The 
acute  form  extends  so  rapidly  from  the  mucosa  toward  the  peri- 
toneum, with  such  small  lateral  involvement,  that  Rokitansky’s 
original  comparison,  “ as  if  the  ulcer  were  cut  out  with  a punch,” 
has  become  the  classical  expression  of  the  text-books.  In  the 
chronic  form  the  destructive  process  is  not  so  rapid;  it  extends 
more  laterally,  producing  a terraced  or  shelving  appearance  of  the 
edges  and  sides,  so  that  it  may  be  funnel-shaped.  Perforation  into 
an  artery,  vein,  or  into  the  peritoneal  cavity  occurs  in  both  forms. 
The  chronic  form  has  a tendency  to  healing,  but  in  so  doing 


SELF-DIGESTION  OF  THE  STOMACH. 


487 


causes  cicatricial  contractions  and  deformity.  The  acute  form 
may  terminate  in  healing,  but  owing  to  its  limited  lateral  extent, 
the  small  cicatrix  rarely  causes  deformity.  It  is  very  probable 
that  the  acute  ulcers  have  a different  etiology  (corrosives,  toxic 
action,  trauma  by  sharp,  hard  materials  in  the  food,  in  conjunction 
with  other  factors  to  be  considered)  from  the  chronic  eroding  type, 
to  which  the  following  description  appertains  more  especially. 

Self-digestion  of  the  Stomach  (Gastromalacia). — If  an  animal 
be  killed  while  in  full  digestion,  the  stomach  may  undergo  self- 
digestion after  death  if  the  body  is  kept  warm.  In  human  beings 
who  died  suddenly  while  the  gastric  digestion  was  at  its  hei'ght,  it 
was  found  at  the  autopsy  that  not  only  the  stomach  had  been 
digested,  but  also  the  spleen,  and  that  this  process  had  extended 
through  the  diaphragm  into  the  lungs.  The  question  naturally 
arises,  What  protects  the  stomach  from  autodigestion  from  its  own 
secretions  under  normal  conditions  ? This  is  an  inquiry  that  con- 
cerns the  fundamental  properties  of  living  matter,  for  it  includes 
the  non-digestion  of  the  intestinal  tract  by  the  alkaline  pancreatic 
juice  and  succus  entericus,  the  same  property  as  observed  in  the 
digestive  tracts  of  invertebrates  and  even  in  the  unicellular  organ- 
isms, the  amebae  and  plasmodia  of  mycetozoa.  For  instance, 
Metschnikofif,  C.  Le  Dantec,  Greenwood,  Saunders,  and  the  author 
have  shown  that  a secretion  is  formed  in  the  digestive  vacuoles  of 
these  unicellular  organisms  which  digests  foreign  proteid  material, 
but  not  the  living  substance  of  the  cell  itself  (see  “ On  the  Role  of 
Acid  in  the  Digestion  of  Certain  Rhizopods,”  by  J.  C.  Hemmeter, 
Philos.  D.,  etc.,  in  “American  Naturalist,”  August,  1896,  p.  619). 

The  following  explanations  have  been  offered  for  the  protection 
of  the  human  stomach  from  its  own  secretion : 

1.  By  Hunter:  That  the  principle  of  life  in  living  things  pro- 

tected the  stomach  from  digestion. 

Bernard  succeeded  in  demonstrating  that  the  hind  leg  of  a living 
frog,  introduced  into  a dog’s  stomach  through  a fistula,  under- 
goes digestion.  This  will  also  happen  if  the  leg  be  placed  in  a 
vessel  containing  gastric  juice  at  the  proper  temperature. 

2.  Bernard  explained  the  exemption  of  the  normal  stomach 
from  autodigestion  by  assuming  a protective  power  in  the  living 
epithelium,  which  he  thought  prevented  the  absorption  of  gastric 
juice. 

3.  Strieker  believed  that  the  mucus  formed  on  the  surface  of  the 
stomach  acts  as  a protective  covering. 


488 


ULCER  OF  THE  STOMACH. 


4.  Pavy  (“Guy’s  Hospital  Reports,”  vol.  xiv,  1868)  held  that  the 
alkaline  blood  circulating  through  the  gastric  walls  saved  them 
from  digestion,  since  it  neutralized  the  acid  as  fast  as  it  was  ab- 
sorbed. None  of  these  explanations  is  sufficient.  Bernard’s  sug- 
gestion simply  shifts  the  problem  by  assuming  an  immunity  of  the 
living  epithelial  cells  without  attempting  to  explain  why  these  are 
not  digested.  The  coating  of  mucus  which  Strieker  believed  to 
be  a protection  is  digested  by  gastric  juice. 

Pavy’s  theory  that  the  alkaline  reaction  of  the  gastric  circulation 
prohibits  self-digestion,  is  untenable,  because  under  these  condi- 
tions one  could  not  explain  why  the  pancreas  does  not  digest  itself, 
and  is  also  disproved  by  Samelson,  who  produced  a neutral  reac- 
tion of  the  blood  by  gradual  introduction  of  acid,  and  then  poured 
dilute  HC1  into  the  animals’  stomachs;  but  even  then  no  auto- 
digestion was  observed.  When  Hunter,  over  one  hundred  years 
ago  (1786),  referred  the  immunity  to  a specific  property  of  the 
living  cells,  the  “ vital  principle,”  he  gave  as  good  an  explanation 
as  any  given  up  to  date.  The  expression  “ vital  principle  ” may 
sound  mysterious  in  the  light  of  modern  physiological  knowledge, 
but  it  undoubtedly  implied  that  gastric  immunity  from  self-diges- 
tion was  due  to  physical  and  chemical  forces  possessed  by  the 
protoplasm  of  living  cells  and  which  are  not  as  yet  understood. 
In  the  latter  term  we  use  more  accurate  expressions,  but  give  no 
better  explanation  than  Hunter. 

Elsasser  agreed  that  gastromalacia  was  always  a cadaverous 
process,  and  was  supported  in  this  view  by  Virchow,  Foster, 
Oppolzer,  Bamberger,  and  others,  so  that  his  opinion  became  the 
prevailing  one.  A contrary  view  was  held  by  Rokitansky,  who 
represents  the  belief  that  there  is  a gastromalacia  that  occurs  intra 
vitam}  particularly  in  the  end  stages  of  grave  diseases  of  the  brain 
and  its  membranes  (basal  and  tuberculous  meningitis)  and  in  other 
severe  exhausting  affections.  The  occurrence  of  intravital  autodi- 
gestion was  proved  in  a case  reported  both  by  W.  Mayer  and  Leube 
from  Ziemssen’s  clinic,  and  also  by  numerous  animal  experiments. 

Results  of  animal  experiments  in  producing  secondary  injury 
and  consequent  self-digestion  of  the  stomach  are  the  following : 
Schiff,  by  intersection  of  the  thalami  and  cerebral  peduncles,  pro- 
duced hemorrhagic  infiltrations,  partial  softenings,  erosions,  and 
even  ulcer  formation  in  the  gastric  mucosa,  and  interpreted  his 
results  as  consequences  of  neuroparalytic  hyperemia  caused  by 
injury  to  the  central  vasomotor  nerve- tracks  of  the  stomach. 


EXPERIMENTS  BEARING  ON  THE  ETIOLOGY. 


489 


Ebstein  and  Brown-Sequard  obtained  identical  effects  after  circum- 
scribed destruction  of  the  anterior  corpora  quadrigemina.  Panum 
injected  an  emulsion  of  tiny  wax  globules  into  the  femoral  arteries 
of  dogs  and  effected  small  gastric  hemorrhagic  infarcts  and  ulcers. 
Cohnheim  injected  suspensions  of  plumbic  chromate  into  the 
stomach  circulation,  by  which  he  succeeded  in  blocking  only  the 
branches  of  the  mucosa  and  submucosa,  while  the  circulation  of 
the  muscularis  remained  free.  At  the  autopsy  he  discovered  large 
ulcers  with  abruptly  descending  edges  and  clean  bases.  Koch  and 
Ewald  brought  about  gastric  hemorrhagic  infarcts  by  intersection 
of  the  spinal  cord  (Schiff’s  method),  and  after  this  introduced 
strong  solutions  of  hydrochloric  acid  (5  per  1000)  into  the 
stomach,  thereby  producing  penetrating  ulcerations.  After  severe 
traumatism, — for  example,  bruising  the  epigastric  region  with  a 
hammer, — and  after  thermic  irritation,  as  by  introducing  very  hot 
gruel,  Ritter  and  Decker  produced  ulcus  ventriculi.  Silbermann 
brought  on  gastric  ulcers  that  healed  with  difficulty  by  causing 
hemoglobinemia  with  substances  that  dissolved  the  blood-cor- 
puscles. 

His  results  are  significant,  as  explaining  the  pathogenesis  of  gas- 
tric ulcer  after  extended  skin  burns  and  malaria.  This  is  to  a 
certain  entent  explained  by  the  investigations  of  Klebs  and  Welti, 
who  have  shown  that  broken-down  red  corpuscles,  blood-pigment 
and  thrombi  of  blood-plaques,  or  undeveloped  elements  may 
occlude  the  gastric  vessels  and  cause  ulcer;  and  London  explains 
the  gastric  ulcers  in  malaria  by  the  occurrence  of  pigment  emboli. 
Talma  produced  gastromalacia  and  gastric  ulcers  by  ligating  the 
esophagus  of  dogs  above  the  cardia  and  the  duodenum  below  the 
pylorus  (Talma,  “ Untersuch.  fiber  Ulcus  ventric,”  etc.,  “ Zeitschr. 
f.  klin.  Med.,”  Bd.  xvii,  S.  10).  This  experiment  constitutes  too  vio- 
lent an  interference  with  normal  gastric  physiology  to  permit  of 
any  correct  deductions. 

It  is  impossible  to  differentiate  the  effects  of  violent  trauma,  inter- 
ference with  the  venous,  arterial,  and  lymph-supply,  intragastric 
stagnation,  fermentation,  and  sepsis,  that  the  experiment  of  Talma 
brings  about. 

Views  Concerning  Causative  Circulatory  Disturbances. — 

Virchow  called  attention  to  the  frequency  of  gastric  ulcers  in 
anemia  and  chlorosis,  explaining  it  by  the  diseases  of  the  vessel 
walls,  fatty  degenerations,  aneurysmal  and  varicose  dilatations,  and 
their  consequences,  viz. : thrombosis  and  embolism.  Cohnheim 


490 


ULCER  OF  THE  STOMACH. 


conceded  the  casual  relations  of  these  states,  but  disputed  the  fre- 
quency of  their  occurrence,  (i)  because  the  abundant  anastomoses 
between  the  gastric  vessels  facilitate  a compensatory  collateral  cir- 
culation ; (2)  because  the  diseases  of  the  vessel  walls  referred  to 
are  rare  in  young,  but  frequent  in  old  persons,  which  would  indi- 
cate that  in  these,  gastric  ulcer  should  be  found  frequently,  whereas 
in  later  life  it  is  very  rare.  Klebs  has  a theory  attributing  gastric 
ulcer  to  local  ischemia,  supposed  to  be  caused  by  spastic  arterial 
contractions.  Rindfleisch’s  opinion  is  that  venous  stasis  in  the  gas- 
tric walls  may  lead  to  ulcer,  since  occlusion  of  the  exit  of  the  blood 
may  occur  easily  on  account  of  the  compressibility  and  the  few  anas- 
tomoses in  the  gastric  veins  ; this,  he  thinks,  may  cause  hemorrhage, 
erosions,  and  ulcer.  Cohnheim  opposes  this  view  also,  because 
gastric  ulcer  is  a rare  thing  in  the  passive  congestion  due  to  hepatic 
cirrhosis.  One  must  not  overlook  the  fact,  however,  that  in  this 
state  the  secretion  of  HC1  is  much  reduced.  Axel  Key  assumes 
that  long  and  persisting  contractions  of  the  musculature  may  cause 
local  ischemias  or  disturbances  in  the  venous  outflow.  From 
these  observations  it  is  clear  that  interruption  of  the  blood-current 
in  localized  areas  of  the  mucosa  may  lead  to  formation  of  ulcer. 
The  blood  stream,  then,  is  a protective  against  autodigestion,  not 
because  it  keeps  the  gastric  mucosa  alkaline,  as  Pavy  held, — for  the 
mucosa  is  acid  throughout  the  glandular  layer, — but  because  the 
blood  keeps  the  mucosa  nourished  and  alive. 

When  the  internal  surface  of  the  stomach  is  no  longer  nour- 
ished, it  must  die  in  areas,  which  are  then  digested,  as  other  dead 
proteid  matter  would  be. 

The  degree  of  alkalinity  of  the  human  blood  is  far  too  low  to 
neutralize  the  degree  of  HC1  acidity  present  in  any  part  of  the 
mucosa. 

The  digestion  of  the  hind  leg  of  a live  frog  (Bernard)  in  the 
stomach  of  an  animal  does  not  prove  that  living  tissue  will  be 
digested  there.  For  the  cells  of  cold-blooded  animals  die  rapidly  at 
the  temperature  of  the  warm-blooded  animal ; furthermore,  the  epi- 
dermis of  the  frog’s  leg  may  be  killed  by  the  HC1,  and  once  dead, 
it  is  rapidly  digested. 

Bottcher  and  Letulle  attribute  the  causation  of  ulcer  to  bacteria, 
which  they  could  demonstrate  in  colonies  in  the  floor  and  in  the 
surroundings  of  ulcer. 

Most  of  the  observers  mentioned  make  the  statement  that  gastric 
ulcers  produced  experimentally  in  animals  heal  rapidly.  The 


Edge  of  the  Sphincter 

nomatous  ulcer.  of  the  pylorus. 


PLATE  VII 


ETIOLOGY  OF  PEPTIC  ULCER. 


49  1 


mucosa  is  replaced  almost  completely;  a new  formation  of  peptic 
glands  has  been  observed  by  Grifinni,  Hauser,  and  Vassali.  At 
autopsies,  cicatrices  are  often  found  in  the  human  stomach,  where 
no  symptoms  referable  to  ulcer  were  evident  during  life.  It  is 
known,  also,  that  pieces  have  been  torn  loose  by  the  suction  of  the 
lower  end  of  the  stomach-tube,  and  yet  this  loss  of  substance 
healed  without  forming  an  ulcer;  so  that  repair  may  follow  injury 
to  the  human  stomach,  and  it  is  very  evident  that  some  other 
causatory  factors  besides  injury  are  necessary  to  bring  about  an 
ulcer.  A pathological  composition  of  the  blood  has  been  thought 
to  be  one  of  these  factors,  particularly  as  gastric  ulcer  is  very  fre- 
quently found  in  anemia  and  chlorosis.  I have  analyzed  the  gastric 
contents  of  32  cases  of  chlorosis — of  these,  24  had  marked  hyper- 
acidity; in  6 the  acidity  was  normal  and  in  2 it  was  subnormal. 
This  frequent  coexistence  of  hyperacidity  with  chlorosis  has  been 
observed  by  Riegel,  Cantu,  and  Bouveret,  and  is  important  for  the 
etiology.  This  view  is  supported  by  the  experiments  of  Quinke 
and  Daettwyler,  who  produced  a high  degree  of  anemia  by  gradual 
withdrawal  of  blood  from  dogs.  Thereafter,  they  produced  gastric 
injuries  by  mechanical,  chemical,  and  thermic  irritants,  and  discov- 
ered that  ulcers  were  formed  that  healed  with  much  difficulty. 
Clinical  experience  confirms  these  observations,  that  an  impaired 
state  of  the  blood  may  greatly  protract  healing.  On  the  other 
hand,  there  are  numerous  records  of  severe  and  recurrent  attacks 
of  gastric  ulcer  in  persons  whose  blood  was  found  perfectly 
normal. 

Etiology. — The  deductions  from  the  preceding  summary  of 
experiments  and  observations  are,  above  all,  the  establishing  of 
four  principal  factors  in  the  etiology  of  ulcer: 

I.  An  impaired  vitality  or  resistance  of  portions  of  the  mucosa. 

II.  Hyperacidity  or  supersecretion. 

III.  An  altered  state  of  the  blood. 

IV.  Local  bacterial  infection. 

There  are  a number  of  well-authenticated  cases  on  record  prov- 
ing that  direct  trauma  may  cause  gastric  ulcer  (vide  Einhorn,  loc . 
cit.,  p.  191  ; also  others  reported  by  C.  Hoffmann,  Leube,  and 
Eichhorst). 

According  to  Sidney  Martin  (loc.  cit.,  p.  410),  there  are  three 
common  causes  of  the  death  of  the  tissue  which  precedes  ulceration : 

I.  Mechanical  and  Chemical  Causes. — Ingested  fish-bones,  egg 
and  oyster  shells,  seeds,  etc.  Corrosive  poisons  lead  to  ulceration 


49  2 


ULCER  OF  THE  STOMACH. 


by  directly  destroying  the  tissue;  and  an  injury  to  the  mucous 
membrane,  which  is  subsequently  exposed  to  the  continued  action 
of  an  irritant,  will  also  lead  to  an  ulcer. 

Direct  injury  and  wounding  of  the  gastric  mucosa  occurs  very 
frequently,  and,  as  a rule,  heals  very  rapidly.  There  are  a number 
of  cases  on  record  of  persons  swallowing  glass,  nails,  and  knives, 
which  passed  through  the  entire  intestine  without  causing  injury. 
Marcet  (“  Med.  Chirur.  Transactions,”  vol.  xn,  p.  72)  narrates  the 
case  of  an  American  sailor  swallowing  some  thirty  pieces  of  knife- 
blades,  which  were  found  in  his  stomach,  together  with  a number 
of  handles.  Two  blades  were  in  the  colon  and  rectum,  placed 
transversely,  and  had  perforated  the  intestinal  wall  without  causing 
peritonitis.  No  recent  or  old  ulcers  were  found  in  the  stomach. 

The  following  report  from  the  German  Hospital,  of  Kansas  City, 
goes  to  show  that  this  class  of  human  ostrich  has  not  died  out. 
The  main  fact  that  is  proved  by  such  cases  is  that  something  else 
is  needed  in  addition  to  direct  injury  to  the  stomach  in  order  to 
produce  an  ulcer. 

German  Hospital,  Kansas  City,  Mo.,  June  14,  1897. — Harry  Whallen,  the 
“human  ostrich,”  who  was  operated  upon  at  the  German  Hospital  last  Satur- 
day, and  from  whose  stomach  the  surgeon  took  an  assortment  of  cutlery  and 
hardware,  died  at  two  o’clock  this  morning,  the  result  of  the  operation. 

Whallen  got  into  trouble  by  swallowing  a big  Barlow  knife,  in  Pilot  Grove, 
Mo.  When  he  was  operated  upon  at  the  German  Hospital  these  articles  were 
removed  from  his  stomach  : 

Two  jack-knives,  one  3 inches  long  and  the  other  4 inches  ; 5 knife-blades, 
from  1 to  3 inches  long ; 32  wire  nails,  eightpenny  or  larger ; 34  sixpenny 
nails,  26  shingle  nails,  16  carpet  tacks  and  small  wire  nails,  1 barbed  wire 
staple,  1 horseshoe  nail,  3 screws,  3 ounces  of  glass,  and  several  bits  of  crockery. 

He  was  a professional  showman.  He  began  swallowing  glass  and  nails 
when  he  was  ten  years  old,  and  says  he  has  eaten  a lamp  chimney  nearly 
every  day  during  the  seventeen  years  he  has  been  at  it,  but  the  Barlow  knife, 
which  he  swallowed  last  week,  was  too  much,  even  for  his  long-suffering 
stomach. 

When  the  surgeons  operated  upon  him,  the  stock  of  hardware  inventoried 
was  found  imbedded  in  a solid  mass  in  his  stomach  and  partially  encysted. 
After  it  was  removed,  the  stomach  was  thoroughly  washed  out  and  sewed  up. 

2.  Interference  with  the  Vitality  of  the  Tissue. — The  vitality  of  a 
particular  part  of  the  mucous  membrane  may  be  diminished  by 
local  and  chronic  disease  or  by  interference  with  the  circulation 
over  a certain  area.  This  latter  usually  occurs  by  means  of 
thrombosis  or  embolism.  Thrombosis  takes  place  in  connection 
with  disease  of  the  vessels  and  in  association  with  inferior  quality 


BACTERIAL  INFECTION.  493 

of  the  blood  and  a slowing  of  the  local  circulation  ; embolism  may 
be  infective  or  non-infective,  and  is  usually  capillary. 

3.  Bacterial  Infection. — The  infective  processes  of  the  digestive 
mucosa  with  which  we  are  most  familiar  are  the  ulceration  pro- 
cesses of  typhoid  fever,  certain  dysenteries,  and  tuberculosis.  In 
the  gastric  ulcer,  however,  there  is  another  kind  of  bacterial  infec- 
tion, which  is  not  accompanied  with  the  signs  of  active  inflam- 
mation, and  is  termed  by  some  authors  “ bacterial  necrosis.” 

The  process  is  characterized  by  the  invasion  of  bacteria,  usually 
in  the  lower  depths  of  the  mucous  membrane,  by  their  growth 
and  subsequent  necrosis  of  the  tissue.  Although  the  secretion  of 
HC1  is  germicidal  to  many  bacteria,  it  must  be  remembered  that 
the  spores  are  not  destroyed  by  it,  and  that  the  invasion  may  take 
place  during  the  periods  of  rest  of  the  glands  in  the  intervals  of 
digestion  when  no,  or  very  little,  HC1  is  secreted.  There  is  room 
for  the  suggestion  that  the  primary  necrosis  is  due  to  bacteria  and 
the  ensuing  ulceration  caused  by  the  action  of  the  gastric  juice. 
The  bacteria  can  exist  in  the  cells  around  and  beneath  the  floor  of 
the  ulcer,  and  notwithstanding  a very  high  degree  of  hyperacidity 

In  a number  of  cases  which  I examined  by  the  most  approved 
cellular  and  bacterial  stains  the  bacteria  were  present  throughout 
the  layers,  even  in  the  peritoneum,  while  the  floor  of  the  ulcer  was 
in  the  muscularis.  It  is  conceivable  that  they  pave  the  way  for 
autodigestion  by  causing  necrosis  of  the  tissues  in  which  they  are 
imbedded.  No  bacterium  was  so  far  obtained  in  pure  culture,  but 
the  one  most  frequently  observed  was  a bacillus  very  much  re- 
sembling that  of  anthrax,  and  in  two  cases  of  ulcus  carcinomatosum 
the  Oppler-Boas  bacillus. 

Thermic  causes  are  the  ingestion  of  very  hot  food  and  drink, 
taken  when  the  organ  is  empty. 

An  interesting  etiological  relation  exists  between  cutaneous 
burns  and  gastric  or  duodenal  ulcers. 

The  last  two  factors,  hot  food  and  large  cutaneous  burns,  are 
given  in  explanation  of  the  reported  frequency  of  gastric  ulcer 
among  cooks,  who  are  in  the  habit  of  tasting  foods  that  are  still  on 
the  fire,  and  who  are  also  liable  to  frequent  burns.  However, 
there  is  no  satisfactory  statistical  evidence  that  gastric  ulcer  is 
more  frequently  diagnosed  in  cooks  than  in  other  trades. 

Constitutional  causes  are  generally  brought  about  by  such  dis- 
eases as  effect  alterations  and  degeneration  either  in  the  com- 
position of  the  blood  or  in  the  vessels.  These  are  chlorosis, 


494 


ULCER  OF  THE  STOMACH. 


anemia,  syphilis,  tuberculosis,  arteriosclerosis ; fatty,  amyloid,  and 
aneurysmal  degenerations  of  arteries ; thrombi,  emboli,  trichinosis, 
and  malaria. 

Effect  of  pressure  exerted  upon  the  stomach  by  the  costal  mar- 
gins is  claimed  to  induce  anemia  and  atrophy  of  the  mucosa, 
especially  in  the  region  of  the  smaller  curvature.  Habershon  and 
Rasmussen  have  advanced  this  view,  in  explanation  of  the  fre- 
quency of  gastric  ulcer  in  those  whose  occupations  necessitate 
continual  pressure  on  the  stomach. 

Influence  of  Age. — In  order  to  determine  from  postmortem 
records  the  age  at  which  gastric  ulcer  most  frequently  occurs,  all 
cases  in  which  only  cicatrices  are  found  should  be  excluded, 
because  a cicatrix  gives  no  evidence  as  to  the  age  at  which  the 
ulcer  existed.  The  best  statistics  on  this  subject  are  contained  in 
Welch’s  article  on  Gastric  Ulcer  in  Pepper’s  “ System  of  Medicine,” 
volume  ii,  page  483.  The  statistics  of  Brinton,  which  are  still 
cited  in  the  last  editions  of  Boas,  Fleischer,  Sidney  Martin,  Fleiner, 
Debove  and  Remond,  and  others,  include  all  cicatrices  found  at 
autopsies  as  open  ulcers.  The  following  table  is  given  by  Welch, 
representing  the  age  in  607  cases  of  open  ulcer,  collected  from 
hospital  statistics : 


Age,  . 

[-10 

10-20 

20-30 

30-40 

40-50 

50-60 

0 

r-^ 

O 

70-80 

80-90 

90-100 

Over 

100 

No.  of 
Cases, 

- 

32 

119 

107 

114 

108 

84 

35 

6 

0 

* 

Totals, 

33 

226 

222 

II9 

7 

From  this  table  it  is  apparent  that  the  largest  number  of  cases 
is  found  between  twenty  and  thirty.  Three-fourths  of  the  cases 
occur  between  twenty  and  sixty. 

In  41,688  cases,  constituting  the  clinical  material  in  Zurich  and 
Breslau  between  the  years  1853  and  1 873,  252  cases  of  gastric 
ulcer  were  diagnosed  during  life  by  Lebert;  nearly  seven-tenths 
were  between  twenty  and  forty  years  of  age, — a preponderance 
sufficiently  great  to  be  of  diagnostic  value  in  the  differentiation,  as 
we  shall  see  later  from  carcinoma,  for  in  this  disease  the  largest 
number  of  cases  is  found  between  fifty  and  sixty  years.  Goodhart 
has  described  a case  of  gastric  ulcer  in  an  infant  thirty  hours 
old. 


THE  FREQUENCY  OF  GASTRIC  ULCER.  495 

Influences  of  Sex. — Females  are  more  frequently  affected  than 
males;  the  following  are  the  figures  given  by  various  authors: 


Males.  Females. 

Welch, 40  per  cent.  60  per  cent,  in  1699  cases  of  gastric  ulcer 

found  at  autopsy. 

Brinton’s  ratio,  . . 1 male  to  every  2 females. 

Anderson,  ....  3 males  and  32  females  in  35  cases. 

Habershon,  ...  74  males  and  127  females  in  201  cases. 

Steiner’s  ratio,  . . 8 males  to  1 1 females. 


The  nursing  period,  puerperium,  and  menstruation  are,  it  is 
claimed,  liable  to  increase  the  susceptibility  to  ulcer. 

Geographical  Distribution. — There  seems  to  be  an  unequal  geo- 
graphical distribution  of  the  disease,  which  seems  to  be  more 
coVnmon  in  northern  than  in  southern  countries.  It  is  less  com- 
mon in  this  country  than  in  England  and  Germany,  according  to 
Da  Costa,  Keating,  and  Welch  ( loc . cit .,  p.  485).  The  last-men- 
tioned author  found  only  six  cases  of  gastric  ulcer  in  800  autopsies 
made  by  him  in  New  York.  In  444,564  deaths  in  New  York  City, 
from  1868  to  1882,  ulcer  of  the  stomach  was  assigned  as  the  cause 
in  only  410  cases.  To  these  statistics  little  importance  can  be 
attached,  because  they  are  compiled  from  reports  of  practitioners 
of  varying  diagnostic  skill,  and  concern  a disease  that  presents 
many  difficulties  of  recognition. 

The  Frequency  of  Gastric  Ulcer. — We  quote  the  following 
from  Professor  Welch’s  article  {loc.  cit.) : 

In  32,052  autopsies  made  in  Prague,  Berlin,  Dresden,  Erlangen, 
and  Kiel,  there  were  found  1522  cases  of  open  ulcer  or  of  cicatrix 
in  the  stomach.  If  all  the  scars  be  reckoned  as  healed  ulcers, 
according  to  these  statistics  gastric  ulcer,  either  cicatrized  or  open, 
is  found  in  about  five  per  cent,  of  persons  dying  from  all  causes. 

It  is  important  to  note  the  relative  frequency  of  open  ulcers  as 
compared  with  that  of  cicatrices.  In  11,888  bodies  examined  in 
Prague,  there  were  found  164,  or  1.4  per  cent.,  with  open  ulcers, 
and  373,  or  3.1  per  cent.,  with  cicatrices.  Here  scars  were  found 
about  two  and  one-fourth  times  as  frequently  as  open  ulcers.  The 
observations  of  Grunfeld  in  Copenhagen  show  that  when  especial 
attention  is  given  to  searching  for  cicatrices  in  the  stomach,  they 
are  found  much  more  frequently  than  the  figures  here  given  would 
indicate.  It  would  be  a moderate  estimate  to  place  the  ratio  of 
cicatrices  to  open  ulcers  at  three  to  one. 

The  statistics  concerning  the  average  frequency  of  open  ulcers 


496 


ULCER  OF  THE  STOMACH. 


are  much  more  exact  and  trustworthy  than  those  relating  to  cica- 
trices. It  may  be  considered  reasonably  certain  that,  at  least  in 
Europe,  open  gastric  ulcers  are  found,  on  the  average,  in  from  one 
to  two  per  cent,  of  persons  dying  from  all  causes. 

It  is  manifestly  impossible  to  form  an  accurate  estimate  of  the 
frequency  of  gastric  ulcer  from  the  number  of  cases  diagnosed  as 
such  during  life,  because  the  diagnosis  is  in  many  cases  uncertain. 
Hence  the  importance  of  autopsy  statistics. 

Von  Jaksch  (cited  by  Bamberger,  “ Handbuch  d.  speciel.  Path  u. 
Therap.,”  von  Virchow,  vi,  i.  Abth.,  280)  states  that  1 13  ulcers  or 
cicatrices  were  found  in  2330  autopsies,  i.  e.y  4.8  per  cent.  Orth 
gives  five  per  cent. 

Berthold’s  statistics  from  the  “ Charite,”  Berlin,  from  1868  to 
1882,  give  294  cases, — 2.7  per  cent.  (“  Statist.  Beitrage  z.  Kennt.  d. 
chronischen  Magengeschwiirs,”  Sections-Protocoll  d.  Path.  Inst., 
Berlin). 

Nolte,  Munchen,  1876  to  1883,  gives  3500  autopsies,  with  43 
ulcers,  or  1.23  per  cent.  (“  Haufigkeit  d.  Magengeschwiirs  in 
Munchen,”  Dissert.,  1883). 

Berthold  (cited  from  Ewald,  “ Diseases  of  the  Stomach,”  p.  233) 
gives  the  percentage  of  ulcer  of  the  stomach  for  Berlin  as  2.7  per 
cent.;  Nolte,  for  Munich,  as  1.23;  Gries,  for  Kiel,  as  8.3;  Stark, 
for  Copenhagen,  as  13  per  cent.  Von  Sohlern  (“  Der  Einfluss  der 
Ernahrung  auf  die  Entstehung  des  Magengeschwiirs,”  “ Berlin, 
klin.  Wochenschr.,”  1889,  No.  14)  has  lately  called  attention  to  the 
fact  that  the  Roen  Mountains  and  the  Bavarian  Alps  (Germany) 
and  the  greater  part  of  Russia  are  nearly  exempt  from  gastric 
ulcer.  The  diet  upon  which  the  inhabitants  of  these  countries 
subsist  consists  largely  of  amylaceous  and  vegetable  substances 
containing  a large  percentage  of  potassium  salts.  The  blood  of 
persons  living  largely  or  exclusively  on  a vegetarian  diet  (Japanese) 
is  very  rich  in  potassium  phosphate.  According  to  von  Sohlern, 
the  exemption  from  gastric  ulcer  observed  among  these  peoples  is 
due  to  the  large  amount  of  potassium  introduced  in  their  food. 
We  are  not  aware  that  von  Sohlern  has  supported  his  theory  by 
quantitative  blood  analyses  ; this  constitutes  a weak  point  in  his 
argument. 

Location  of  Gastric  Ulcer. — This  table  gives  the  situation  of 
793  ulcers  reported  in  hospital  statistics  (from  article  on  “ Simple 
Ulcer  of  the  Stomach,”  by  W.  H.  Welch,  M.D.,  Pepper’s  “ System 
of  Medicine,”  vol.  11) : 


SYM  PTO  MATO  LOGY. 


497 


Lesser  curvature, 288  (36.3  per  cent.) 

Posterior  wall,  235  (29.6  “ “ ) 

Pylorus, 95  ( 12  “ “ ) 

Anterior  wall, 69  ( 8.7  “ “ ) 

Cardia,  50  ( 6.3  “ “ ) 

Fundus, 29  ( 3.7  “ “ ) 

Greater  curvature, 27  ( 3.4  “ “ ) 


Symptomatology. — The  most  characteristic  subjective  signs  of 
gastric  ulcer  are  localized  pain,  vomiting,  hematemesis,  disturb- 
ances of  secretion,  the  presence  of  blood  in  the  stools,  and  the  state 
of  the  appetite.  Frequently  all  these  symptoms  occur  together; 
at  other  times  only  one  or  the  other  single  symptom  becomes 
prominent.  There  are  cases  of  gastric  ulcer  that  run  a latent 
course,  without  any  characteristic  symptoms  whatever. 

We  will  begin  with  a consideration  of  the  excessive  secretion  of 
HC1.  This  is  a result  of  the  irritation  of  the  gastric  nerves,  either 
by  the  inflammation  caused  by  the  ulcer  itself,  or  by  irritation  of 
exposed  nerve-fibers,  caused  by  the  contents  of  the  stomach.  Since 
the  publication  of  the  first  edition  of  this  work,  Prof.  J.  P.  Pawlow 
has  demonstrated  the  secretory  nerves  of  the  stomach  in  the  vagus 
and  sympathetic  by  methods  irreproachable  from  the  standpoint  of 
physiological  technique.  By  admirable  patience  he  succeeded  in 
preparing  such  vagus  fibers  as  caused  only  a prompt  secretion  of 
gastric  juice  and  others  that  responded  to  stimulation  by  prompt 
inhibition  of  secretion  (Pawlow,  “ Arbeit  d.  Verdauungsdriisen,” 
S.  78).  Just  as  the  eye  will  overflow  with  tears  until  an  offending 
foreign  body  has  been  removed,  and  just  as  the  saliva  will  be 
secreted  when  the  mucous  membrane  of  the  mouth  is  stimulated 
by  food,  or  when  there  are  ulcers  or  inflammations  present  in  the 
buccal  cavity,  so  in  a similar  manner  the  gastric  mucosa  will  re- 
spond to  irritation  of  its  nerve-fibers  by  an  augmented  secretion. 

The  entire  gastric  nerve  apparatus  is  placed  in  a state  of  increased 
excitability  through  the  presence  of  an  ulcer,  and  when  food 
reaches  the  stomach  the  mucosa  is  stimulated  to  a degree  much 
greater  than  in  the  normal  stomach.  The  percentage  of  HC1 
present  varies  from  three  to  five  per  1000;  this  strong  gastric  juice 
rapidly  dissolves  albuminous  constituents  of  the  food,  while  the 
carbohydrates  remain  undigested.  Organic  acids  are  absent.  It 
may  happen,  in  rare  cases,  that  the  peristalsis  of  the  stomach  is  in- 
hibited, causing  retention  of  the  food ; in  such  cases  the  irritation 
of  the  nerves  is  kept  up  as  long  as  food  is  present  in  the  stomach, 


498 


ULCER  OF  THE  STOMACH. 


constituting  continued  hypersecretion.  We  have  to  distinguish  in 
these  cases  between  two  kinds  of  excess  of  gastric  juice:  (i)  the 
digestive  hyperacidity , which  occurs  when  the  motility  is  good,  only 
during  the  normal  presence  of  ingesta  in  the  stomach ; (2)  the  con- 
tinued hypersecretion , which  occurs  as  soon  as  the  motility  is  im- 
paired, when  food  is  present  at  all  times  in  the  organ.  With  a 
continued  hypersecretion  the  glandular  cells  gradually  become 
exhausted;  they  eventually  secrete  a juice  which  is  much  poorer 
in  HC1  and  pepsin  than  the  normal  product,  just  as  the  exhausted 
salivary  gland-cells  secrete  a saliva  which  is  very  poor  in  ptyalin. 
The  exhaustion  of  the  gastric  gland-cells  may  explain  the  observa- 
tion referred  to,  where  hyperacidity  was  absent  in  cases  of  un- 
doubted gastric  ulcer.  The  fact  probably  was,  the  glands  had 
become  so  exhausted  by  continued  overwork  that  it  was  impossi- 
ble for  them  to  form  their  characteristic  product. 

The  pain  of  gastric  ulcer  is  caused  by  irritation  of  the  sensory 
nerves  in  the  base  of  the  corroded  area.  It  occurs  with  great  in- 
tensity after  the  ingestion  of  food,  and,  as  a rule,  increases  with 
the  augmentation  of  acid  during  digestion.  The  pain  during  the 
digestive  act  is  most  probably  caused  also  by  the  peristaltic  move- 
ments, drawing  upon  and  compressing  the  ulcer.  External  pres- 
sure will  produce  sharp  pain  in  the  locality  of  the  ulcer.  The 
pain  is  of  a burning,  stinging  character,  and  in  some  cases  it 
causes  a spastic  contraction  of  the  sphincter  of  the  pylorus  re- 
flexly — a reflex  pylorospasm,  which  in  itself  may  be  very  painful. 
Some  patients  complain  frequently  of  a sore  spot  in  the  epigas- 
trium. In  cases  of  gastric  ulcer  associated  with  pylorospasm  the 
pain  radiates  from  the  epigastrium  toward  the  right  and  left,  reach- 
ing the  spinal  column.  Traube  called  attention  to  well-defined 
irradiations  of  the  pain  into  the  domain  of  other  nerves  outside  of 
the  stomach.  Attacks  of  angina  pectoris,  intercostal  neuralgias, 
and  neuralgias  in  the  left  brachial  plexus  have  been  described  by 
Brinton ; sympathetic  neuralgias  in  the  arms  and  legs  have  been 
referred  to  by  M.  Muller. 

The  intercostal  nerves  of  the  left  side  may  be  in  a more  sensi- 
tive condition  earlier  than  those  of  the  right  side.  This  may  reveal 
itself  by  a hyperesthesia  of  the  skin  and  soft  parts  in  the  lower 
left  parts  of  the  thorax,  upper  portions  of  the  abdomen,  and  in  the 
lumbar  region.  The  slightest  touch,  the  pressure  of  the  clothes 
and  bed-covers,  may  be  unpleasant  to  such  patients.  Female 
patients  can  not  wear  a corset. 


PYROSIS. 


499 


Very  frequently  the  pain  has  a penetrating,  lancinating  char- 
acter, shooting  from  the  epigastrium  straight  through  to  the 
spinal  column.  The  influence  of  the  ingestion  of  food  on  the 
pain  is  very  evident,  although  there  are  painful  sensations  when 
the  stomach  is  empty;  these  sensations  partake  more  of  the  nature 
of  soreness  and  hunger.  This  may  be  momentarily  relieved  by 
the  taking  of  food,  only  to  become  more  severe  by  the  stimulation 
and  the  hyperacid  secretion  that  are  set  up  by  it.  Liquid  food  may 
pass  through  the  stomach  without  causing  much  annoyance, 
whereas  solid  food  is  always  distressing.  Very  cold  or  very  hot 
food  invariably  causes  this  gastralgia.  The  pain  usually  occurs 
within  a half  hour  after  ingestion.  Should  it  not  occur  until  an 
hour  and  a half  to  two  hours  after  meals,  this  would  justify  the 
suspicion  of  an  ulcer  below  the  pylorus  in  the  duodenum,  whereas 
if  the  pain  occurs  at  once,  during  the  act  of  deglutition,  an  ulcer 
in  the  lower  part  of  the  esophagus  should  be  suspected.  Lying 
on  the  left  side  increases  the  pain  (Leube),  whereas  absolute  quiet 
and  resting  on  the  back  relieve  it. 

Pyrosis. — There  is  in  most  cases  a very  annoying  burning  feeling 
in  the  left  hypochondrium  and  epigastrium,  frequently  rising  to  the 
throat.  Some  patients  locate  it  posterior  to  the  sternum,  or  even 
between  the  shoulder-blades  ; this  so-called  “ heart-burn  ” is  caused 
by  irritation  of  the  stomach  and  esophagus  by  excessively  acid 
gastric  contents.  If  the  burning  is  very  marked  in  the  esophagus, 
we  may  presume  that  abnormal  peristalsis  of  the  stomach  and  in- 
sufficiency of  the  cardia  are  cooperative  in  bringing  about  the 
pyrosis. 

The  Condition  of  the  Appetite. — In  our  experience  the  appetite  is 
either  normal  or  increased  in  the  majority  of  cases.  The  instances 
where  the  appetite  is  positively  lost  are  very  rare.  Before  accept- 
ing a state  of  anorexia  it  is  necessary  to  distinguish  whether  food 
is  refused  because  the  patients  have  no  feeling  of  hunger,  or 
whether  they  will  not  eat  because  they  dread  the  pain  caused 
thereby.  Thirst  is  usually  increased,  and  the  tongue  is  clean. 

Vomiting. — The  irritation  and  the  hyperacidity  set  up  by  the 
presence  of  the  ulcer  cause  increased  peristalsis  and  antiperistalsis. 
The  peristaltic  unrest  is  accompanied  by  a feeling  of  boring  undu- 
lation in  the  epigastrium.  It  may  involve  the  intestine,  causing 
gurgling,  rumbling  noises.  The  rapid  evacuation  of  the  stomach, 
caused  by  the  intensified  peristalsis,  is  rather  favorable  to  recovery, 
because  it  brings  on  a speedy  return  of  the  contracted  state  which 
33 


Soo 


ULCER  OF  THE  STOMACH. 


favors  approximation  of  the  edges  of  the  ulcer  and  healing.  When 
the  pylorus  is  tightly  closed  by  spasmodic  contraction,  the  food 
masses  remain  much  longer  in  the  stomach,  and  the  mucosa  is 
excessively  irritated  by  the  intensely  acid  contents.  The  stomach 
is  then  distended  by  the  constant  afflux  of  gastric  juice  and  saliva; 
also  by  the  aspiration  of  air,  which  occurs  frequently  in  these  con- 
ditions. The  distention  causes  a drawing  apart  of  the  edges  of 
the  ulcer,  pain,  antiperistaltic  movements,  and  eventually  vomiting. 
Pylorospasm  is  a very  grave  accompaniment,  since  it  gives  rise  to 
gastric  hemorrhages  and  new  erosions  by  the  development  of  the 
conditions  just  described.  The  vomited  matter  generally  shows  a 
good  digestion  of  proteids  and  imperfect  digestion  of  carbohy- 
drates. 

Hematemesis. — This  is  probably  the  most  characteristic  sign  of 
ulcer.  It  only  occurs  in  about  half  the  cases.  Jaworski  and 
Korczynski  (loc.  cit.)  assert  that  the  acidity  is  very  much  increased 
immediately  before  and  after  the  hematemesis.  This,  of  course, 
would  explain  the  digestion  of  the  blood  and  the  conversion  of 
oxyhemoglobin  into  hematin  hydrochlorate.  The  amount  of  the 
vomited  blood  does  not  give  a correct  impression  of  the  degree  of 
the  hemorrhage,  because  considerable  quantities  of  the  blood 
escaping  into  the  stomach  reach  the  intestine  and  are  passed  out  in 
form  of  tarry  stools.  The  intestinal  evacuations  may  contain 
blood  several  days  after  the  hematemesis. 

The  production  of  gastric  hemorrhage  is  favored  by  bodily 
movement,  but  it  may  occur  during  rest,  even  during  sleep. 
When  very  small  quantities  of  blood  escape  into  the  stomach,  they 
mix  with  the  contents,  are  partially  digested,  and  eventually  come 
up  in  the  form  of  coffee-ground  material.  When  larger  vessels 
are  corroded  by  the  ulcer,  we  have  copious  hemorrhages  of  dark- 
red,  pure  blood.  A profuse  hemorrhage,  therefore,  as  a rule,  points 
to  a deep  ulcer.  Gastric  hemorrhages  are  accompanied  by  the 
systemic  phenomena  of  internal  hemorrhages  in  any  other  part  of 
the  body,  such  as  sinking  of  arterial  pressure,  marked  pallor, 
sensations  of  warmth  and  pain  in  the  stomach,  cardiac  oppression, 
nausea,  cold  sweat,  fainting,  and  collapse.  Death  has  been  known 
to  occur  in  the  state  of  collapse  before  any  blood  was  vomited,  the 
stomach  containing  at  the  autopsy  enormous  quantities  of  liquid 
and  coagulated  blood.  In  one  case  a solid  blood-clot  filled  the 
entire  stomach.  Bodily  exertions,  the  external  application  of  force 
of  any  kind  to  the  region  of  the  stomach,  and  straining  at  stool 


RELATION  OF  HYPERACIDITY  AND  PEPTIC  ULCER. 


50 


have  repeatedly  been  reported  as  the  direct  causes  of  gastric 
hemorrhage.  In  patients  with  persistent  pain  in  the  stomach, 
and  dark-colored  stools,  the  latter  should  be  examined  for  blood- 
coloring matters  by  testing  for  the  hemin  crystals.  Iron,  bismuth, 
tannic  acid,  tea,  claret,  and  huckleberries  may  produce  a black 
color  of  the  stools,  and  must  be  excluded  in  the  diagnosis. 

The  Relation  of  Hyperacidity  and  Peptic  Ulcer. — Hyperacidity  (as  an 
etiological  factor). — In  the  second  volume  of  Reynolds’  “System 
of  Medicine,”  page  930,  W.  Fox  expresses  the  opinion  that  the 
cause  of  chronicity  of  ulcer  may  be  “ an  excessive  acidity  or 
secretion  of  the  gastric  juice,  particularly  when  the  stomach  was 
empty.”  But  to  Riegel  belongs  the  credit  of  having  placed  this 
condition  of  hyperacidity  with  gastric  ulcer  upon  a scientific  basis. 
His  results  were  confirmed  by  von  den  Velden,  Jaworski,  Kor- 
cynski,  Ewald,  and  Boas. 

According  to  my  experience,  hyperacidity  is  present  in  90  per 
cent,  of  undoubted  gastric  ulcers.  Riegel  at  first  asserted  that  it 
was  a constant  accompaniment  (F.  Riegel,  “ Beitrage  zur  Diag- 
nostik  d.  Magenkrankheiten,”  “ Zeitschr.  f.  klin.  Med.,”  Bd.  xii, 
S.  434).  But  Gerhardt,  Rosenheim,  Ritter,  von  Mehring,  Cahn, 
and  Hirsch  published  cases  of  gastric  ulcer  with  normal  and  even 
subnormal  acidities. 

We  have  thoroughly  tested  the  method  of  analysis  of  Cahn  and 
v.  Mehring,  and  assured  ourselves  that  it  gives  values  that  are  too 
low  for  the  free  HC1,  which  may  explain,  in  part,  some  of  the  results 
and  discrepancies  of  Rosenheim  and  the  originators  of  the  method. 
We  do  not  deny  that  there  are  undoubted  cases  of  gastric  ulcer  in 
which  there  is  a subnormal  amount  of  HC1,  but  they  are  exceed- 
ingly rare.  (This  may  come  about  as  a result  of  exhaustion  of  the 
gland-cells  consequent  upon  continued  supersecretion.  See  p.  334.) 
Whenever  the  glandular  layer  is  intact,  it  is  reasonable  to  expect 
hyperacidity,  because  the  presence  of  an  ulcer  is  a never-ceasing 
irritation. 

Riegel  has  argued  that  the  hyperacidity  is  a primary  causative 
disturbance  and  the  ulcer  a secondary  result  of  this,  but  Ewald’s 
opinion  is  that  the  reverse  may  be  possible,  and  that  in  individuals 
with  great  irritability  of  the  secretory  nerves  an  injury  to  the 
mucosa  may  secondarily  bring  about  the  hyperacidity.  Although 
this  view  of  Ewald’s  is  plausible, — and  we  do  not  wish  to  deny  the 
possibility  of  the  hyperacidity  being  a secondary  result  in  excep- 
tional cases, — nevertheless  the  results  of  experiments  on  animals 


502 


ULCER  OF  THE  STOMACH. 


are  opposed  to  such  a conception.  Many  injuries  to  the  mucosa, 
hemorrhagic  erosions,  etc.,  lead  to  recovery  and  do  not  cause  peptic 
ulcer;  only  in  individual  cases  do  ulcerations  develop. 

In  experimental  injuries  that  were  produced  in  the  stomachs  of 
animals  by  Cohnhein  and  Matthes  it  was  found  that  prompt  heal- 
ing occurred;  but  the  healing  process  was  very  much  prolonged 
if  hyperacidity  was  artificially  caused  by  continued  addition  of  HC1 
to  the  contents  of  the  stomach.  On  the  other  hand,  hyperacidity 
was  never  caused  by  these  injuries  secondarily,  although  some  ot 
them  were  very  extensive. 

That  a mechanical  injury  to  the  stomach  can  not  of  itself  pro- 
duce hyperacidity,  and  thus  be  converted  into  a peptic  ulcer,  is 
proved  by  the  cases  where  human  beings  swallowed  such  things 
as  knives,  bits  of  glass,  nails,  etc.,  and  still  no  ulceration  was  found 
at  the  operation  or  autopsy. 

If  this  kind  of  trauma  in  a stomach  previously  healthy  can  not 
produce  peptic  ulcer,  one  must  naturally  assume  that  a special 
predisposition  must  previously  exist  if  such  an  ulcer  shall  develop. 
It  can  hardly  be  accepted  that  this  kind  of  a disposition  should 
develop  at  the  moment  an  injury  is  received.  I have  personally 
observed  the  continuance  of  the  hyperacidity  after  the  ulcer  was 
healed,  and  I agree  with  Riegel  in  the  opinion  that  the  hyperacidity 
is  the  primary  disturbance,  and  its  continuance  explains  the  frequent 
returns  of  peptic  ulcers  after  supposed  cures  had  been  effected. 

In  stomachs  that  show  hyperchlorhydria  the  normal  digestive 
stimulation  of  food  is  followed  by  an  excessive  production  of  HC1. 
If  an  individual  afflicted  in  this  manner  receives  an  injury  to  the 
gastric  mucosa  leading  to  an  erosion,  this  will  not  heal  as  it 
would  in  a healthy  person,  for  the  hyperchlorhydria  that  occurs 
every  time  food  is  taken  into  the  stomach  will  prevent  the 
healing  ; more  than  that,  it  will  in  itself  be  a factor  for  further 
destruction  in  the  injured  area.  Nauwerck  and  D.  Gerhardt  have 
recently  demonstrated  the  transition  of  hemorrhagic  erosions  into 
ulcerations.  Any  necrosis  in  the  mucosa  may  lead  to  an  ulcer.  A 
slight  hemorrhagic  infiltration  may  be  the  first  step  in  the  process, 
and  later  the  infiltrated  area  becomes  necrosed.  Then  the  necrotic 
tissue  is  dissolved  under  the  influence  of  the  hyperchlorhydria. 
Two  factors,  then,  are  essential — hemorrhagic  infiltration  and  a very 
active  hyperacid  gastric  juice. 

Nauwerck  has  pointed  out  that  erosions  may  also  be  a secondary 
result  caused  by  mycotic  and  bacterial  necroses  of  the'mucosa. 


RELATION  OF  HYPERACIDITY  AND  PEPTIC  ULCER.  503 

Inasmuch  as  the  ulcer  is  not  the  cause  of  the  hyperacidity,  but 
rather  the  result,  one  can  not  be  surprised  to  find  occasionally  that 
ulcer  cases  are  not  accompanied  by  hyperacidity.  These  are  the 
exceptions.  As  a rule,  it  can  be  stated  that  gastric  ulcer  is  asso- 
ciated with  hyperacidity. 

The  state  of  the  bowels  is  mostly  that  of  persistent  constipation; 
sometimes  the  evacuations  are  normal ; this  is  generally  the  case 
when  much  water  has  been  ingested  to  quench  the  intense  thirst. 
The  small  quantity  of  the  evacuations  is  explained  by  the  fact  that 
very  little  food  is  ingested,  and  this  is  so  thoroughly  dissolved  in 
its  proteid  constituents  by  the  very  active  gastric  juice  that  little 
work  remains  for  the  intestine.  Often  the  pylorospasm,  the 
cicatricial  contraction  of  the  pylorus,  and  the  frequent  vomiting 
are  agents  in  producing  constipation,  because  they  prevent  the 
transit  of  the  food  into  the  duodenum.  Colitis  and  membranous 
dysentery  may  coexist  with  gastric  ulcer  in  rare  instances. 

The  urine  is  very  much  diminished  in  quantity,  and  is  frequently 
highly  acid  when  no  emesis  has  occurred ; but  when  there  has 
been  much  vomiting,  or  when  the  stomach  has  been  washed  out 
frequently,  the  urine  may  become  alkaline.  Maly  and  Quincke 
have  observed  that  the  excretion  of  the  alkaline  constituents  of  the 
blood  goes  hand-in-hand  with  the  increased  acid  secretion  of  the 
stomach ; at  the  same  time  the  total  chlorids  of  the  urine  are  very 
much  reduced.  The  results  of  Charles  E.  Simon  (loc.  cit.)  indicate 
that  exact  analyses  of  the  urine  respecting  its  alkalinity,  the  sub- 
normal amount  of  chlorids,  and  the  excess  of  indican,  etc.,  may 
eventually  instruct  us  concerning  the  secretory  processes  in  the 
stomach,  where  it  is  impossible  to  obtain  the  gastric  contents  for 
examination.  (For  detailed  information  see  chapter  on  The  Urine 
in  Gastric  Diseases.) 

The  development  of  tumor  or  palpable  swelling  is  a very  rare 
occurrence  in  gastric  ulcer  cases.  Very  old  ulcers  may  show  con- 
siderable thickenings  at  the  edges,  which  at  times  become  palpa- 
ble. Gerhardt  has  described  the  following  varieties  of  palpable 
gastric  ulcer  indurations  or  tumors  : (i)  The  ulcer  itself,  with  its 

hard  base  and  indurated  edges,  is  palpable.  This  can  only  be  felt 
if  it  is  located  in  that  small  area  of  the  anterior  gastric  wall  that 
can  be  palpated.  Gerhardt  stated  that  in  some  cases  the  induration 
could  be  felt  through  the  left  lobe  of  the  liver.  I have  never  observed 
a case  of  indurated  peptic  ulcer,  either  clinically  or  at  autopsy,  at 
which  such  palpation  was  possible.  The  existence  of  gastric  tumor, 


504 


ULCER  OF  THE  STOMACH. 


as  a rule,  speaks  against  ulcer  and  for  carcinoma;  but  in  painful 
gastric  affections  of  over  two  years’  standing  the  existence  of  a 
small  narrow  tumor  speaks  for  ulcer.  (2)  In  cases  of  hyperacidity 
and  gastralgia  a functional  hypertrophy  of  the  pyloric  musculature 
may  develop  and  become  palpable ; this  occurs  most  frequently 
when  the  ulcer  is  located  at  the  pylorus.  This  type  is  only  palpa- 
ble if  the  stomach  is  dilated  or  prolapsed.  If  the  pylorus  is  in  its 
normal  position,  it  can  not,  in  my  experience,  be  palpated.  (3) 
After  a gastric  ulcer  has  perforated,  a tumor  mass  may  develop  on 
the  outside  of  the  stomach  by  an  exudate,  or  an  encapsulated 
abscess  may  form.  In  these  extremely  rare  cases  a rapidly  devel- 
oping tumor  mass  develops  after  a long-standing  gastric  disease, 
and  is  very  likely  to  be  mistaken  for  a carcinoma.  (4)  Old  large 
peptic  ulcers  frequently  envelop  neighboring  organs  with  their 
broadened  bases.  It  is  claimed  that  pancreas,  spleen,  and  left 
lobe  of  the  liver  may  project  into  the  ulcer,  the  projecting  part 
becoming  chronically  inflamed,  hard  to  palpation,  quite  massive, 
and  even  capable  of  growth.  The  demonstration  of  excess  of  HC1 
in  the  stomach  contents  will  prevent  the  diagnosis  of  cancer  in 
these  cases. 

In  sixteen  cases  of  tumor  in  connection  with  gastric  ulcer,  re- 
ported by  Reinhard,  six  were,  at  autopsy,  found  to  be  due  to  cica- 
tricial stenosis  of  the  pylorus,  six  to  adhesions  of  the  stomach  with 
adjacent  organs,^one  to  an  encapsulated  abscess,  and  three  to  for- 
eign bodies  (hair,  vegetable  debris,  lime,  etc.). 

Diagnostic  Pain  Points. — Of  these,  there  are  two  that  are  of  im- 
portance : ( a ) the  epigastric ; ( b ) the  dorsal.  The  epigastric  pain 
point  is  in  the  median  line,  or  slightly  to  the  left,  very  rarely  to 
the  right  of  it.  It  can  not  be  correctly  called  a point,  because  the 
pain  is  more  or  less  diffuse,  at  times  spreading  over  an  area  as  large 
as  the  palm  of  the  hand.  The  exact  limitation  of  the  epigastric 
painful  area  varies  with  the  location  of  the  stomach.  In  most 
cases  it  is  close  to  the  xyphoid  cartilage,  but  it  may  be  several 
centimeters  below  that  in  cases  of  descent  of  the  stomach, 
gastroptosis,  dilatation,  etc.  The  pain  area  described  by  Head 
(“  Brain,”  1896)  as  a reflected  pain  in  gastric  disease  is  localized  by 
him  as  a small  triangular  spot  in  the  left  epigastrium.  The  pain 
in  Head’s  epigastric  triangle  is  elicited  on  the  slightest  touch,  and 
is  not  discovered  if  pressure  is  used,  such  as  is  necessary  to  localize 
the  pain  spots  of  ulcer. 

The  epigastric  pain,  which  is  very  sharply  circumscribed  and 


CLINICAL  FORMS  OF  GASTRIC  ULCER. 


505 


intense,  may  be  associated  with  a sensation  of  throbbing  and 
pulsation.  The  dorsal  pain  region,  which  was  first  described  by 
Cruveilhier,  is  also  sharply  circumscribed.  It  was  found  in  about 
one-third  of  our  cases  at  a level  with  the  tenth  to  the  twelfth 
thoracic  vertebra.  Its  lateral  extent  amounts  to  from  two  to  three 
cm.  and  its  vertical  extent  from  two  to  five  cm.  In  very  rare  in- 
stances there  is  a painful  zone  corresponding  to  the  fourth  or  fifth 
thoracic  vertebra.  Usually,  the  dorsal  pain  point  is  only  present 
on  the  left  side,  and  Boas  mentions  a case  in  which  the  dorsal  pain 
was  present  and  no  epigastric  pain  complained  of.  The  only 
gastric  sensation  this  patient  had  was  a feeling  of  pressure  after 
the  ingestion  of  food.  There  was  no  vomiting  and  no  blood  in  the 
stools.  Pressure  on  the  epigastric  region  did  not  cause  pain,  but 
there  was  an  intensely  painful  spot  at  the  level  of  the  twelfth  dorsal 
vertebra.  The  patient  later  on  suffered  from  severe  hematemesis. 
The  localization  of  pain  is,  in  our  experience,  only  exceptionally 
of  diagnostic  aid.  The  so-called  pain  points  are  frequently  absent, 
or,  if  present,  they  are  not  in  the  places  designated  by  Boas. 
Neurasthenic  patients  often  have  pain  points  in  these  locations 
without  any  other  evidence  of  ulcer. 

Clinical  Forms  of  Gastric  Ulcer. — 1.  Hemorrhagic  Form. — 
This  type  may  be  acute  or  chronic.  In  the  acute  type  there  are, 
as  a rule,  no  well-marked  symptoms  of  gastric  ulcer,  which  runs  a 
latent  course,  until  suddenly  a severe  gastric  hemorrhage  makes  the 
diagnosis  clear.  The  patient  may  die  as  a result  of  a profuse  loss 
of  blood.  If  the  hemorrhage  does  not  result  in  death,  an  intense 
anemia  remains.  In  the  chronic  type  the  loss  of  blood  is  not  so 
considerable,  but  the  hemorrhages  occur  more  frequently.  I have 
personally  observed  a case  in  which  twelve  hemorrhages  occurred 
in  one  year,  and  the  stool  contained  blood  at  all  times  during  that 
year.  Such  cases  become  extremely  cachectic,  and  pernicious 
anemia  has  been  known  to  result. 

2.  The  Gastralgic  Form . — This  type  is  frequently  confounded 
with  purely  nervous  gastralgia  and  the  attacks  of  pain  occurring 
in  cholelithiasis. 

3.  Acute  Perforating  Type. — The  ulcerative  process  runs  a latent 
course,  showing  only  slight  dyspeptic  symptoms.  The  acute  per- 
foration in  most  cases  occurs  suddenly  and  generally  ends  fatally. 

4.  Chronic  Dyspeptic  Form. — This  type  gives  the  impression  of 
chronic  gastritis  or  nervous  dyspepsia ; symptoms  of  gastric  ulcer 
are  wanting.  The  epigastric  region  may  be  sensitive  to  pressure, 


5°6 


ULCER  OF  THE  STOMACH. 


and  there  may  be  vomiting  and  pain  occurring  occasionally  after 
eating,  but  they  are  not  the  characteristic  sharp  pains  peculiar  to 
typical  ulcer;  they  partake  more  of  the  discomfort  shown  in 
other  chronic  diseases  of  the  stomach.  If  such  cases  show  ex- 
cess of  HC1  in  the  gastric  contents,  and  no  abundance  of  mucus, 
the  diagnosis  will  most  probably  be  ulcer. 

5.  The  Cachectic  Form. — These  very  emaciated  and  cachectic 
patients  frequently  give  the  impression  of  being  afflicted  with  a 
cancer.  The  condition  is  most  frequently  seen  in  advanced  stages 
of  long-existing  ulcers,  in  dilatations  caused  by  cicatrices,  or  in 
chronic  cases  of  hypersecretion.  Attacks  of  pain  and  vomiting  are 
still  present,  but  the  general  appearance  is  that  of  cachexia  and 
even  marasmus. 

6.  Vomitive  Form. — Here  the  emesis  is  the  most  annoying  symp- 
tom, which  is  so  persistent  that  the  sufferers  rapidly  assume  an 
advanced  stage  of  emaciation.  These  types  of  gastric  ulcers  are 
sufficient  to  demonstrate  how  variable  the  clinical  picture  may  be. 

The  Duration. — It  is  impossible  to  determine  how  long  a 
gastric  ulcer  has  existed,  and  it  is  difficult  to  determine  when  a 
complete  cure  has  been  effected.  Even  the  cessation  of  pain  is 
no  proof  of  perfect  healing.  Large  gastric  ulcers,  with  extensive 
lateral  and  vertical  destruction,  probably  never  heal  perfectly.  As 
a rule,  the  disease  runs  a chronic  course.  There  are  cases  that 


DESCRIPTION  OF  PLATE  VIII.— ULCUS  CARCINOMATOSUM  OF  THE 
PYLORUS. 

Fig.  1. — A Section  Through  the  Wall  of  the  Stomach,  Showing  the  Edge 
and  a Portion  of  the  Base  of  the  Ulcer. 

Objective,  two-thirds ; eyepiece,  two  inches.  Stained  with  hematoxylin  and  eosin. 
The  drawing  is  built  up  from  a series  of  microscopic  fields.  X about  15  dia- 
meters. 

d.  Mucous  membrane,  m.  Muscularis  mucosae,  s.  Submucosa,  a.  Base  of  the 
ulcer,  mm.  Muscle-coat  of  stomach,  me.  Groups  of  cancer  cells  between  the  bundles 
of  muscle-fibers,  dc.  Groups  of  cancer  cells  in  the  edge  of  the  ulcer  in  the  mucous 
membrane.  sc.  Groups  of  cancer  cells  in  the  submucosae.  a.  Necrotic  membrane 
lining  the  base  of  the  ulcer. 

Fig.  2. — A Small  Nodule  from  the  Serous  Coat  of  the  Stomach  Over  the 
Base  of  the  Ulcer. 

Objective,  two-thirds ; eyepiece,  two  inches.  Stained  with  hematoxylin  and  eosin. 
X about  15  diameters. 

This  figure  gives  a good  idea  of  one  of  the  nodules  in  the  serosa.  It  is  composed 
entirely  of  a collection  of  groups  and  masses  of  cancer  cells,  so  closely  packed 
that  the  outlines  of  the  individual  cells  can  not  be  made  out.  Except  for  these  nodular 
thickenings,  the  serosa  was  not  altered,  pc.  Cancer  masses  in  peritoneal  coat. 


PLATK  VIII. 


DIAGNOSIS. 


507 


run  an  acute  course  and  become  perfectly  healed  within  a period 
of  from  four  to  six  weeks.  The  long  duration  of  the  majority  of 
cases  is  largely  explained  by  the  irritating  character  of  the  food 
and  by  the  late  recognition  of  the  character  of  the  trouble.  Com- 
plications may  greatly  prolong  the  disease. 

The  course  is  a very  variable  one,  and  a complete  cure  should 
not  be  spoken  of  until  the  patient  has  been  perfectly  free  from  all 
gastric  distress  for  six  months.  In  some  cases  the  symptoms  may 
disappear  very  rapidly  under  strict  diet  and  appropriate  treatment. 
After  a few  weeks,  months,  or  years  the  same  symptoms  return. 

The  question  now  arises  whether  this  has  been  caused  by  a new 
ulcer  or  whether  the  old  ulcer  has  not  yet  healed.  It  is  almost 
impossible  to  decide  this  point,  though  it  is  probable  that  the  old 
ulcer  has  not  yet  been  perfectly  cured.  This  is  particularly  the 
case  if  the  distress  has  only  been  relieved  as  long  as  the  patient 
strictly  keeps  to  a careful  diet.  If  the  pains  recur  whenever  an 
ordinary  diet  is  taken,  the  case  is  not  cured.  The  hyperacidity 
may  continue  after  the  ulcer  has  been  cured,  but  need  not  neces- 
sarily cause  a relapse. 

Diagnosis. — If  the  symptoms  of  pain  in  the  stomach,  gastric 
hemorrhages,  and  hyperchlorhydria  are  present  simultaneously, 
the  diagnosis  is  assured  ; but  in  the  majority  of  cases  pain  is  the 
only  symptom.  If  the  pain  occurs  only  at  the  height  of  digestion 
and  at  a circumscribed  area  in  the  epigastrium,  and  if  the  dorsal  pain 
point  is  present,  gastric  ulcer  should  be  suspected.  Hyperchlor- 
hydria, in  connection  with  continued  pain,  should  also  suggest 
ulcer.  The  pain  or  cardialgia  of  hyperchlorhydria  is  sometimes 
indistinguishable  from  that  of  gastric  ulcer.  Both  kinds  of  pain 
are  caused  by  the  digestive  irritation  of  the  food.  Both  cease  when 
the  ingesta  have  left  the  stomach.  The  only  important  point  of 
difference  between  these  two  pains  is  their  regularity  with  ulcer 
and  their  irregularity  in  hyperchlorhydria.  In  the  latter  there 
may  be  days  in  which  the  patients  are  entirely  free  from  pain.  In 
doubtful  cases  it  is  always  safe,  according  to  Leube’s  plan,  to  insti- 
tute treatment  for  ulcer. 

Wherever  a chronic  morbid  process  can  be  determined  upon 
with  accuracy  and  the  characteristic  pain  points  are  present  at 
the  same  time,  the  diagnosis,  according  to  Boas,  should  be  cer- 
tain ( loc . cit.y  p.  41).  He  attributes  less  importance  to  analysis 
of  the  gastric  contents.  There  are,  however,  atypical  forms  which 
present  some  difficulty  in  diagnosis.  Thus  there  are  cases  rarely 


508 


ULCER  OF  THE  STOMACH. 


observed  in  which  the  patients  never  complain  of  pain,  nor  has  the 
food  any  distressing  effect  upon  the  stomach.  In  other  cases, 
although  pain  is  present,  it  is  not  aggravated  by  taking  food.  In 
some  well-diagnosticated  cases  food  of  all  kinds  was  well  borne. 
In  all  of  these  well-authenticated  forms  the  diagnosis  was  assured 
by  characteristic  unmistakable  symptoms,  such  as  hematemesis 
and  bloody  stools,  coming  on  afterward.  Concerning  hematemesis, 
it  should  be  said  that  the  differentiation  of  pulmonary  from  gastric 
hemorrhage  may  become  necessary.  This  may  be  facilitated  by 
a study  of  the  subjoined  scheme: 


HEMORRHAGES  FROM  THE 
Lung.  Stomach. 


1.  Blood  is  bright  red,  foamy. 

2.  Physical  signs  point  to  a pulmonary  or 
cardiac  affection — the  stomach  may  be 
affected  secondarily. 

3.  Pulmonary  hemorrhages  followed  by 
rusty-colored  sputa  for  days  (gener- 
ally), but  there  is  no  blood  in  the  stools. 

4.  Physical  signs  of  pulmonary  or  cardiac 
disease — moist  rales. 


1.  Blood  is  dark  brown,  partly  coagulated, 
frequently  mixed  with  food,  sometimes 
acid. 

2.  Physical  examination  evinces  a gastric 
or  hepatic  affection,  or  stasis  in  portal 
circulation. 

3.  Gastric  hemorrhages  are  frequently  as- 
sociated with  tar-colored  stools. 

4.  Physical  examination  of  heart  and  lungs 
usually  negative. 


The  diagnosis  becomes  complete  if  the  characteristic  pain  points 
are  present,  with  prompt  aggravation  of  pain  soon  after  taking  food, 
vomiting  showing  hyperacidity,  hematemesis,  and  a history  of 
chronic  trouble. 

The  blood  coming  from  the  stomach  does  not  necessarily  origi- 
nate from  an  ulcer.  One  may,  in  rare  instances,  be  called  upon  to 
exclude  carcinoma,  portal  vein  stasis  producing  passive  conges- 
tion, gastric  varicosities,  toxic  corrosions,  traumatisms,  scurvy,  acute 
yellow  atrophy  of  the  liver,  and  yellow  fever.  The  hemorrhages  of 
carcinoma  are  small  in  quantity  compared  to  those  of  ulcer,  and  in 
cancer  the  blood  is  more  frequently  decomposed  and  of  a coffee-  or 
chocolate-brown  color,  and  there  are  rarely  any  bloody  stools. 
Charcot  has  reported  hematemesis  in  hysteria  (crises  gastriques), 
but  Debove  suggests  (Joe.  cit.)  that  organic  and  functional  nervous 
diseases  may  be  coincident  with  ulcer.  In  sudden  gastric  hemor- 
rhages the  previous  history  will,  as  a rule,  enable  one  to  distinguish 
between  the  above-mentioned  possibilities.  In  hemorrhage  from 
passive  congestion  due  to  stasis  of  the  portal  vein  the  epigastric 
pain  is  very  slight  or  entirely  absent. 


CHOLELITHIASIS. 


509 


Affections  of  the  transverse  colon, — some  forms  of  colitis  (mem- 
branous and  simple  catarrhal  types), — as  well  as  severe  colic, 
coprostasis,  and  prolapse  of  the  colon,  may  closely  mimic  the 
clinical  picture  of  gastric  ulcer.  The  pain  area  of  the  transverse 
colon  can  not,  in  my  experience,  be  definitely  separated  from  that 
of  the  stomach  by  palpation.  In  this  connection  I would  empha- 
size that  pains  of  the  colon  cease  and  frequently  disappear  entirely 
after  this  part  of  the  intestines  is  thoroughly  evacuated.  In  the 
greater  proportion  of  these  diseases  of  the  colon  the  amount  of 
free  HC1  in  the  stomach  is  markedly  reduced,  or  occasionally  may 
be  absent  entirely.  In  ulcer  there  is  hyperacidity,  as  a rule. 
Careful  inspection  and  examination  of  the  stool  is  necessary  in 
both  diseases,  and  will  often  instruct  us  regarding  the  condition  of 
the  colon. 

Whether  colitis  may  lead  up  to  functional  disturbances  of  the 
stomach,  as  Fleiner  asserts,  is  still  uncertain. 

Cholelithiasis  may  be  confounded  with  ulcer  when  there  has  been 
no  blood  in  the  vomit  or  stools,  nor  any  grit,  sand,  or  stones  in  the 
evacuations.  The  following  signs  and  symptoms  are  then  of  value  : 
The  pain  in  hepatic  colic  is  not  in  connection  with  the  taking  in  of 
food ; it  draws  from  the  median  line  to  the  right.  The  dorsal  pain 
point  of  ulcer,  if  present,  is  located  at  the  level  of  the  twelfth  tho- 
racic vertebra,  to  the  left  and  very  close  to  the  body  of  the  twelfth 
vertebra.  But  the  dorsal  pain  point  of  cholelithiasis,  if  present,  is 
located  to  the  right,  about  two  or  three  fingers’  breadths  from  the 
twelfth  dorsal  or  first  lumbar  vertebra.  In  ulcer  there  is  rarely  any 
pain  on  the  right  side;  even  if  there  is,  it  is  much  less  intense,  and 
in  cholelithiasis  there  is  rarely  any  pain  to  the  left  of  the  spinal 
column. 

In  cholelithiasis  the  right  lobe  of  the  liver  and  the  gall-bladder 
are  enlarged  after  an  attack;  and  during  the  intervals  between  the 
attacks  all  kinds  of  foods  can  be  eaten  with  impunity.  In  chole- 
lithiasis the  amount  of  HC1  in  the  gastric  contents  is  normal  or  sub- 
normal, or  the  contents  may  not  show  any  free  HC1;  in  ulcer  there 
is  hyperacidity.  Icterus,  when  repeatedly  observed,  following  attacks 
of  pain,  strengthens  the  diagnosis  of  cholelithiasis,  but  it  must  be 
emphasized  that  with  duodenal  ulcer  icterus  is  occasionally  observed. 
In  private  practice  I have  observed  two  cases  in  which  chole- 
lithiasis and  gastric  ulcer  occurred  contemporaneously. 

Diagnosis  of  the  Complications  and  Consequences  of  Gastric  Ulcer. — 
These  are:  (1)  The  perforation  peritonitis;  (2)  cicatricial  stenosis 


5io 


ULCER  OF  THE  STOMACH. 


of  the  pylorus;  (3)  the  transition  of  ulcer  into  carcinoma,  or  ulcus 
carcinomatosum ; (4)  hour-glass  stomach  from  cicatricial  contrac- 
tions ; (5)  subphrenic  abscess ; (6)  progressive  pernicious  anemia. 

The  diagnostic  signs  of  perforative  peritonitis  are : (a)  great 
rigidity  of  the  abdominal  muscles,  flat  abdomen  ; ( b ) disappearance 
or  diminution  of  liver  dullness;  this  sign  may  be  absent,  however, 
if  only  liquid  gastric  contents  and  no  air  escape  into  the  peri- 
toneum ; ( c ) vomiting.*  According  to  Rosenheim  (“  Zeitschr.  f. 
klin.  Med.,”  Bd.  xvu,  S.  116),  about  five  to  six  per  cent,  of  gastric 
ulcers  develop  carcinomata  at  their  margins,  and  these  carcinomata 
are  said  to  be  associated  with  a pronounced  hyperacidity. 

The  so-called  hour-glass  stomach  may  be  produced  by  one  or 
more  cicatrices  in  the  neighborhood  of  the  antrum  pylori. 
Cicatrices  of  the  duodenum  may  cause  a dilatation  beyond 
the  pylorus,  by  which  the  latter  will  itself  constitute  the 
narrowing  or  isthmus  of  what  very  much  resembles  an  hour- 
glass stomach  (Reiche,  “Jahrb.  d.  Hamburger  Staatskrankenan- 
stalt,”  1890,  p.  180). 

Subphrenic  Abscess  (Pyopneumothorax  subphrenicus). — In  1880, 
Leyden  first  described  a combination  ol  diseases  which  followed 
perforative  peritonitis  or  escape  of  pus  from  the  intestines  into  the 
peritoneum.  A purulent  exudate  forms  in  the  lower  parts  of  the 
right  or  left  thoracic  cavity  under  symptoms  of  inflammation,  but 
no  coughing  or  expectoration  is  connected  therewith.  The  poste- 
rior and  lower  thoracic  regions  give  dullness  on  percussion,  absence 
of  vesicular  murmur,  and  fremitus.  Metallic  sounds  can  be  made 
out  when  one  percusses  and  auscults  simultaneously.  The  succus- 
sion  sound  is  distinct.  The  lung  is  distinctly  intact  above  these 
parts.  The  respiratory  murmur  is  vesicular  and  the  fremitus  is 
maintained  down  to  the  fourth  or  fifth  rib  ; from  here  on,  the  respira- 
tory murmur  suddenly  ceases.  The  dullness  that  corresponds  to 
the  exudate  changes  with  various  positions  of  the  body.  The  signs 
of  equally  distributed  pressure  in  the  pleura  are  wanting.  The 
movements  of  the  corresponding  half  of  the  thorax  are  not  coordi- 


*The  diagnosis  of  perforation  has  been  attempted,  when  other  signs  failed,  by  punc- 
turing through  the  abdominal  walls  with  a sterilized  hypodermic  needle,  when  the 
gaseous,  bacterial,  and  cellular  evidences  of  perforation  can  at  times  be  aspirated.  (Test 
for  H2S  by  lead-acetate  paper ; when  the  abdomen  is  very  tympanitic,  this  sign  is  almost 
pathognomonic.)  The  puncture  is  made  when  the  patient  is  in  the  dorsal  position.  The 
escaped  gases  will  rise  upward  between  the  intestines  and  the  peritoneal  wall.  There  is 
danger  of  puncturing  the  intestines  in  this  method. 


TREATMENT  OF  GASTRIC  ULCER. 


5 


nated,  the  intercostal  spaces  are  almost  obliterated,  and  the  heart  is 
slightly  pushed  to  the  other  side. 

If  the  exudate  is  on  the  right  side,  the  liver  projects  far  into  the 
abdomen,  and  can  be  felt  at  or  below  the  umbilicus.  The  exudate 
may  perforate  into  the  respiratory  passages  and  cause  sudden  and 
abundant  expectoration  of  foamy  pus  containing  hepatic  cells.  In 
1894  Maydl  collected  179  cases  of  subphrenic  accumulations  of  pus. 
In  twenty  per  cent,  of  these  cases  perforating  ulcers  of  the  stomach 
or  duodenum  were  found  to  be  the  causes.  (“  Subphrenic  Abscess,” 
Meltzer,  in  the  “ New  York  Med.  Jour.,”  June  24,  1893.)  Progres- 
sive pernicious  anemia  as  a concomitant  phenomenon  of  ulcer  can  be 
recognized  by  the  reduction  of  the  number  of  red  corpuscles  with 
relative  increase  of  percentage  of  hemoglobin  and  the  appearance 
of  the  poikilocytes,  gigantoblasts,  microcytes,  and  macrocytes.  (See 
chapter  on  The  Blood  in  Gastric  Diseases,  p.  400  et  seq.) 

Senator  suggests  that  a left-sided  pleurisy  immediately  or 
remotely  following  gastric  ulcer  should  suggest  the  possibility  of 
a subphrenic  abscess.  The  following  are  further  suggestive  points 
in  these  cases  : First,  violent  pains  in  the  epigastrium,  or  in  one  or 
other  hypochondrium.  Second,  pain  and  stiffness  in  the  back  dur- 
ing efforts  to  sit  up.  Third,  painful  eructation,  sobbing  and  singultus. 
Fourth,  reclining  posture  of  the  patient  on  his  back,  because,  as  a 
rule,  with  extensive  pleuritic  extravasations  the  patient  maintains  a 
position  on  the  diseased  side.  Fifth,  edema  of  the  lower  lateral 
and  posterior  thoracic  walls,  at  times  extending  to  the  loins. 

In  the  presence  of  extensive  pleurisy  or  empyema,  the  coexist- 
ence of  these  five  conditions  would  justify  the  supposition  of  a 
subphrenic  abscess. 

The  general  subcutaneous  emphysema  as  a complication  of  perfor- 
ation of  gastric  ulcer  is  a very  rare  occurrence,  to  which  Demarquay 
first  called  attention. 

Treatment  of  Gastric  Ulcer. — Prophylactic. — If  gastralgias  are 
frequent  in  a person  afflicted  with  hyperacidity,  the  diet  must  be 
very  mild  and  unirritating;  two  weeks  of  a milk  diet  will  be  the 
safest.  Sudden  deviations  in  the  temperature  of  the  food  must  be 
avoided,  daily  evacuations  must  be  effected  by  suitable  diet,  and,  if 
need  be,  Carlsbad  salts,  and  the  hyperacidity  remedied.  The 
dietetic  and  medicinal  treatment  will  vary  according  to  the  presence 
or  absence  of  hematemesis. 

Treatment  of  Hematemesis  and  the  Period  Immediately  Follozving 
It. — During  the  stages  of  blood  vomiting  the  patient  must  remain 


512 


ULCER  OF  THE  STOMACH. 


absolutely  quiet  in  bed  and  not  even  arise  for  urination  or  defeca- 
tion. Positively  nothing  should  be  permitted  by  the  mouth,  not 
even  ice.  If  the  patient  is  well  nourished  no  alimentation  by  the 
rectum  is  advisable,  because  this  necessarily  disturbs  the  rest  and 
compels  the  stomach  to  move  because  of  the  changes  in  position 
required.  If  the  patient  is  weak  and  anemic,  a nourishing  enema 
may  be  imperatively  indicated  every  four  hours.  The  enema  most 
favored  is  that  of  Boas,  consisting  of  250  gm.  of  milk,  the  yolks 
of  two  eggs,  a teaspoonful  of  salt,  one  ounce  of  good  claret  (we 
favor  Beaune-Burgundy  for  this  purpose),  and  one  tablespoonful  of 
aleuronat  flour.  Previous  to  giving  an  enema  for  nutritive  pur- 
poses, the  rectum  and  colon  must  be  cleaned  by  a high  irrigation 
with  one  liter  of  warm  water.  The  above  ingredients  are  thor- 
oughly mixed  by  means  of  an  egg-beater,  warmed  to  about  990  F., 
and  permitted  to  run  in  under  gentle  pressure,  care  being  taken 
that  the  tube  is  introduced  as  far  up  into  the  sigmoid  flexure  as 
possible. 

When  the  hematemesis  is  copious  and  persistent,  a hypodermic 
injection  of  ergotal,  20  to  30  minims,  should  be  given  at  once. 
With  this  preparation  of  ergot  we  have  had  extensive  experimental 
and  clinical  experience  (see  “Med.  News”  for  Jan.  31,  Feb.  7, 
Mar.  7 and  14,  1891,  “An  Experimental  and  Clinical  Study  of 
Ergot,”  by  J.  C.  Hemmeter).  The  use  of  ergot  for  hematemesis 
has  the  indorsement  of  Riegel  (loc.  cit.),  Ewald,  and  Nothnagel.  At 
the  same  time  an  ice-bag  is  placed  over  the  epigastrium,  and  if  the 
pain  is  severe  an  injection  of  of  a grain  of  morphin  should  not 
be  delayed,  as  this  drug  acts  as  an  adjuvant  to  the  hemostatic  by 
the  ease  and  quiet  it  brings  about.  For  three  days  following 
hematemesis  this  treatment  should  not  be  changed,  and  no  food 
allowed  by  mouth.  The  treatment  from  the  fourth  to  the  seventh 
day  after  consists  of  absolute  rest  in  bed,  a wet  pack  covered  with 
oiled  silk  and  bandage  being  applied  to  the  epigastrium.  And 
now  one  may  resume  feeding  by  the  mouth,  but  in  form  of  liquids 
only, — half  milk,  half  lime-water ; or  milk  with  a small  addition 
of  coffee  or  tea,  never  more  than  lukewarm  ; also  beef-tea,  to  which 
nutrose,  meat-powder,  or  somatose  have  been  added,  and  egg- 
albumen  water.  Chocolate,  yolks  of  eggs,  and  all  alcoholic 
beverages  must  be  forbidden  in  this  stage. 

In  the  second  week  after  the  hemorrhage  a typical  cure  for  ulcer, 
according  to  principles  laid  down  by  Wilson  Fox  (“  Diseases  of  the 
Stomach,”  1872,  p.  146),  v.  Leube  (“  Ziemssen’s  Handbuch,”  Bd. 


TREATMENT  OF  GASTRIC  ULCER. 


513 


vii,  2,  p.  120),  and  v.  Ziemssen  (Volkmann’s  “ Sammlung  klin.  Vor- 
trage,”  No.  7 5),  should  be  instituted.  These  systematic  treatments 
are  in  the  main  rest-cures  combined  with  the  daily  use  of  a glass  of 
Carlsbad  Miihlbrunnen  water,  liquid  or  semiliquid  diet,  and  hot 
applications  to  the  epigastrium.  Every  morning  the  patient  takes 
a glass  of  (40°  R.)  warm  Miihlbrunnen  in  which  five  to  ten  gm.  of 
natural  or  artificial  Carlsbad  salts  have  been  dissolved.  Spongiopi- 
lin  cut  into  any  requisite  shape  and  dipped  into  hot  water  is  applied 
externally  to  the  epigastrium,  and  renewed  every  three  hours  night 
and  day.  The  diet  consists  mainly  of  milk  and  whipped  eggs  ; if  there 
is  great  weakness,  the  Boas  enema,  containing  perhaps  two  ounces 
of  claret,  should  be  given,  and  if  the  pulse  is  feeble,  hypodermic 
injections  of  digitalin  To  of  a grain,  and  strychnia  ^ of  a grain.  In 
one  case  of  profuse  hematemesis  we  gave  an  intravenous  injection 
of  500  c.c.  of  sterilized  normal  salt  solution.  The  pulse  had  left  the 
wrist,  and  was  barely  perceptible  at  the  carotid ; the  effect  was 
prompt,  and  the  opinion  of  the  assisting  colleagues  was  that  life 
was  saved  thereby, — the  case  recovering  later  on  under  the  nitrate 
of  silver  treatment. 

In  the  third  week,  when  the  pain  in  the  epigastrium  and  general 
cardialgia  have  ceased,  the  patient  may  be  permitted  to  rest  on  the 
sofa,  and  the  Carlsbad  water  is  continued.  We  might  remark  here 
that  the  Saratoga  Carlsbad  and  the  Hathorn  spring  waters  act  quite 
as  well  as  the  imported.  In  fact,  the  only  objects  of  the  Carlsbad 
water  in  the  cures  of  Leube  and  Ziemssen  are  the  neutralization  of 
the  hyperacidity  and  the  promotion  of  intestinal  evacuation.  One 
must  not  gain  the  impression  that  Carlsbad  waters  or  salts  have  any 
direct  or  specific  curative  effect.  Ewald  {loc.  cit .,  p.  275)  declares 
that  many  a patient  who  went  to  Carlsbad  might  have  recovered 
more  rapidly  if  he  had  taken  the  rest-cure  at  home.  To  neutralize 
the  hyperacidity  and  prevent  autodigestion  I usually  give  the  fol- 
lowing : 

R . Magnesias  ustae, 

Sodii  carbonatis, 

Potassii  carbonatis,  ....  aa  ...  . 5.0  3 j -f-  grs.  xv 

Sacchar.  lactis, 25.0  3 vj  T grs-  xx* 

SlG. — Half  a teaspoonful  dry  on  the  tongue  every  three  hours. 

In  the  third  week  one  may  permit  dipped  cakes,  toast,  or  zwie- 
back; broiled  sweetbread  or  calf’s  brain,  dumplings  made  of  finely 
divided  meat,  broiled  pike,  bluefish,  trout,  oysters,  in  very  small 
quantities.  In  the  fourth  week  purees  made  of  potatoes,  peas,  or 
34 


5 14 


ULCER  OF  THE  STOMACH. 


beans  rubbed  through  a sieve,  stewed  apples,  pears,  and  plums. 
Saratoga  Vichy  may  be  allowed;  all  vegetables  that  can  be  prepared 
in  puree  (gruel)  form,  such  as  spinach,  carrots,  peas,  etc.  For 
many  years  the  patient  must  avoid  raw  fruits,  all  sour,  acid,  or  spiced 
food  and  drink,  ice-cream,  and  all  cold  and  hot  beverages.  If  there 
has  been  no  hematemesis  the  treatment  had  best  be  carried  out  along 
these  lines  also.  On  page  241  detailed  diet-lists  for  cases  of  gastric 
ulcer  are  given.  In  rebellious  cases  of  recurrent  gastralgias, 
vomiting,  and  hyperacidity,  McCall  Anderson  (“Brit.  Med.  Jour.,” 
May  10,  1890)  and  H.  B.  Donkin  (“The  Lancet,”  Sept.  27,  1890) 
recommend  a total  abstinence  cure  of  two  to  three  weeks,  during 
which  the  patients  are  fed  exclusively  by  rectal  enemata  (three  to 
four  in  the  day);  hot  applications  to  the  epigastrium  are  also  used. 
After  ten  days  of  rectal  feeding  they  cautiously  and  slowly  return 
to  feeding  by  the  mouth  (milk,  bouillon,  egg-albumen).  We  have 
tried  this  in  a number  of  cases  in  which  relapses  had  occurred 
after  the  rest-cure,  and  can  speak  in  favor  of  the  method.  (See, 
also,  A.  P.  Gros,  “ Traitement  de  Malad.  de  l’estomac,  par  la  cure 
de  Repos  absolu,”  etc.,  Paris,  1898.)  Gerhardt  and  Boas  speak 
very  favorably  of  nitrate  of  silver  in  light  cases  of  gastric  ulcer.  The 
latter  begins  with:  3^.  Argenti  nitratis  0.25  to  120  of  peppermint 
water;  one  tablespoonful  three  times  a day  on  an  empty  stomach. 
Then  the  dose  is  increased  to  0.3  to  120  of  water,  of  which  two 
bottles  are  taken,  and  finally  0.4  to  120  of  water,  of  which  also  two 
bottles  are  advised.  This  is  combined  with  a sparing  diet  and  as 
much  rest  as  possible. 

Fleiner  and  Kussmaul  recommend  bismuth  subnitrate  in  all 
irritative  conditions  of  the  gastric  mucosa — old  ulcers,  erosions, 
excoriating  carcinomata.  Fleiner  employs  it  in  the  following 
manner:  10  to  20  gm.  (150  to  300  grs.)  of  bismuth  subnitrate  are 
stirred  in  200  c.c.  of  warm  water ; after  the  stomach  has  been 
thoroughly  cleansed  by  lavage,  this  suspension  is  poured  into  the 
stomach  and  allowed  to  remain  three  minutes;  then  the  clear 
water  is  siphoned  out,  the  bismuth  remaining  behind  and  forming 
a coating  to  the  injured  places  in  the  stomach.  It  is  a modified 
direct  or  local  treatment.  We  usually  employ  three  drams  of 
bismuth  subnitrate  and  one  dram  of  bismuth  subgallate  in  a pint 
of  warm  water,  having  previously  thoroughly  cleansed  the  stomach 
with  solutions  of  sodium  bicarbonate  (5ss  to  a pint),  the  state  of 
the  ulcer  permitting.  Recently  we  have  used  the  bismuth  salts  by 
insufflating  them  into  the  stomach  in  a dry  form  by  a powder  blower. 


SURGICAL  TREATMENT  OF  GASTRIC  ULCER. 


515 


In  chronic  cases  in  which  Fleiner’s  treatment  can  be  employed 
it  relieves  pain  promptly,  reduces  the  hyperacidity,  and  promotes 
healing;  it  is  worth  trying  in  cases  of  long  standing.  Direct  or 
local  treatment  of  this  kind  is  permissible  when  there  have  been  no 
hemorrhages  or  tarry  stools  for  one  month.  During  this  time  the 
ordinary  cures  by  diet,  rest,  Carlsbad  Miihlbrunnen,  etc.,  must 
have  been  employed.  There  must  be  no  sensitiveness  to  pressure 
on  the  epigastrium.  Chronic  ulcers  that  have  resisted  dietetic  and 
medicinal  treatment  have  been  successfully  treated  by  this  method 
by  Matthes  (loc.  cit.),  O.  Fischer  ( loc . cit.),  and  Stintzing  (Joe.  cit .). 
The  anemia  following  ulcer  may  require  iron,  arsenic,  strychnin. 
Iron  preparations  must  contain  no  acid. 

J.  Petruscky  has  reported  two  cases  of  primary  tubercular  ulcers  of 
the  stomach  which  were  apparently  cured  by  injections  of  tubercu- 
lin (“  Verhandlung  d.  XVII  Congress  f.  innere  Med.,”  1899,  S.  366). 

Surgical  treatment  becomes  necessary  when,  after  a trial  of  the 
aforesaid  methods,  the  ulcer  or  ulcers  prove  very  obstinate  and  not 
amenable  to  medical  treatment,  or  because  hemorrhages  may  be- 
come so  abundant  and  frequent  as  to  endanger  life,  or,  lastly, 
because  of  perforation.  Nelson  C.  Dobson  (“  Bristol  Medical  and 
Surg.  Jour.,”  1883)  first  advocated  surgical  interference  for  per- 
forating gastric  ulcer.  In  this  country,  Robert  F.  Weir,  of  New 
York,  has  contributed  the  most  important  work  to  this  domain  of 
surgery.  His  last  important  paper  (Robert  F.  Weir  and  E.  M. 
Foote,  “The  Surgical  Treatment  of  Round  Ulcer  of  the  Stomach 
and  Its  Sequelae,”  etc.,“  Medical  News,”  April  25  and  May  2,  1896) 
contains  an  account  of  78  cases  of  laparotomy  for  acute  perforation 
of  gastric  ulcer.  Keen  and  Tinker  have  added  statistics  of  78 
further  cases  (“  Phila.  Med.  Jour.,”  vol.  1,  p.  1106);  these  articles 
contain  also  the  indications,  prognosis,  etc.,  of  operations  for 
gastric  ulcer. 

Gastric  ulcers  have  been  excised  entirely,  the  sequelae  thereof 
have  been  removed  by  the  severing  of  peritonitic  adhesions,  and 
hour-glass  stomach  much  improved  by  gastro-anastomosis  (see  von 
Hacker,  “ Ueber  Magenoperationen  bei  Carcinom  u.  b.  narbigen 
Stenosen,”  published  by  Wilh.  Braumuller,  Wien  and  Leipzig,  1895). 

For  further  details  concerning  the  operations  on  the  stomach  for 
recent  ulcers  and  for  cicatrices,  we  refer  to  the  sections  on  Sur- 
gery of  the  Stomach. 

Treatment  of  Exhaustive  Gastric  Hemorrhage  by  Transfusion  and 
Intravenous  Injection  of  Normal  Salt  Solution. — Michel  transfused 


5 16 


ULCER  OF  THE  STOMACH. 


successfully  in  a case  of  extreme  anemia  following  gastrorrhagia 
(“  Berl.  klin.  Wochenschr.,”  1870,  No.  49).  In  a case  of  profuse  and 
repeated  hematemesis,  which  followed  washing  out  the  stomach, 
Michaelis  infused  into  the  veins  350  c.c.  of  solution  of  common  salt. 
Reaction  gradually  followed,  and  the  patient  recovered.  This  case, 
which  was  one  of  probable  ulcer,  illustrates  the  advantages  of  infus- 
ing a small  quantity  {ibid.,  June  23,  1884).  The  sudden  infusion  of 
quantities  of  liquid  exceeding  500  c.c.  will  cause  such  an  abrupt  rise 
in  arterial  pressure  that  the  injured  blood-vessels  in  the  gastric 
mucosa  may  reopen,  causing  renewed  profuse  hemorrhages.  The 
dangers  are  illustrated  by  a case  reported  by  von  Hacker,  who 
infused  1500  c.c.  of  salt  solution  into  a patient  in  a state  of  extreme 
collapse  resulting  from  hemorrhage  from  gastric  ulcer.  The  patient 
rallied,  but  he  died  three  hours  after  the  infusion  from  renewed 
hemorrhage  (“Wiener  med.  Wochenschr.,”  1883,  No.  37).  In 
Legroux’s  case  of  gastric  ulcer,  renewed  hemorrhage  and  death 
followed  the  transfusion  of  only  80  gm.  of  blood  (“Arch.  Gen. 
de  Med.,”  Nov.,  1880).  In  a case  quoted  by  Roussel,  Leroy 
transfused  130  gm.  of  blood  into  a girl  twenty  years  old,  who  lay 
at  the  point  of  death  from  repeated  hemorrhages  from  a gastric 
ulcer.  In  the  following  night  renewed  hemorrhage  and  death 
occurred  (“  Gaz.  des  Hop.,”  September  22,  1883).  According  to 
the  experiments  of  Schwartz  and  Ott,  the  transfusion,  or, 
rather,  infusion,  of  physiological  salt  solution  is  as  useful  as 
that  of  blood,  and  it  is  simpler  and  unattended  with  some  of 
the  dangers  of  blood  transfusion.  The  formula  is  chlorid  of 
sodium,  6 parts;  distilled  water,  1000.  Our  personal  experience 
is  confirmatory  of  the  observations  of  these  last-mentioned  ex- 
perimenters. 

Fleiner  ( loc . cit .)  favors  the  excision  of  simple  gastric  ulcer,  when 
external  (social)  conditions  render  a suitable  diet  and  treatment 
impossible.  We  can  not  advocate  this  heroic  treatment  for  simple, 
uncomplicated  ulcer,  feeling  convinced  that  the  various  treatments 
with  which  we  are  now  acquainted  are  eminently  successful.  But 
if  a laparotomy  has  been  undertaken  and  the  stomach  has  been 
opened  for  other  indications  (suspicion  of  peritonitis,  perigastritis, 
appendicitis,  carcinoma,  perforation),  and  an  uncomplicated  ulcer  is 
discovered,  the  excision  of  the  latter  is  undoubtedly  justifiable,  and 
has  been  successfully  carried  out  by  Cordua,  Kansche,  Maurer  (at 
Czerny’s  clinic),  and  Mintz  {loc.  cit.).  In  the  latter  case  the  gastric 
functions  were  entirely  recovered.  Extreme  and  persistent  gastric 


LITERATURE  ON  ULCER  OF  THE  STOMACH. 


517 

pain  has  been  the  indication  for  gastroenterostomy  in  a case  of 
Cahn’s  ( loc . cit.). 


LITERATURE 

ON  ULCER  OF  THE  STOMACH, 

In  addition  to  the  text-books  mentioned  in  the  literature  on  gastritis. 

1.  Abaytia,  W.,  “ Trataimento  de  la  ulcera  heptica  en  plena  actividad 
gastrica  mitigado  por  la  alimentacion  rectal,”  “ Rev.  de  med.  y cirug.  pract.,” 
Madrid,  1898,  xliii,  401,  489,  529. 

2.  Adamson,  R.  O.,  “ The  Symptoms  of  Perforated  Gastric  Ulcer,  with  Two 
Recent  Cases,”  “ Scot.  M.  and  S.  J.,”  Edinb.,  1898,  11,  317-326. 

3.  Affleck,  J.  O.,  “ Edinburgh  Hospital  Reports,”  1894,  vol.  11,  pp.  198-238. 

4.  Alexander,  W.  C.,  “A  Case  Illustrating  the  Difficulty  of  Diagnosis  in 
Gastric  Ulcer,”  “Brit.  M.  J.,”  1897,  1,  1345. 

5.  Allen,  J.  E.,  “ Hereditary  Influence  or  Family  Tendency  as  a Predis- 
posing Cause  of  Gastric  Ulcer,”  “Yale  M.  J.,”  New  Haven,  1897-98,  iv,  229- 
232. 

6.  Altmann,  J.  F.,  “ Ulcer  of  the  Stomach,”  “ Tr.  M.  Soc.  Tennessee,”  Nash- 
ville, 1898,  105-113. 

7.  Anderson,  “ British  Medical  Journal,”  May  10,  1890. 

8.  Anderson,  G.  R.,  “Note  on  a Case  of  Perforated  Gastric  Ulcer,”  “ Brit. 
M.  J.,”  Lond.,  1898,  1,  1448. 

9.  Ardouin,  “Ulcere  d’estomac,  Gastrotomie,”  “Soc.  Anat.,”  17  Dec.,  1897. 

10.  Assaky,  “Ulcer  stomacal,”  “ Spitalul  Bucuresci,”  1898,  xvm,  77-84. 

11.  Auffray,  “Contribution  a l’etude,  du  diagnostic  de  la  peritonite 
suraigne  dans  l’ulcere  perforede  l’estomac,’’  “ These  de  Paris,”  23  Juin,  1896. 

12.  Barling,  “ Birmingham  Medical  Review,”  August,  1895. 

13.  Beck,  C.,  “ Medical  Record,”  Feb.  15,  1896. 

14.  Begouin,  “Ulcere  latent  de  l’estomac  ; perforation;  mort,”  “ Journ.  de 
med.  de  Bordeaux,”  24  Jan v.,  1897. 

1 5.  Bellrose,  N.  W.,  “ Gastric  Ulcer,  Probably  Tubercular,  Report  of  a Case,” 
“ Colorado  M.  J.,”  Denver,  1897,  III,  169-174. 

16.  Benedict,  A.  L.,  “ Gastric  Ulcer,”  “ Med.  News,”  N.  Y.,  1898,  lxxiii, 
675-678. 

17.  Bensley,  C.  N.,  “A  Case  of  Chronic  Ulcer  of  the  Stomach,”  “Indian 
Lancet,”  Calcutta,  1897,  x,  171. 

18.  Berg,  A.  A.,  “The  Etiology  of  Gastric  Ulcer  and  an  Outline  of  Its 
Therapeutics,”  “ Med.  Record,”  July  30,  1898. 

19.  Bernardbeig,  “ De  l’Ulcere  de  l’Estomac,”  “Normandie  Med.,”  Rouen, 
1897,  XII. 

20.  Blackader,  A.  D.,  “Gastric  Catarrh  and  Gastric  Ulcer,”  “ Am.  Text- 
book Dis.  Child.”  (Stan.),  2d  ed.,  Phila.,  1898. 

21.  Bohland,  “ Ueber  die  Hernia  epigastrica  und  ihre  Folgezustande,” 
“ Berl.  klin.  Wochenschr.,”  1894,  No.  34. 

22.  Bondet,  “ Gastrorrhagie  par  Ulcere  de  l’Estomac,  Traitement,”  “ Province 
Med.,”  Lyon,  1898,  xn,  380-383. 

23.  Borchgrevink,  “ Ulcus  Ventriculi  Perforatum,  Laporotomie,”  “ Norsk. 
Magaz.  f.  Laegevidensk,”  1897,  Heft.  1. 


ULCER  OF  THE  STOMACH. 


24.  Bottcher,  A.,  “ Zur  Genese  des  perforirenden  Magengeschwiirs,” 
“ Dorpat.  med.  Zeitschr.,”  1874. 

25.  Bramwell,  B.,  “Clinical  Remarks  on  a Case  of  Acute  Perforative 
Peritonitis  Due  to  Ulceration  of  the  Stomach,”  “ Internat.  Clin.,”  Phila.,  1898, 
8 s.,  1,  1 16-122. 

26.  Brenner,  “Zur  Magensecretion  bei  Ulcus  ventriculi,”  “Wiener  klin. 
Wochenschr.,”  No.  48,  1897. 

27.  Brinton,  W.  {Joe.  cit.). 

28.  Broadbent,  W.,  “ Perforated  Gastric  Ulcer,”  “Brit.  M.  J.,”  Lond.,  1897, 
hi,  1254-1257. 

29.  Bugge,  “ Ulcer  of  the  Stomach  Causing  Death  by  Internal  Hemorrhage,” 
“ Forh.  med.  Selsk.  i.  Kristiania,”  1897,  203-205. 

30.  Bush,  J.  Paul,  “Cases  of  Perforative  Gastric  Ulcer  Treated  by  Opera- 
tion,” “Brit.  M.  Jour.,”  Nov.  5,  1898. 

31.  Cabot,  A.  T.,  “ A Case  of  Perforating  Gastric  Ulcer  ; Operation  at  End  of 
Twenty-four  Hours;  Recovery,”  “Boston  M.  and.  S.  Jour.,”  Aug.  11,  1898. 

32.  Cade,  “Ulcere  Perforant  de  l’Estomac  Chez  un  Enfant  de  Deux  Mois,” 
“ Soc.  des  Scienc.  med.  de  Lyon,”  Oct.  20,  1897. 

33.  Cahn,  “ Berlin,  klin.  Wochenschr.,”  1894,  No.  28. 

34.  Campbell,  J.,  “A  Case  of  Operation  for  Perforated  Gastric  Ulcer,” 
“ Brit.  med.  Journal,”  July  16,  1898. 

35.  Caro,  “ Ueber  Blutungen  aus  Oesophagusvaricceen,”  Diss.,  Wurzburg, 
Heidelberg,  1896. 

36.  Cathcart,  C.  W.,  “Ruptured  Gastric  Ulcer,”  “Tr.  Med.-Chir.  Soc.,” 
Edinb.,  1896-97,  n.  s.,  xvi,  195. 

37.  Caussade,  “Ulceration  Gastrique,  Hematemese  Foudroyante,  Mort,” 
“ Presse.  Med.,”  30  Janvier,  H.  9. 

38.  Chaput,  “ Traitement  des  Ulceres  Gastriques,”  “ Gaz.  de  Hop.  Par.,”  1898, 
lxxi,  67. 

39.  Chaput,  “ Ulcere  Gastrique  avec  Tumeur  Volumineuse,  Gastro-enteros- 
tomie,  Disparition  des  Accidents  et  Persistance  de  la  Tumeur,”  “ Soc.  Med. 
des  Hopitaux,”  31,  1,  1897. 

40.  Chauffard,  “Ulcere  Simple  de  l’Estomac  avec  Hemorrhagies  Abon- 
dantes,  Guerison  ; Mort  par  Coma  Diabetique,”  “Jour  de  Med.  et  Chir.  Prat.,” 
10  Mar.,  1898. 

41.  Choppin,  “ De  la  Perforation  dans  l’Ulcere  Latent  d’Estomac,”  “ These 
de  Paris,”  1896. 

42.  Claisse,  “ Ulcere  Rond  del’Estomac;  Perforation;  Peritonite  Suraigue, 
Mort,”  “Soc.  Anat.,”  Paris,  8 Janvier,  1897. 

43.  Clubbe,  C.  P.  B.,  “ Four  Cases  of  Operation  for  Perforated  Gastric 
Ulcer,”  “Austral.  Med.  Gaz.,”  June  20,  1898. 

44.  Connelly,  A.  W.,  “ Ulcer  of  the  Pyloric  Orifice,”  “ Intercolon.  M.  J. 
Austral.,”  Melbourne,  1898,  ill,  536-538. 

45.  Cramer,  “Ueber  die  Behandlung  des  Ulc.  ventr.  mit  gross'en  Wismuth- 
dosen,”  “ Miinchener  med.  Wochenschr.,”  1896,  No.  25. 

46.  Cruveilhier,  “ Anatomia  Pathologique,”  1829-1835,  Livraison  x. 

47.  Czygan,  “Zur  Behandlung  der  ulcusartigen  Magenerkrankungen,” 
“ Therap.  Monatsschr.,”  Berk,  1898,  xil,  494-496. 

48.  Debove  et  Remond,  “ Traite  des  Maladies  de  l’Estomac,”  Paris,  p.  255. 


LITERATURE  ON  ULCER  OF  THE  STOMACH.  519 

49.  Decker,  “Exp.  Beitrag  zur  Aetiologie  der  Magengeschwtire,”  “Berl. 
klin.  Wochenschr.,”  1887. 

50.  Diddens,  E.  J.,  “ Een  paar  complicatier  van  het  maagulcus  en  haar- 
chirurgische  behandeling,”  “ Nederl.  Tijetschr.  v.  Geneesk.,”  Amst.,  1898,  2 
R.  xxxiv,  d.  2,  441-453. 

51.  Dieulafoy,  “Ulcdres  Latents  de  l’Estomac,”  “ Presse  Med.,’’  25,  vii,  1897. 

52.  Dieulafoy,  “ Sur  l’Exulceratio  simplex  de  l’Estomac,”  “ Acad,  de  Med.,” 
18  Janv.,  1898. 

53.  Dieulafoy,  “ Hematemese  dans  l’Exulceration  simplex,”  “ Rev.  prat, 
d.  Trav.  de  Med.,”  Par.,  1898,  lx,  259. 

54.  Diriart  et  Apert,  “ Double  Ulcere  latent  de  l’Estomac,  double  perfora- 
tion, Laporotomie ; Mort,”  “ Soc.  Anat.,”  17,  1,  1896. 

55.  Dobson,  “ Bristol  Medical  and  Surgical  Journal,”  1893,  p.  196. 

56.  Duplay,  “Sur  la  Traitement  operatoire  de  l’Exulceration  simple  de 
l’Estomac,”  “ Bull.  Acad,  de  Med.,”  Par.,  1898,  3 s.,  xxxix,  90-92. 

57.  Ebstein,  Wilh.,  “ Experimented  Untersuchungen  iiber  das  Zustande- 
bekommen  von  Blutextravasaten  in  der  Magenschleimhaut,”  “Arch.  f.  exp. 
Pathologie  u.  Pharm.,”  11,  1878. 

58.  Ebstein,  Wilh.,  “ Ueber  die  Beziehungen  zwischen  Trauma  und  Magen- 
erkrankung,”  “ Deutsch.  Arch.  f.  klin.  Med.,”  Bd.  liv. 

59.  Einhorn,  Max,  “Medical  Record,”  June  23,  1894. 

60.  Elsasser,  “ Die  Magenerweichung  der  Sauglinge,”  Stuttgart  und 
Tubingen,  1846. 

61.  Etienne,  “ Ulcere  latent,”  “ Soc.  de  Med.  de  Nancy,”  11,  xi,  1896. 

62.  Ewald,  C.  A.  ( loc.cit .),  p.  234;  “ Diseases  of  the  Stomach,”  p.  233. 

63.  Ewald,  C.  A.,  “ Klinik  der  Verdauungskrankheiten,”  1.  Theil,  3.  Aufl., 
p.  122. 

64.  Fanoe,  “ Fall  von  Ulcus  perforans  ventriculi,  durch  Laparotomie  und 
Sutur  geheilt,”  “ Hospital  stidende,”  52,  1896  (Casuistik). 

65.  Fenwick,  C.,  “ A Case  of  Gastric  Ulcer  Perforating  into  the  Pericardium,” 
“ Lancet,”  Lond.,  1897,  11,  388. 

66.  Fenwick,  W.  S.,  “ Ulcer  of  the  Stomach  in  Children,”  “ Internat.  Clin.,” 
Phila.,  189 7,7  s.,  11,  165-177. 

67.  Fischer,  O.,  “ Bismuth  Treatment,”  “ Dissertation,”  Jena,  1893. 

68.  Fisher,  H.  M.,  “ Perforating  Round  Ulcer  of  the  Stomach,”  “ Tr.  Path. 
Soc.,”  Phila.,  1898,  xviii,  46,47. 

69.  Fleiner,  “ Verhandl.  des  XII.  Congresses  f.  innere  Medicin,”  1893;  also 
“ Volkmann’s  Vortrage,”  No.  103. 

70.  Flexner.  S.,  “ Exhibition  of  a Specimen  of  Round  Ulcer  of  the  Stomach  ; 
Erosion  of  the  Gastric  Artery;  Postmortem  Perforation,”  “Johns  Hopkins 
Hosp.  Bull.,”  Balt.,  1898,  ix,  41. 

71.  Fox,  Wilson,  “ The  Diseases  of  the  Stomach,”  1872,  p.  146. 

72.  Fyffe,  W.  K.,  “ Gastric  Ulcer  with  Perforation,”  “Australas.  M.  Gaz.,” 
1897,  xvi,  331. 

73.  Gemiind,  “ Beitrage  zur  pathol.  Anatomie  des  Ulcus  ventriculi,  insbes. 
des  gurtelformigen,”  Dissert.,  Leipzig,  1895-96. 

74.  Glaeser,  A.,  “Ulcus  ventriculi  fur  Aneurysma  gehalten,”  “Allg.  med. 
Central-Ztg.,”  Berl.,  1897,  lxvi,  561. 


520 


ULCER  OF  THE  STOMACH. 


75.  Godart-Danhieux,  “ l’Emploi  des  Alcalins  dans  l’Ulcere  de  l’Estomac,” 
“ Policlin.  Brux.,”  1898,  vii,  33-43. 

76.  Gongora,  J.,  “ Acerca  del  tratamiento  farmacologico  de  la  ulcera  cronica 
simple  del  estomago,”  “ Rev.  de  cier.  med.  de  Barcel.,”  1897,  xxm,  t.  2,401- 
408. 

77.  Griffini  und  Vassale,  “ Beitrage  zur  patholog.  Anat.,”  von  Ziegler  und 
Nauwerclc,  Bd.  ill,  Heft  5,  p.  425. 

78.  Griffini  und  Vassale,  “Ueberdie  Reproduction  der  Magenschleimhaut,” 
“Ziegler’s  Beitrage,”  111. 

79.  Giinzburg,  “ Zur  Kritik  des  Magengeschwiirs,”  “ Arch,  fiir  physiol. 
Heilkunde,”  ix. 

80.  Hainebach,  J.,  “ Zwei  Falle  von  Perigastritis  adhaesiva  nach  Ulcus 
ventriculi,”  “ Deutsche  med.  Wochenschr.,”  Leipz.  u.  Berl.,  1897,  xxm,  657— 
660. 

81.  Hall,  A.  J.,  “On  Two  Cases  of  Perigastric  Abscess  Arising  from  Gastric 
Ulceration  and  Rupturing  into  the  Left  Lung,”  “ Clin.  Jour.,”  London,  1898, 
XU,  353-357. 

82.  Hamilton,  H.  L.,  “Treatment  of  a Case  of  Gastric  Ulcer,”  “Louisville 
Med.  Monthly,”  1898-99,  v,  131. 

83.  Hartmann,  “ Peritonite  par  Perforation  d’un  Ulcere  Simple  de  l’Estomac, 
Laparotomie ; Guerison,”  “ Bull,  de  la  Soc.  de  Chir.,”  Bd.  xxii,  1896. 

84.  Hartmann,  “ Ulcere  de  l’estomac  ; gastro-enterostomie,”  “ Soc.  de  Chir.,” 
20  aout,  1897. 

85.  Harttung,  O.,  “ Ueber  Faltenblutungen  und  hamorrhagische  Erosionen,” 
“ Deutsche  med.  Wochenschr.,”  1890,  No.  38,  p.  847. 

86.  Hauser,  “ Das  chronische  Magengeschwur,”  Leipzig,  1883. 

87.  Heidenreich,  “ De  1’ Intervention  Chirurgicale  dans  l’Ulcere  d’Estomac,” 
“ Sem.  Med.,”  2 fevrier,  1898. 

88.  Herald,  J.,  “ Ulcer  and  Cancer  of  the  Stomach,”  “Kingston  Med.  Quart.,” 
1897-98,  11,  124-128. 

89.  Herrick,  J.  B.,  “ The  Treatment  of  Ulcer  of  the  Stomach  by  Rest  in  Bed 
and  Rectal  Feeding,”  “Jour.  Amer.  Med.  Asso.,”  1898,  xxxi,  1303. 

90.  Hibbard,  C.  M.,  “ A Case  of  Gastric  Ulcer  in  a Child  Four  Months  Old,” 
“ Boston  Med.  and  Surg.  Jour.,”  1897,  cxxxvii,  177. 

91.  Hirsch,  “ Zur  Casuistik  und  Therapie  der  lebensgefahrlichen  Magenblut- 
ungen,”  “Berl.  klin.  Wochenschr.,”  No.  38,  1896. 

92.  Hoffmann,  “ Ueber  die  Erweichung  und  den  Durchbruch  der  Speiserohre 
und  des  Magens,”  “ Virchow’s  Archiv,”  Bd.  xliv. 

93.  Hone,  F.  S.,  “ Gastric  Ulcer  and  Secondary  Parotiditis,”  “ Australas.  Med. 
Gaz.,”  Sydney,  1898,  xvn,  50-54. 

94.  Hood,  D.,  “A  Case  of  Gastric  Ulcer,”  “Clin.  Jour.,”  London,  1898-99, 
xiii,  136. 

95.  Horner,  “ Cardialgie  durch  Einklemmung  praperitonealer  Lipome,” 
“ Prager  med.  Wochenschr.,”  1892. 

96.  Jacot-Descombes,  Ch.,  “ Contribution  anatomique  a l’etude  de  la  patho- 
genic de  l’ulcere  rond  de  l’estomac,”  “ These  de  Paris,”  1897. 

97.  James,  A.,  “Gastric  Ulcer,”  “ Internat.  Clin.,”  Philadelphia,  1898,  8 s., 
126-135. 


LITERATURE  ON  ULCER  OF  THE  STOMACH.  521 

98.  Jaworski  und  Korczynski,  “ Deutsche  med.  Wochenschr.,”  1886,  Nos. 

47-49- 

99.  Jonas,  A.  F.,  “Operation  for  Ulcus  Ventriculi  Chronicum,  Three  Cases, 
with  Remarks  on  Indications  for  Operation,”  “West.  Med.  Rev.,”  Lincoln, 
Neb.,  1897,  11,  285-287. 

100.  Jones,  Eleanor  C.,  “A  Case  of  Gastric  Ulcer  Terminating  in  Hemor- 
rhage and  Death,”  “ Med.  News,”  New  York,  1897,  lxxi,  499. 

101.  Key,  Axel,  “ Gurlt-Virchow’s  Jahresb.,”  1871. 

102.  Klaussner,  “ Ein  Beitrag  zur  operativen  Behandlung  des  Ulcus  ven- 
triculi,” “ Munch,  med.  Wochenschr.,”  1897,  No.  37. 

103.  Kohler,  “ Beitrag  zur  Kenntniss  der  Symptomatologie  bei  Ulcus  ven- 
triculi simplex,”  Dissert.,  Berlin,  1895-96. 

104.  Kolisch,  R.,  “ Zur  Frage  der  posthamorrhagischen  Azoturie  (speciell 
beim  Ulcus  ventriculi),”  “Wien.  klin.  Wochenschr.,”  1897,  x,  628. 

105.  Krokiewicz,  A.,  “ Ein  Beitrag  zur  Lehre  vom  runden  Magengeschwiir,” 
“ Wien.  klin.  Wochenschr.,”  1897,  x. 

106.  Krupetski,  Aleksiei,  “ Kucheniga  ob  Ulcus  ventriculi  rotundum,”  “Yur- 
yev,” 1897,  K.  Matisen,  256,  p.  8. 

107.  Laine,  J.,  “Des  erosions  hemorrhagiques  de  l'estoniac,”  “ These  de 
Paris,”  1 7 Novembre,  1897. 

108.  Lammert,  “ Das  perforierte  Ulcus  ventriculi  rotundum  in  gerichtlich- 
medicinischer  Beziehung,  nebst  Bemerkungen  uber  die  Haufigkeit  des  runden 
Magengeschwiirs  zu  Miinchen  in  den  Jahren  1883-88,”  Dissert.,  Miinchen, 
1895-96. 

109.  Landerer,  A.,  und  G.  Glucksmann,  “ Mittheilungen  aus  den  Grenz- 
gebieten  der  Medizin  und  Chirurgie,”  Bd.  1,  p.  168,  Jena,  1896. 

no.  Langerhaus,  “ Virchow’s  Archiv,”  Bd.  cxxiv,  p.  373. 

111.  Lanzer,  O.,  “ Zur  Diagnose  und  Therapie  des  runden  Magengeschwiirs,” 
“ Wien.  med.  Presse,”  1898,  xxxix,  1127-1131. 

1 12.  Lanenstein,  “Arch.  f.  klin.  Chirurgie,”  vol.  xiv. 

1 13.  Leblanc,  “ Gastrorrhagie  et  perforation  dans  l’ulcere  de  l’estomac,” 
“ These  de  Paris,”  3,  xn. 

1 14.  Leith,  R.  F.  C.,  “ Edinburgh  Hospital  Reports,”  1894,  vol.  11,  pp.  198- 
238. 

1 1 5.  Lennander,  K.  G.,  “The  Treatment  of  the  Perforating  Stomach  and 
Duodenal  Ulcer,”  “ Upsula  Lakaref.  Forh.,”  1897-98,  N.  F.,  ill,  350-403. 

1 16.  Levi,  “ Retrecissement  fibreux  du  pylore  consecutif  a un  ulcere  de 
l’estomac,”  “ Soc.  Anat.  de  Paris,”  31,  1,  1897. 

1 17.  Le  Wald,  L.  U.,  “Ulceration  of  Both  Stomach  and  Duodenum,  with 
Perforation  of  the  Splenic  Artery,”  “ Med.  Rec.,”  New  York,  1898,  liv,  892. 

1 18.  Leyden,  E.,  “ Ueber  Pyopneumothorax  subphrenicus  und  subphren- 
ische  Abscesse,”  “ Zeitschr.  f.  klin.  Med.,”  1880,  p.  320. 

1 19.  Liebermeister,  “ Ueber  das  einfache  Magengeschwiir,”  “ Volkmann’s 
Sammlung  klin.  Vortrage,”  1892,  No.  61. 

120.  Lincoln,  J.  R.,  “ Gastric  Ulcer  in  the  Newborn,  Etiology,  Maternal 
Impressions,”  “ Boston  Med.  and  Surg.  Jour.,”  1897,  cxxxvu,  178. 

121.  Litten,  “Ulcus  ventriculi  tuberculosum,”  “Virchow’s  Archiv,”  Bd. 
LX  vi  1. 


522 


ULCER  OF  THE  STOMACH. 


122.  Liitzeler,  “ Statistisches  liber  Magengeschwiire  und  operative  Eingriffe 
bei  denselben,”  Dissert.,  Bonn,  1895-96. 

123.  Luys,  G.,  “ Ulceration  gastriques  chez  un  alcoolique  mort  subite  par 
hemorrhagie,”  “ Bull.  Soc.  Anat.  de  Par.,”  1896,  lxxi,  660-667. 

124.  Lyell,  “A  Case  of  Gastric  Ulcer  with  Perforation  in  Two  Places,” 
“ Brit.  Med.  Jour.,”  London,  1898,  1,  818. 

125.  Lyon,  G.,  “ Traitement  de  l’ulcere  simple  de  l’estomac,”  “ Gaz.  d. 
Hop.,”  Paris,  1898,  3 s.,  xv,  356-358. 

126.  Lyon,  “ Discussion  sur  le  traitement  de  l’ulcere  de  l’estomac,”  “ Bull, 
gen.  de  therap.,”  etc.,  Paris,  1898,  cxxxvi. 

127.  Mackenzie,  J.,  “ A Case  of  Gastric  Ulcer  with  Characteristic  Seat  of 
Pain,”  “ Edinb.  Med.  Jour.,”  1897,  n.  s.,  II,  591. 

128.  Mackenzie,  J.,  “ The  Site  of  Pain  in  Gastric  Ulcer,”  “ Edinb.  Med. 
Jour.,”  1897,  n.  s.,  11,  154-158. 

129.  Mackenzie,  W.  G.,  “ Perforation,  Ulcer  of  Stomach  with  Hour-glass 
Contraction,”  “ Tr.  Path.  Soc.,”  London,  1896-1897,  XLViii. 

130.  Marcet,  “ Medico-Chirurgical  Transactions,”  vol.  xil,  p.  72. 

1 3 1 . Marchand,  “ Gastromalacie  (und  CEsophagomalacie),”  “ Real-Encyklo- 
padie,”  xil. 

132.  Marcille,  “ Ulcere  gastrique  ; abces  de  la  rate,  abces  sous  phrenique,” 
“ Soc.  Anat.,”  Paris,  10  juin,  1898. 

133.  Marin  Perujo,  “Ulceration  del  estomago  por  el  uso  inadecuado  de  la 
quinina,”  “ Siglo  med.,”  Madrid,  1897,  xliv,  706. 

134.  Matthes,  “ Ueber  den  Vorschlag  Fleiner’s,  Reizerscheinungen  des 
Magens  mit  grossen  Dosen  Wismuth  zu  behandeln,”  “ Centralblatt  fiir  innere 
Med.,”  1894. 

135.  Mauwerk,  C.,  “ Gastritis  ulcerosa  chronica,  ein  Beitrag  zur  Kenntnis 
des  Magengeschwiirs,”  “ Miinch.  med.  Wochenschr.,”  1897,  xliv,  955,  987. 

136.  Mayer,  W.,  “ Gastromalacia  ante  mortem,”  “ Deutsches  Arch,  fiir  klin. 
Med.,”  ix,  1872. 

137.  McCohs,  A.  J.,  "A  Case  of  Perforating  Gastric  Ulcer;  Operation, 
Recovery,”  “Med.  News,”  16,  1,  1897. 

138.  Metcalfe,  W.  B.,  “ Etiology  and  Diagnosis  of  Ulcer  of  the  Stomach,” 
Matthews,  O.  J.,  “ Rectal  Dis.,”  Louisville,  1897,  IV,  335-344. 

139.  Merigot  de  Freigny,  “Traitement  de  l’ulcere  Gastrique  par  le  repos 
absolu  de  l’Estomac,”  “ Rev.  gen,  de  clin.  et  de  Therap.,”  Par.,  1897,  xi,  5 1 7— 
520. 

140.  Mintz,  “ Operative  Behandlung  der  Magenkrankheiten,”  “ Zeitschr.  f. 
klin.  Med.,”  Bd.  xxv,  1894. 

141.  Morely,  “Ulcere  rond  de  l’Estomac  devolution  lente,  Perforation 
peritonite  generalisee,”  “Soc.  Anat.,”  10  Dec.,  1897. 

142.  Muller,  L.,  “ Das  corrosive  Geschwiir  im  Magendarmkanal,”  Erlangen, 
i860. 

143.  Murrell,  W.,  “Gastric  Ulcer  and  Its  Treatment,”  “ Med.  Brief,”  St. 
Louis,  1898,  xxvi,  673-676. 

144.  Neuwerck,  C.,  “Ueber  den  mycotischen  Ursprung  des  peptischen 
Magengeschwiirs,”  “ Miinchener  med.  Wochenschr.,”  1895. 

145.  Nissen,  “Zur  Frage  der  Indication  der  operativen  Behandlung  des 
runden  Magengeschwiirs,”  “ Petersburger  med.  Wochenschr.,”  1890. 


LITERATURE  ON  ULCER  OF  THE  STOMACH.  523 

146.  Nitka,  “Ueber  embolische  Magengeschwiire,”  Dissert.,  Freiburg  i. 
Br.,  1895-96. 

147.  v.  Noorden,  “ Magensaftsecretion  und  Blutalkaleszenz,”  “Arch,  fur 
exp.  Pathologie  u.  Pharm.” 

148.  v.  Noorden,  “ Zwei  operative  Eingrifife  wegen  Folgezustanden  von 
Magengeschwiiren,”  “ Miinch.  med.  Wochenschr.,”  No.  35,  1896. 

149.  Nolte,  see  Ewald  {loc.  cit.,  239). 

150.  O’Donovan,  C.,  “On  the  Treatment  of  Gastric  Ulcers  after  Hemor- 
rhage,” “ New  York  Med.  Jour.,”  1897,  lxvi,  51-53. 

1 5 1.  Oliver,  F.,  “ Ulceration  of  the  Pylorus  and  Its  Consequences,”  “ Inter- 
nat.  Clin.,”  Philadelphia,  1898,  8 s.,  1,  146-157. 

152.  Openchowski,  “ Zur  pathologischen  Anatomie  der  geschwiirigen  Pro- 
cesse  im  Magendarmtractus,”  “ Virchow’s  Archiv,”  Bd.  cxvn. 

153.  Panum,  “ Experimented  Beitrage  zur  Lehre  von  der  Embolie,”  “Vir- 
chow’s Archiv,”  Bd.  xxv,  1862. 

154.  Pariser,  “ Die  Behandlung  des  frei  in  die  Bauchhohle  perforierten  Ulcus 
ventriculi,”  “ Allg.  medic.  Centralz.,”  1896. 

155.  Pauly,  “Zur  Lehre  vom  traumatischen  Magengeschwiir,”  “ Aerztl. 
Sachverst.-Ztg.,”  No.  2,  1898. 

156.  Pavy,  “On  Gastric  Erosion,”  “Guy’s  Hospital  Reports,”  vol.  xiv, 
1868. 

1 57.  Petruschky,  J.,  “ Zur.  Diag.  u.  Therap.  d.  Primar.  Ulcus  ventric.  tubercu- 
losum,”  “ Verhandlung  d.  XVII.  Congress,  f.  innere  Medicin,”  1899,  S.  366. 

158.  Pfuhl,  “ Berliner  klin.  Wochenschr.,”  1877,  p.  57. 

159.  Potain,  “ Ulcere  Simple  Duodenal  et  Ulcere  Simple  de  l’Estomac,” 
“ Bull,  med.,”  1,  1,  1897. 

160.  Poulain,  “ Du  role  del’Infection  dans  la  Pathogenie  de  l’Ulcere  rond,” 
“ These  de  Paris,”  1897. 

161.  Qaife,  F.  H.,  “ An  Interesting  Case  of  Gastric  Ulcer,”  “ Australas.  Med. 
Gaz.,”  1898,  xvii. 

162.  Quincke,  “ Die  Entstehung  des  Magengeschwiirs,”  “ Deutsche  med. 
Wochenschr.,”  1882. 

163.  Quincke  und  Daettwyler,  “ Correspondenzbl.  f.  Schweizer  Aerzte,”  1875, 
p.  101. 

164.  Rabe  et  Rey,  “ Double  Ulcere  de  l’Estomac ; Ulceration  du  foie  et  du 
Pancreas,  Retraction  Cicatricielle  Intense,  avec  Biloculation  de  l’Estomac  ; 
Abcess  sus-hepato-phrenique,  Epanchement  Pleuritique  Double,  Purulent  a 
Gauche,  Sereux  a Droite,”  “ Bull.  Soc.  Anat.  de  Par.,”  1897,  lxxii. 

165.  Rasmussen,  “Ueber  die  Magenschwiirfurche  und  die  Ursache  des 
chronischen  Magengeschwiirs,”  “ Centralblatt  fur  die  med.  Wissenschaften,” 
1887. 

166.  Ratjen,  “ Ulcus  ventriculi,  ausschliesslich  mit  Rectal-Ernahrung  be- 
handelt,”  “ Deutsche  med.  Wochenschr.,”  No.  52,  1897. 

167.  Reichel,  “Zur  Lehre  vom  traumatischen  Magengeschwiir,”  “Aerztl. 
Sachverst.  Ztg.,”  Nr.  6,  1898. 

168.  Riegel,  F.,  “ Zeitschr.  f.  klin.  Med.,”  Bd.  xn,  S.  434,  and  “ Deutsche 
med.  Wochenschr.,”  1886,  Nr.  52. 

169.  Rindfleisch,  “ Lehrbuch  der  patholog.  Anatomie.” 


524 


ULCER  OF  THE  STOMACH. 


170.  Ritter,  “ Ueber  den  Einfluss  von  Traumen  auf  die  Entstehung  des 
Magengeschwiirs,”  “ Zeitschr.  f.  klin.  Med.,”  xii. 

1 7 1 . Rivet,  “ Perforation  par  ulcere  de  l’estomac,”  “ Soc.  med.  de  Nantes,” 
10  Dec.;  “ Gaz.  med.  de  Nantes,”  1897. 

172.  Rokitansky,  “ Lehrbuch  der  patholog.  Anatomie.” 

173.  Rolleston,  H.  D.,  “ A Case  of  Latent  Ulcer  of  the  Pylorus  with  Jaun- 
dice, Simulating  Malignant  Disease,”  “ Practit.,”  London,  1897,  Liv,  465- 
470. 

174.  Rommelaere,  “ Ulcere  rond  phagedenique  de  l’estomac  deux  lesions, 
une  cicatrice  a fond  pancreatique  et  un  ulcere  perforant  en  activite  bouche 
pir  un  cartilage  costal,  sclerose  de  la  parvi  prepylorique ; mort,  autopsie,” 
“ Clinique  Brux.,”  1897,  xi,  521-529. 

175.  Rosenheim,  Th.,  “ Pathologie  und  Therapie  der  Krankheiten  der 
Speiserohre  und  des  Magens,”  Wien  und  Leipzig,  1891,  S.  161. 

176.  Rosenheim,  Th.,  “ Zur  Kenntniss  des  mit  Krebs  complicirten  runden 
Magengeschwiirs,”  “ Zeitschr.  f.  klin.  Med.,”  Bd.  xvii,  S.  116. 

177.  Rosenheim,  Th.,  “ Deutsche  med.  Wochenschr.,”  1890,  Nr.  15. 

178.  Rosenheim,  “ Die  neueren  Behandlungsmethoden  des  Magens,”  “ Ber- 
liner Klinik,”  May,  1894. 

179.  Roughton,  E.  W.,  “Perforating  Gastric  Ulcer;  Operation,  Death; 
Necropsy,”  “ Brit.  Med.  Jour.,”  July  9,  1898. 

180.  Sansoni,  L.,  “ II  sottonit  rato  di  bismuto  ad  alte  dosi  nella  cura  del 
l’ulcera  semplice  dello  stomaco,”  “ Gior.  d.  r.  accad.  di  med  di  Torino,”  1897, 
3 s.,  xlv,  463-468. 

181.  Saundby,  “ Ein  Fall  von  sanduhrformiger  Einschniirung  des  Magens 
in  Verbindung  mit  einem  kolossalen  Magengeschwiir,”  “ Deutsche  med. 
Wochenschr.,”  1891. 

182.  Savelieff,  “ Ueber  die  Wismuthbehandlung  des  runden  Magenge- 
schwiirs,”  “ Therap.  Monatshefte,”  1894,  Nr.  10. 

183.  Scheel,  V.,  “ Et  Tifaelde  af  Ulcus  ventriculi,”  “ Hosp.-Tid.  Kjobenh.,” 
1898,  4.  R.,  vi. 

184.  Scheurmann,  “Ueber  die  Haufigkeit  des  runden  Magengeschwiirs  in 
Miinchen,”  Dissert.,  Miinch.,  1895-96. 

185.  Schiff,  “ Beitrag  zur  Kenntniss  des  motorischen  Einflusses  der  in  Seh- 
hiigel  vereinigten  Gebilde,”  “ Arch.  f.  physiol.  Heilkunde,”  v,  1846. 

186.  Schiff,  “ Ueber  die  Gefassnerven  des  Magens,”  ibid.,  xm,  1854,  S.  30. 

187.  Schmidt,  “ Anatomische  Beitrage  zur  Genese  des  Ulcus  ventriculi,” 
Dissert.,  Leipzig,  1895-96. 

188.  Schiitz,  R.,  “ Differential  Diagnose  d.  UlcuS  Ventriculi,”  ibid.,  S.  417. 

189.  Sehrwald,  “ Was  verhindert  die  Selbstverdauung  des  lebenden  Magens  ? 
Ein  Beitrag  zur  Aetiologie  des  runden  Magengeschwiirs,’-’  “Miinch.  med. 
Wochenschr.,”  1888. 

190.  Shaw,  G.  F.,  “ Hematemesis  as  a Sequence  of  Chronic  Ulcer,”  “ Med. 
Rec.,”  New  York,  1898,  liv,  138. 

191.  Silbermann,  “ Deutsche  med.  Wochenschr.,”  1886,  Nr.  29. 

192.  Sohlern,  V.,  “ Der  Einfluss  der  Ernahrung  auf  die  Entstehung  des 
Magengeschwiirs,”  “ Berl.  klin.  Wochenschr.,”  1889,  Nr.  14. 

193.  Stawell,  R.  de  S.,  “ Perforating  Gastric  Ulcer,”  “ St.  Barth.  Hosp.  Jour.,” 
London,  1897-98,  v. 


LITERATURE  ON  ULCER  OF  THE  STOMACH. 


525 


194.  Stepp,  “ Zur  Behandlung  des  chronischen  Magengeschwiirs,”  “ Ver- 
handlungen  der  65.  Versammlung  deutscher  Naturforscher  und  Aerzte,”  1893. 

195.  Sticker,  “ Ueber  den  Einfluss  der  Magensaftabsonderung  auf  den 
Chlorgehalt  des  Harns,”  “ Berl.  klin.  Wochenschr.,”  1887. 

196.  Sticker  und  Hubner,  “ Wechselbeziehungen  zwischen  Secreten  und 
Excreten,”  “ Zeitschr.  f.  klin.  Med.,”  xil,  1887. 

197.  Stockton,  Chas.  G.,  “ The  Etiology  of  Gastric  Ulcer,”  “ Med.  News,” 
Jan.  14,  1893. 

198.  Sutherland,  L.  R.,  “ A Series  of  Specimens  of  Perforating  Ulcer  of  the 
Stomach  and  Duodenum,”  “ Glasgow  Med.  Jour.,”  1898,  XLIX,  207-215. 

199.  Talma,  “ Untersuchungen  iiber  Ulc.  ventr.  simpl.  Gastromalacie  und 
Ileus,”  “ Zeitschr.  f.  klin.  Med.,”  xvn,  1890. 

200.  Taylor,  S.,  “ Gastric  Ulcer,”  “ Med.  Press  and  Circ.,”  London,  1898. 
n.  s.,  LXV,  297-300. 

201.  Thorspecken,  “ Ein  Fall  von  Magenerweichung  ante  mortem,” 
“ Deutsches  Arch.  f.  klin.  Med.,”  xxxm. 

202.  Tournier,  C.,  “ D’un  type  cle  catarrhe  gastrique  avec  hyperesthesie  de 
la  muqueuse  et  colite  mucomembraneuse ; difficultes  diagnostiques  avec 
l’ulcere,”  “ Province  med.,”  Lyon,  1898,  xil,  457-461. 

203.  Troisfontaines,  “ Ulcere  simple  de  l’estomac,  chez  une  jeune  homme  ; 
mort;  examen  anatomique,”  “Ann.  de  la  Soc.  de  med.  de  Liege,”  Juin,  1896, 

204.  Tuffier,  “ Epaississement  des  parois  stomacales  du  a un  ulcere  prob- 
able,” “ Soc.  de  Chir.,”  27  Oct.,  1897. 

205.  Uhlrich,  Chr.,  “ Sequelae  ulceris  ventriculi  perforati,”  “ Biblioth.  for 
Laeger,”  p.  367. 

206.  Vasilin,  C.,  “ Ulcerul  simpiu  al  stomac  uli  si  tratamentul  Boas,” 
“ Spitalul,”  Bucuresci,  1898,  xvn. 

207.  Virchow,  R.,  “ Virchow’s  Archiv,”  Bd.  V,  p.  363. 

208.  Von  Leube  und  Mikulicz,  “ Chirurgische  Behandlung  des  Magenge- 
schwiirs,”  Abstr.  “ Deutsche  med.  Wochenschr.,”  1897,  xxm,  Ver.  Beil.,  83. 

209.  Warren,  J.  C.,  “ The  Surgery  of  Gastric  Ulcer,  with  the  Report  of  a 
Case  of  Gastrolysis,”  “ Boston  Med.  and  Surg.  Jour.,”  Sept.  29,  1898. 

210.  Weir,  Robt.  F.,  and  E.  M.  Foote,  “ The  Surgical  Treatment  of  Round 
Ulcer  of  the  Stomach  and  Its  Sequelae,  with  an  Account  of  a Case  Successfully 
Treated  by  Laparotomy,”  “ Med.  News,”  April  25  and  May  2,  1896. 

21 1.  Welch,  cited  from  Osier’s  “ Practice  of  Medicine,”  p.  369. 

212.  Welti,  “ Drei  Falle  von  Verbrennungstod,”  “ Centralblatt  fur  allg. 
Path.,”  1890. 

213.  Widal  et  Meslay,  “ Ulcere  rond  developpe  au  cours  dune  pyhemie  a 
staphylocoques ; de  lorigine  infectieuse  de  certains  ulceres  ronds  perforants  de 
l’estomac,”  “ Bull,  et  mem.  Soc.  med.  d.  hop.  de  Par.,”  1897,  3 s.,  xiv,  pp. 
379-385- 

214.  Winternitz,  W.,  “ Die  Hydrotherapie  des  Ulcus  rotundum  ventriculi,” 
“ Deutsche  med.  Wochenschr.,”  Nr.  46,  1897. 

215.  Wynter,  W.  E.,  “ On  Gastric  Ulcer  Treatment,”  London,  1897,  1,  462- 
464. 

216.  Ziemssen,  “Ueber  die  Behandlung  des  einfachen  Magengeschwiirs,” 
“Volkmann’s  Sammlung  klinischer  Vortrage,”  1871,  Nr.  15. 


526 


ULCER  OF  THE  STOMACH. 


We  refer  also  to  “ Literature  on  Gastric  Ulcer”  in  Prof.  William  H.  Welch’s 
article  in  “American  System  of  Medicine,”  vol.  ir,  p.  480,  in  which  over  140 
important  bibliographical  references  are  given. 

In  the  fourth  volume  of  Penzoldt  and  Stintzing’s  “ Handbuch  d.  speciellen 
Therapie,”  vol.  iv,  pp.  316,  317,  also  pp.  437  and  438,  are  contained  150  biblio- 
graphical references  on  the  treatment  of  Gastric  Ulcer. 


BIBLIOGRAPHY  OF  ULCUS  CARCINOMATOSUM. 

1.  Berthold,  Inaug.-Dissert.,  Berlin,  1883. 

2.  Biach,  “Wien.  med.  Presse,”  1890,  Nr.  3. 

3.  Boas,  “ Diagnostik  u.  Therapie  d.  Magenkrankh.,”  p.  8. 

4.  Bouveret,  “ Traite  de  malad.  d.  l’estomac,”  Paris,  1893,  p.  274  (three 
cases). 

5.  Brinton,  “ Lectures  on  Diseases  of  the  Stomach,”  London,  1864. 

6.  Dittrich,  “ Prager  Vierteljahresschrift,”  v,  1848,  S.  1. 

7.  Eisenlohr,  “ Deutsche  med.  Wochenschr.,  ’ 1890,  Nr.  52. 

. 8.  Ewald,  “ Klinik  d.  Verdauungskrankh.,”  1885. 

9.  Feiertag,  Inaug.-Dissert.,  Dorpat,  1894. 

10.  Hauser,  “ Das  chronische  Magengeschwur,”  Leipzig,  1883. 

11.  Heitler,  “Wien.  med.  Wochenschr.,”  1883,  Nr.  31. 

12.  Koch,  R.,  “ St.  Petersburger  med.  Wochenschr.,”  1893,  Nr.  43. 

13.  Kollmann,  “ Zur  Differentialdiagnose  zwischen  Magengeschwur  und 
Magenkrebs,”  1891,  Nr.  5,  6. 

14.  Krukenberg,  Inaug.-Dissert.,  Heidelberg,  1888. 

15.  Kulcke,  Inaug.-Dissert.,  Berlin,  1889. 

16.  Langguth,  “ Archiv  f.  Verdauungskrankh.,”  von  Boas,  Bd.  1,  S.  355,  “ On 
Significance  of  Lactic  Acid.” 

17.  Lebert,  “ Die  Krankheiten  d.  Magens,”  Tubingen,  1878,  S.  440. 

18.  Leube,  “ Ziemssen’s  Handbuch,”  Bd.  vii,  S.  124. 

19.  Meyer,  C.,  Inaug.-Dissert.,  Heidelberg,  1885. 

20.  Oppler  und  Boas,  “ Zur  Kenntniss  d.  Mageninhalts  b.  Carcinome,”  etc., 
“ Deutsche  med.  Wochenschr.,”  1895,  Nr.  5. 

21.  Pignal,  “ These  de  Lyon,”  1891  (two  cases). 

22.  Plange,  Inaug.-Dissert.,  Berlin,  1859. 

23.  Riegel,  F.,  “ Die  Erkrankungen  d.  Magens,”  p.  174.  (On  the  Oppler- 
Boas  bacillus.) 

24.  Rokitansky,  “ Lehrbuch  d.  patholog.  Anatomie,”  third  edition. 

25.  Rosenheim,  “ Zur  Kenntniss  des  mit  Krebs  complicirten  runden  Magen- 
geschwurs,”  “ Zeitschr.  f.  klin.  Med.,”  Bd.  xvii,  S.  116. 

26.  Schlesinger  und  Kaufmann,  “Wien.  klin.  Rundschau,”  1895,  Nr.  15. 
(On  the  Oppler-Boas  bacillus.) 

27.  Steiner,  Inaug.-Dissert.,  Berlin,  1868. 

28.  Sticker,  “ Verhandl.  d.  Congresses  f.  innere  Med.,”  1887. 

29.  Tapret,  “Union  medic.,”  1891,  No.  98. 

30.  Thiersch,  “Munch,  med.  Wochenschr.,”  1886,  Nr.  13. 

31.  Waltzold,  “ Charite-Annalen,”  Bd.  xiv. 

32.  Wollmann,  Inaug.-Dissert.,  1868. 


CARCINOMATA. 


527 


CHAPTER  IV. 

MALIGNANT  TUMORS  OF  THE  STOMACH. 

(A)  CARCINOMATA. 

Pathology. — In  accordance  with  leading  pathologists  we  may 
distinguish  four  types: 

1.  The  cylindrical  cell,  or  adenocarcinoma. 

2.  The  soft  glandular,  or  medullary  carcinoma. 

3.  The  hard  glandular  carcinoma,  or  scirrhus. 

4.  The  mucous,  or  colloid  carcinoma. 

In  the  section  on  the  Surgical  Operations  on  the  Stomach  we 
have  spoken  of  the  relative  frequency  with  which  these  various 
types  of  carcinoma  attack  this  organ.  It  is  an  error  for  clinicians 
to  speak  of  gastric  cancer  as  if  this  were  the  only  type  of  malig- 
nant neoplasm  that  can  attack  the  stomach.  Inasmuch  as  these 
various  types  show  different  rates  of  mortality  after  operation,  and 
as  they  can  occasionally  be  distinguished  clinically  by  small  bits 
of  the  new  growth,  which  come  up  in  the  wash-water  or  are  found 
caught  in  the  eyes  of  the  stomach-tube,  it  is  essential  that  a brief 
pathological  description  of  them  should  be  given.  The  types 
which  we  have  mentioned  are  not  sharply  distinguished  from  each 
other,  but  many  gradations  and  transitions  exist  between  them. 
The  structure  of  a gastric  malignant  neoplasm  is  by  no  means  a 
matter  of  indifference,  both  for  the  clinical  history  and  the  pros- 
pective surgical  treatment.  The  scirrhus  exhibits  the  most  pro- 
tracted course ; the  medullary  (soft  glandular)  a disposition  to 
disintegration  and  formation  of  metastases  ; while  the  colloid  has  a 
tendency  to  extend  to  the  peritoneum,  and  rarely  forms  metastases. 

The  cylindrical  cell,  or  adenocarcinoma , presents  a soft,  distinct 
prominence,  or  tumor,  upon  the  surface  of  which  smaller  fungoid 
elevations  develop,  being  attached  to  the  fundamental  tumor  by 
broad  or  narrow  bases,  which  give  the  surface  a papillary  appear- 
ance. In  this  case  the  tumor  regularly  has  a red  color,  because 
each  individual  fungosity  contains  a small  loop  of  blood-vessels. 
The  little  vessels  in  the  outer,  as  well  as  those  in  the  inner,  sections 
of  the  neoplasm  frequently  show  an  irregular  spindle-shaped  or 
spherical  dilatation,  so  that  this  form  of  carcinoma  has  been  called 
by  Orth,  telangiectatic.  This  condition  of  the  blood-vessels  may 


528 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


explain  why,  in  this  type  of  cancer,  smaller  or  larger  extravasations 
of  blood  are  found  on  the  surface,  as  well  as  in  the  parenchyma ; 
and  also  accounts  for  the  frequent  effusion  of  blood  into  the  cavity 


Fig.  35. — Cancerous  Invasion  of  the  Glandular  Layer.  A Portion  of  the  Mucous 
Coat. — ( From  the  Author's  Clinic.') 

Objective,  one-sixth.  Eyepiece,  one  inch.  X about  320  diameters.  Stained  with  hematoxylin 
and  orange  G. 

This  cut  shows  very  well  the  small,  round-cell  infiltration  between  the  cross-sections  of  the 
gastric  tubules,  with  here  and  there  the  cells  very  much  crowded,  A,  A. 

The  exfoliation  of  the  cells  lining  some  of  the  glandular  acini  is  also  shown  in  places,  B. 

At  one  or  two  places  the  proliferation  of  the  epithelial  cells  that  line  the  glands,  with  breaking 
of  these  glandular  structures  and  the  escape  of  some  of  the  cells  into  the  surrounding  tissue,  is 
seen,  C,  C,  C. 

The  entire  obliteration  of  some  of  the  glandular  structures  by  masses  of  cancer  cells,  Z),  D, 
which  in  many  places  are  strung  out  for  some  distance,  E,  E,  and  in  a few  others  have  taken  on 
the  pseudo-glandular  arrangement,  E,  is  also  well  shown. 


of  the  stomach.  On  section,  the  so-called  “ carcinoma  juice  ” ap- 
pears abundantly  on  the  surface,  and  in  this  “juice”  typical  cylin- 
drical cells  are  generally  exclusively  found  in  sections  examined 


ADENOCARCINOMA  OF  THE  STOMACH.  529 

microscopically.  Such  sections  present  varying  pictures,  accord- 
ing to  whether  they  are  taken  from  the  surface  or  from  deeper 
regions  of  the  neoplasm.  On  the  surface  the  aspect  closely  re- 
sembles that  of  a papillary  fibroma,  but  in  the  deeper  regions  a 


C 

Fig.  36.— Cancerous  Infiltration  of  the  Muscularis.  Section  of  a Portion  of  the 
Muscular  Coat  of  the  Stomach. — ( From  the  Author's  Clinic .) 

Objective,  one-sixth.  Eyepiece,  one  inch.  Stain,  hematoxylin  and  orange  G.  X about  320 
diameters. 

Cross-section  of  bundles  of  muscle-fibers  from  the  muscular  coat  are  shown,  A,  between  which 
there  are  a large  number  of  small  round  cells,  B,  B,  in  places,  and  here  and  there  large  clumps 
of  cancer  cells,  C,  C , C,  C,  a few  of  which  show  the  attempt  at  pseudo-glandular  formation,  D , Z>, 
in  some  instances  arranging  themselves  in  complete  circles,  while  in  others  only  a portion  of  an 
acinus  is  formed. 


glandular  structure  becomes  very  distinct,  for  here  cylindrical  cells 
may  be  seen  lining  tubular,  hollow  spaces  in  a regular  manner, 
these  tubular  ducts  being  separated  by  connective  tissue,  which 
35 


530 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


generally  shows  small-celled  infiltration ; nor  are  these  glandular 
hollow  spaces  always  regular  in  distribution  or  in  size.  The  order 
of  the  lining  cell  is,  in  so  far,  a typical  one,  as  the  whole  cavity  is 
filled  with  cells  of  which  only  the  outer  ones  are  cylindrical  and 
arranged  in  regular  order,  while  the  rest  show  very  irregular  re- 
lations, both  in  form  and  position.  The  cylindrical  cell  carcinoma 
is  most  frequently  found  in  the  pyloric  region,  its  favorite  place 
being  close  to  the  valve,  and  generally  sharply  limited  toward  the 
duodenum.  It  is  probable  that  the  neoplasm  originates  here  from 
the  pyloric  glands,  while  at  other  locations  of  the  stomach  the  sur- 
face epithelium  and  the  cylindrical  cells  of  the  gland  vestibules 
form  -the  bases  of  origin.  The  papillary  forms  of  these  cancers 
particularly  have  a tendency  to  grow  toward  the  surface,  for  they 
may  last  a long  time ; i.  e .,  the  cancer  mass  may  assume  a con- 
siderable size  before  the  infiltration  will  invade  the  outer  layers  of 
the  stomach  wall.  The  development  of  secondary  carcinomata 
may  also  take  a long  time,  so  that  with  very  large  malignant 
neoplasms  perhaps  only  one  or  a few  lymph  glands  will  be  found 
secondarily  involved.  Finally,  ulcerations  of  the  surface  may  pro 
long  development ; or,  if  a loss  of  substance  does  occur,  it  may  be 
compensated  for  by  proliferation  of  the  tumor  tissue ; eventually, 
however,  with  the  co-operation  of  necrosis,  a larger  destruction 
occurs.  The  ulceration  is  usually  surrounded  by  a projecting 
fungus-like  wall. 

Occasionally  the  ensuing  necrosis — which  presumably  arises 
from  disturbances  in  the  circulation — may  become  so  extensive 
that  the  entire  tumor,  with  the  exception  of  very  few  remnants, 
•may  be  sloughed  off,  leaving  behind  an  ulcerating  base.  The  break- 
down and  destruction  of  the  tumor  mass  frequently  progresses  in 
a gangrenous  manner,  and  then  we  may  find  not  only  formations 
of  cavities  within  the  tumor,  but  the  entire  stomach  walls  may  also 
be  perforated,  while  large  cancerous  proliferations  are  still  left 
close  to  the  perforation. 

The  second  main  type,  the  soft  glandular  or  medidlary  car- 
cinoma, likewise  forms  knotty  projections  on  the  inner  surface  of 
the  stomach,  but  it  is  very  rare  that  these  are  observed  intact;  on 
the  contrary,  this  type  of  cancer  usually  appears  at  the  necropsy 
as  a cancerous  ulceration.  Its  form  is  quite  characteristic.  It  pre- 
sents a navel-like,  deepened  center  and  an  external  surrounding 
wall  which  is  formed  by  the  mass  of  the  tumor;  it  is  either  broad 
or  narrow,  high  or  low;  at  times  it  exhibits  a uniform  appear- 


ADENOCARCINOMA  OF  THE  STOMACH. 


531 


ance  ; again,  it  is  irregularly  ragged  in  outline.  In  the  bowl-shaped 
central  depression  the  tumor  mass  is  found  breaking  down  in 
fragments,  or,  occasionally,  this  depression  may  be  found  smooth, 
since  the  more  resistant  muscularis  may  have  been  exposed  and  is, 


Fig.  37. — A Portion  of  an  Area  in  the  Submucosa,  Largely  Composed  of  Groups  of 
Cancer  Cells. — ( From  Author's  Clinic .) 

Objective,  one-sixth.  Eyepiece,  one  inch.  Stained  with  hematoxylin  and  orange  G.  X about 
320  diameters. 

The  fibrous  tissue  of  the  mucosa  is  infiltrated  with  many  small  round  cells,  which  in  some 
places  are  very  numerous,  A , A.  The  most  prominent  change  appears  in  the  numerous  clumps 
of  cancer  cells,  most  all  of  which  lie  in  open  spaces  in  the  tissue,  B.  These  clumps  are  like  those 
seen  in  other  coats  of  the  stomach,  but  the  attempt  at  glandular  formation  is  more  marked  here 
than  in  any  other  locality,  C,  C.  In  the  upper  part  of  the  cut  is  seen  the  lower  portion  of  the  mus- 
cularis mucosae,  D,  D,  infiltrated  with  many  small  round  cells,  and  containing  a few  of  the  masses 
of  cancer  cells. 


presumably,  destroyed  much  more  slowly  than  the  other  layers  by 
the  action  of  the  gastric  juice.  In  this  tumor  also  the  destruction 
may  go  on  to  complete  perforation  of  the  gastric  wall.  The  masses 


532 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


of  the  tumor  which  surround  the  ulceration  denote  more  or  less  ex- 
tensive retrogressive  metamorphoses,  accompanied  by  hemorrhages, 
and,  not  rarely,  an  ichorous  deterioration  of  the  tumor  mass.  On 
microscopical  examination  of  these  masses,  it  is  noticed  that  the 
cancer  cells  are,  as  a rule,  quite  small  and  irregularly  shaped,  simi- 
lar to  oxyntic  cells,  but  that  their  numbers  far  exceed  the  stroma, 


Fig.  38. — Section  of  Tissue  Near  the  Base  of  a Carcinomatous  Ulcer,  Showing  Micro- 
organisms.— ( From  Author's  Clinic.) 

Objective,  one-twelfth.  Eyepiece,  one  inch.  Stained  with  methyl-violet,  anilin-oil  solution  by 
Gram’s  method.  X 1060  diapieters. 

a , a , a.  The  Oppler-Boas  bacillus,  singly  and  in  chains.  The  peculiar  base-ball  bat  shape  is 
shown  in  some  cases,  while  in  others  it  is  seen  that  one  end  of  the  rod  is  narrow  and  the  other 
broad,  the  change  in  size  being  sudden.  Some  of  the  rods  stain  solidly,  while  in  others  there  are 
clear  spaces. 

b,  b,  b.  A micrococcus  which  occurs  singly  and  in  clumps,  but  never  in  chains.  These,  as  well 
as  the  Oppler-Boas  bacillus  and  the  next  organism  to  be  described,  were  found  both  in  the  necrotic 
tissue  over  the  base  of  the  ulcer  and  in  the  healthy  tissue  below  the  same. 

c,  c,  c.  A peculiar  yeast-like  organism,  that  is  probably  some  protozoan.  It  is  much  smaller 
than  a yeast  cell.  Budding  forms  are  seen,  and  the  granular  protoplasm  in  some,  and  the  few 
large  deeply  staining  dots  in  others,  are  well  represented. 


which  in  many  places  consists  chiefly  of  very  thin,  delicate  parti- 
tions. Larger  supporting  partitions  of  the  stroma  exist,  of  course, 
in  addition  to  these,  and  in  this  latter  type  “ small-celled  infiltra- 
tion ” is  regularly  present.  Microscopical  examination  evinces  the 
fact  that  the  soft  glandular  cancer  rapidly  invades  the  exterior 
gastric  layers,  for  small  nodules  (tumor  knots)  appear  at  the  serosa  at 
an  early  stage,  which  nodules  distinctly  show,  and  correspond  to, 


MEDULLARY  CARCINOMA. 


533 


the  course  of  the  lymphatic  vessels.  These  nodules  have  arisen 
by  a direct  advance  of  the  cancer  into  and  through  the  muscular 
layer,  in  which,  microscopically,  a distinct  thickening  is  observed, 
this  thickening  being  dependent  upon  proliferation  of  the  mus- 
cular substance  itself,  as  well  as  upon  a broadening  of  the  inter- 
muscular connective  septa.  ( Fig.  36.)  Examining  microscopically 
a section  through  the  muscularis,  it  at  once  becomes  evident 
that  the  cancer  masses,  in  their  invasions  between  the  muscular 
fibers,  follow  the  septa  which  conduct  the  lymphatic  vessels. 
In  older  cases,  small  foci  are  found  in  the  muscle-bundles  them- 
selves, where  they  have  forced  apart  the  muscle  cells  to  assume  the 
shape  of  spindle-like  spaces.  As  the  growth  of  the  carcinoma  is 
much  more  restricted  in  the  denser  and  closer  netted  muscularis 
than  in  the  subserosa,  the  cancer  masses  outside  of  the  muscular 
layer  are  generally  considerably  more  voluminous  than  those 
within  it.  The  (soft)  medullary  carcinoma  may  extend  toward  the 
surface  as  well  as  toward  the  interior,  and  it  will  then  be  seen  that 
it  habitually  follows  preformed  passages — namely,  along  the  peri- 
lymphatic spaces.  In  very  rare  cases  this  neoplasm  may  extend  over 
the  whole  stomach,  except,  possibly,  the  fundus;  and  in  such  a 
case  Orth  has  found  that  the  entire  lymphatic  network  of  the 
mucosa,  as  well  as  of  the  submucosa,  was  filled  with  cancerous 
masses.  The  greater  tendency  of  the  medullary  carcinoma  for 
local  dissemination  corresponds  to  its  relations  toward  the  general 
organism.  With  this  neoplasm  particularly,  one  finds  extensive 
lymphatic  gland  carcinomata,  not  only  in  the  epigastric,  celiac, 
portal,  and  retroperitoneal,  but  also  very  frequently  in  the  left 
supraclavicular  lymph-glands ; one  may  find  metastases  in  the 
lymph-  as  well  as  in  the  blood-channels,  and,  besides,  a dissemina- 
tion of  cancerous  nodules  in  the  abdominal  cavity. 

Concerning  the  seat  of  medullary  cancers,  it  may  be  said  that 
they  are  not  limited  to  any  particular  part  of  the  stomach,  for  they 
may  be  found  at  the  cardia,  the  anterior  and  posterior  walls, and  the 
lesser  curvature  as  well  as  in  the  pyloric  region,  for  which  they 
have  an  unmistakable  affinity.  Frequently,  cancers  of  the  cardia 
extend  to  the  esophagus,  while  the  duodenum  remains  intact. 

The  scirrhus  (meaning  hard  glandular)  is  distinguished  from  the 
two  preceding  types  of  carcinoma  mainly  by  its  hardness.  It  pro- 
duces no  large  tumor  nodules,  but  rather  simple  thickenings  of  the 
entire  wall.  The  surface  of  the  mucosa  shows,  as  a rule,  a flat  ulcer- 
ation, which  has  either  a smooth  or  an  actually  cicatricial  basis,  or 


534 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


else  a papillomatous,  irregular,  and  corroded  appearance.  The  edges 
of  the  ulcerations  are  generally  entirely  flat,  without  a trace  of  the 
wall-like  elevation,  and  for  that  reason  the  transition  into  the  sur- 
rounding mucosa  is  very  gradual.  On  cutting  through  a scirrhous 
gastric  wall  considerable  resistance  is  met  with,  so  that  the 
tissue  actually  grates  on  cutting.  Microscopical  section  reveals  a 
thickening  of  all  layers,  particularly  of  the  muscularis,  by  a gray- 
ish-white, striated,  cicatricial  connective  tissue.  Typical  cancer- 
ous proliferation  is  not  apparent  on  the  mucosa  nor  in  the  remain- 
ing layers  of  the  gastric  wall,  so  that  it  may  be  doubtful  whether 
one  is  dealing  with  a cancer  or  with  a simple  chronic  ulcer.  To 
decide  this  question  one  must  observe  the  relation  of  other  parts, 
and,  particularly,  search  for  secondary  cancer  formation. 

As  a matter  of  fact,  one  occasionally  sees  small,  flat  tumor 
nodules  on  the  serosa  directly  over  the  neoplasm ; but  as  exten- 
sive adhesions  of  the  pylorus  with  neighboring  organs  (liver,  intes- 
tine, omentum)  are  invariably  present  with  this  form  of  cancer, 
implicating  the  peritoneum,  such  nodules  are  difficult  to  recognize, 
even  if  they  are  present.  A more  reliable  sign  is  the  condition  of 
the  lymphatic  glands,  which  usually  show  cancer  formation  ; and, 
besides  this,  the  liver  and  other  organs,  which  are  otherwise  rarely 
invaded  (for  instance,  the  spinal  column),  may  be  found  to  contain 
it.  Such  cases  easily  give  rise  to  deception,  because  these  second- 
ary tumors  may  show  a medullary  structure  and  attain  con- 
siderable size,  in  which  case  the  seemingly  unimportant  scirrhous 
ulceration  in  the  stomach  may  be  overlooked.  The  surest  indica- 
tion of  the  character  of  these  changes  is  obtained  from  microscop- 
ical examination,  though  in  a section-preparation  hardly  anything 
else  but  fibrous  connective  tissue  is  seen,  particularly  in  the  very 
much  thickened  muscularis,  which  is  permeated  with  broad,  gray- 
ish-white stripes.  But  when  a larger  number  of  preparations  are 
carefully  examined  the  histological  peculiarities  of  carcinoma, 
the  connective-tissue  stroma,  and  carcinoma  bodies  are  discovered. 

The  last-named  are  diminutive  and  consist  of  small-celled  rows. 
The  stroma  is  massive,  and  composed  of  tough,  rigidly  fibered  con- 
nective tissue.  The  longitudinal  direction  of  the  small  cell-rows  is 
parallel  to  the  course  of  the  fibers  of  the  stroma.  It  is  noteworthy 
that  the  secondary  cancer  nodules  of  scirrhus  are  richer  in  cells, 
and  therefore  more  closely  resemble  the  medullary  carcinoma; 
and  also  that,  alongside  entirely  fibrous  places  in  the  gastric  wall, 
here  and  there  at  the  edges  of  the  ulcerations  places  can  be  found 


THE  GASTRIC  SCIRRHUS. 


535 


where  the  cancer  cells  are  not  as  yet  so  scarce  in  proportion  to  the 
stroma,  and  where  the  latter  does  not  as  yet  possess  the  character- 
istic callous  consistency.  It  may,  from  this,  be  concluded  that  the 
scirrhus  is,  in  fact,  an  atrophic  cancer  ( cancer  atrophicans) — i.  e.} 
that  the  callous  formation  represents  nothing  more  than  a later 
stage,  or  result,  of  the  initial  cancerous  process.  The  question  has 
arisen  whether  complete  healing  may  not  be  produced  by  a total 
callous  metamorphosis  of  the  neoplasm  ; but,  up  to  the  present 
time,  no  convincing  observations  confirmatory  of  this  question 
have  been  made.  It  is  reasonable  to  assume  that  a very  localized 
callous  cicatricial  healing  may  be  brought  about  in  certain  places, 
while  in  other  portions  (the  very  youngest  parts  of  the  neoplasm) 
very  slow  but  gradual  cancerous  progress  is  made.  The  callous 
stroma  of  the  scirrhus  has  a tendency  to  contract  such  formations. 

This  fact  is  of  great  significance,  when  the  microscopical  rela- 
tion of  the  scirrhus  is  considered,  for  it  explains  the  stenosis  which 
it  causes  at  the  pylorus, — its  almost  exclusive  locality.  This 
constriction  is  further  increased  by  the  very  much  thickened  and 
callus-like  alteration  of  the  gastric  wall,  which  becomes  unresis- 
tant  and  inelastic,  resembling  a hard  rigid  ring,  or  stiff  tube. 
It  is  self-evident  that  a pylorus  changed  in  this  manner  is  no  longer 
capable  of  closing  off  the  stomach  toward  the  duodenum  (incon- 
tinence of  the  pylorus).  The  extent  of  the  scirrhus  from  the 
pylorus  toward  the  cardia  may  be  variable,  rare  cases  occurring  in 
which  the  entire  gastric  wall  is  in  a state  of  scirrhous  degeneration. 
The  entire  organ  is  then,  as  a rule,  considerably  contracted,  and  at 
the  same  time  the  walls  are  very  much  thickened.  On  the  inner 
surface  little  mucous  membrane  remains  in  these  cases.  We  have 
seen  elsewhere  that  a similar  condition  may  be  brought  about  by 
chronic  inflammation  (hyperplastic  gastritis,  cirrhosis  of  the  stom- 
ach). The  differential  diagnosis  is  very  difficult  to  establish  from 
the  local  conditions,  but  the  majority  of  stomach  contractions  are 
to  be  attributed  to  scirrhus  (Orth,  loc.  cit.).  At  any  rate,  it  is  well 
always  to  think  first  of  all  of  this  neoplasm. 

The  colloid  carcinoma  in  typical  cases  has  a very  characteristic 
appearance.  It  does  not  produce  circumscribed  tumor  masses  so 
much  as  diffuse  thickenings  of  the  entire  wall  similar  to  scirrhus. 
In  this  growth  the  stroma  is  not  a bright  fibrillar  tissue,  but  a gela- 
tinous, translucent,  colorless  or  light-brown  material.  These 
masses  are  recognizable  on  the  inner  surface,  which,  as  a rule, 
presents  an  extended  flat  ulceration.  Where  the  tumor  tissue  lies 


536  MALIGNANT  TUMORS  OF  THE  STOMACH. 

exposed  there  appears  a distinct,  alveolar,  grayish  framework, 
which  incloses  the  colloid  granules,  in  dimension  the  size  of  a pin- 
head or  a millet  seed.  The  whole  mass  has  a slimy,  mucoid 
feeling,  but  it  is  not  nearly  so  soft  as  genuine  mucus.  Micro- 
scopically a similar  picture  obtains  ; for  here,  also,  the  connective- 
tissue  alveolar  framework,  containing  a transparent  mucocolloid 
mass  in  its  meshes,  is  prominent.  This  mass  may  be  entirely 
devoid  of  cellular  elements,  but  generally  a number  of  cells  and 
cell  fragments  are  detected,  in  which  it  can  be  distinctly  recog- 
nized that  these  cells  themselves  furnish  the  colloid  material  of  the 
alveoli,  for  one  frequently  sees  many  cells  in  a swollen  state,  either 
with  hyaline  granules  or  in  a condition  of  disintegration.  In  other 
places  cells  may  be  found  in  better  preservation,  while  the  colloid 
matter  is  not  so  pronounced,  so  that,  in  this  form  of  carcinoma, 
just  as  in  scirrhus,  there  are  transitions  to  the  medullary  type. 
Here,  likewise,  the  youngest  portions  of  the  growth  are  those 
most  rich  in  cellular  elements,  and  production  of  colloid  material  is 
a phenomenon  which  occurs  in  the  course  of  further  development 
of  the  tumor. 

“ Colloid  tissue  ” several  centimeters  thick  may  be  found  through- 
out the  entire  gastric  wall,  and  here  again  the  lymph-vessels  offer 
the  channels  in  which  the  cancerous  masses  take  their  course,  and 
in  which  they  ramify  both  interiorly  and  superficially.  Occasionally, 
larger  colloid  tumor  nodules  may  appear  on  the  serosa;  and,  in 
fact,  the  colloid  carcinoma  not  rarely  invades  the  peritoneum  and 
produces  an  extensive  carcinosis — as  a result  of  which  the  omen- 
tum is  transformed  into  a short,  thick,  and  board-like  band.  Af- 
fections of  the  lymphatic  glands,  liver,  lungs,  and  other  organs,  are 
by  no  means  absent.  The  colloid  carcinomata  also  have  their 
favorite  location  in  the  pyloric  region,  whence  they  may  extend  to 
the  duodenum,  and  also  to  the  liver,  by  direct  continuity.  The 
extension  to  the  liver  generally  occurs  after  the  formation  of  a 
previous  adhesion.  A transition  to  the  esophagus  from  the  cardia 
has  likewise  been  observed.  Although  the  colloid  carcinoma  pro- 
duces no  large  prominent  tumors,  it  may  extend  far  over  the  gastric 
surface,  and  frequently  takes  in  the  entire  wall,  reducing  the  size  of 
the  stomach  somewhat,  but  not  to  such  a degree  as  scirrhus.  The 
wall  is  hard  and  immovable,  the  inner  surface  ulcerated,  the  outer 
coarsely  granular  from  small  and  large  cancerous  nodules  of  the 
peritoneal  covering. 

Although  the  ulcerations  of  the  colloid  carcinoma  may  have 


STRUCTURAL  EFFECTS  OF  GASTRIC  CANCERS. 


537 


considerable  superficial  extent,  still  a perforation  rarely  results, 
although  the  ulcerations  may,  at  places,  reach  even  to  the  perito- 
neum. The  colloid  tissue  is  not  subject  to  rapid  disintegration, 
hence  new  tumor  masses  may  be  formed  in  front  of  the  basis  of 
ulceration. 

Structural  Effects  of  Malignant  Gastric  Neoplasms. — The 

development  of  gastric  carcinoma  is  accompanied  by  adhesions  of 
the  serosa  with  the  pancreas,  liver,  the  transverse  colon,  the  anterior 
abdominal  wall,  and  the  omentum  ; and,  at  the  same  time, there  occurs 
a callous  hyperplasia  of  all  connective  tissue  in  the  immediate  neigh- 
borhood. The  result  is  that  the  stomach,  particularly  the  part 
most  frequently  affected  (namely,  the  pylorus),  becomes  fixed, 
while  in  other  rare  cases  such  adhesions  may  not  be  formed,  and 
the  stomach  is  dislocated  downward  by  the  tumor  masses,  in  which 
case  the  pylorus  may  extend  as  far  as  the  symphysis  pubis.  Fre- 
quently the  cancerous  stomach  exhibits  changes  of  size  and  form. 
We  may  have  diminutions  in  size  accompanying  the  total  degen- 
erations of  stenosing  cardiac  carcinomata,  or,  what  is  more  common, 
dilatation  accompanied  by  marked  muscular  hypertrophy.  The 
dilatations  originate  from  the  obstruction  of  the  passage  through 
the  pylorus,  a pyloric  stenosis  existing.  This  may  be  caused  by  a 
variety  of  circumstances.  Among  the  causes  so  operating  may  be 
mentioned,  in  the  first  place,  a large  tumor  mass  located  in  the 
pyloric  orifice,  acting  like  a cork  or  ball-valve ; secondly,  the  rig- 
idity which  the  walls  undergo  in  scirrhus  and  in  colloid  carcinoma; 
finally,  the  effective  contractions  of  the  scirrhus,  whereby  a consid- 
erable resistance  is  offered  against  the  advance  of  the  gastric  con- 
tents. These  disturbances  may  be  increased  by  a large  variety  of 
inflections  and  dislocations  resulting  from  adhesions,  as  well  as  by 
the  weight  of  the  accumulating  gastric  contents.  Incontinence  of 
the  pylorus  may  occur  contemporaneously  with  stenosis,  but  it 
may  also  exist  in  a very  severe  degree  without  stenosis  where  the 
cancerous  ulceration  has  destroyed  more  or  less  of  the  pyloric  ring. 
These  changes  at  the  pylorus  are  important  because  they  are  very 
frequent,  for,  as  is  evident  from  what  we  have  said  concerning  the 
various  types  of  carcinoma,  the  pyloric  antrum  is  the  most  frequent 
seat  of  cancer  formation.  According  to  the  statistics  of  William 
H.  Welch  (“  A System  of  Practical  Medicine  by  American  Authors,” 
edited  by  William  Pepper,  vol.  n,  p.  561),  the  frequency  of  carcino- 
mata occurring  at  the  pyloric  region  is  60.8  per  cent. ; at  the  lesser 
curvature,  1 1.4  per  cent. ; at  the  cardia,  8 per  cent. ; at  the  posterior 


538 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


wall,  5.2  per  cent.;  the  whole,  or  the  greater  part  of  the  stomach, 
4.7  per  cent.  According  to  Orth,  60  per  cent,  of  all  gastric  cancers 
invade  the  pylorus;  20  per  cent.,  the  lesser  curvature;  10  per  cent., 
the  cardia ; and  the  rest,  the  remaining  parts  of  the  stomach.  As 
gastric  carcinoma  makes  up  35  to  45  per  cent,  of  all  carcinomata, 
the  great  importance  of  pyloric  cancer  can  be  appreciated.  In  the 
midregions  of  the  stomach  the  cancers  are  limited  to  a portion  of 
the  circumference,  but  in  the  vicinity  of  the  two  openings  they  fre- 
quently occupy  the  entire  circumference  in  a ring-  or  girdle-shaped 
manner. 

The  growth  of  carcinomata  occurs  partly  through  simple  periph- 
eral extension,  partly  through  daughter  nodules  which  develop  at 
some  distance  from  the  main  tumor,  but  sooner  or  later  coalesce 
with  it.  These  nodules  evidently  lie  underneath  the  mucosa, 
which  may  be  movable  over  them  ; hence,  it  may  be  assumed  that 
they  have  arisen  through  infection  by  way  of  the  lymph-channels. 
The  frequent  occupation  of  lymphatic  vessels  by  cancer  masses 
in  the  neighborhood  of  larger  nodules  argues  in  favor  of  this  view. 
Concerning  the  secondary  infection  of  lymph-glands,  it  may  be 
stated  that,  with  gastric  carcinomata,  it  often  happens  that  glands 
are  diseased  which  do  not  receive  their  lymph  from  the  direction 
of  the  stomach ; for  instance,  the  retroperitoneal.  It  is  possi- 
ble that  this  is  caused  by  the  cancerous  impermeability  of  glands 
located  higher  up,  which  compels  a return  of  the  lymph-current. 
Following  the  current  of  the  lymph,  it  has  been  found,  by  Orth 
and  others,  that  the  thoracic  duct  may  be  infected.  Possibly,  the 
infection  of  the  left  supraclavicular  lymph-glands  occurs  in  con- 
nection with  the  transportation  of  cancer-cells  through  the  lymph 
of  the  thoracic  duct.  The  lymph-vessels  of  the  diaphragm  may  be 
entirely  filled  with  cancerous  masses,  and  may  disseminate  the  ele- 
ments of  the  disease  to  the  pleural  cavity,  bronchial  glands,  and 
lungs.  The  author  has  studied  sections  obtained  by  operation 
during  attempts  to  execute  a Heinecke-Mikulicz  pyloroplastic 
operation  from  two  cases  of  what  proved  to  be  gastric  scirrhus 
later  on.  In  neither  case  did  microscopical  examination  reveal 
any  foci  of  cancer  cells  ; a large  number  of  sections  were  examined, 
and  the  appearance  was  that  of  a chronic  hyperplastic  gastritis. 
Nowhere  could  any  small  cell  rows  of  cancer  bodies  be  discovered 
in  the  dense  connective-tissue  stroma.  Later  on,  metastases 
developed,  which  gkve  evidence  of  the  malignant  nature  of  the 
original  gastric  induration.  This  experience  has  led  the  author  to 


STRUCTURAL  EFFECTS  OF  GASTRIC  CANCERS.  539 

urge  gastroenterostomy,  or,  if  possible,  resection  in  all  doubtful 
cases  of  chronic  hyperplastic  gastritis.  If  it  should  happen  that 
a simple  benign  but  hyperplastic  gastritis  is  treated  in  this  way, 
the  patient  will  be  the  gainer  by  the  operation,  for  this  form  of 
gastritis  is  as  fatal  as  the  malignant  types,  owing  to  the  absolute 
rigidity  of  the  stomach  and  loss  of  peristalsis  which  it  produces. 

In  twenty-five  per  cent,  of  all  gastric  cancers  secondary  nodules 
are  contained  in  the  liver.  The  infection  being  transported  by  direct 
extension  after  “adhesive  invasion,” by  the  lymph-current  from  the 
porta  hepatica  or  transportation  by  the  blood-stream,  the  latter 
mode  being  by  far  the  more  plausible.  The  metastases  may  occur 
through  minute  particles  that  are  not  retained  emboli ; whereas, 
in  other  instances,  emboli  can  be  demonstrated  in  the  larger  ves- 
sels, proving  that  such  emboli  can  originate  from  the  stomach, 
because  the  gastric  veins  are  roots  of  the  portal  vein,  and  cancer- 
ous invasion  of  the  veins  of  the  stomach  is  conceded.  The  spread- 
ing of  gastric  cancer  to  the  esophagus,  duodenum,  spleen,  pancreas, 
and  intestines  occurs  by  direct  extension  along  the  paths  that  are 
either  normally  present  or  newly  formed  pathologically.  Participa- 
tion of  the  peritoneum  has  its  foundation  in  the  direct  extension  of 
the  carcinoma  into  the  gastric  serosa ; when,  however,  the  peri- 
toneum is  once  invaded,  the  rest  of  it  is  not  affected  by  continued 
simple  extension  of  the  growth,  although  this  may  occur  with  col- 
loid carcinomata,  but  by  dissemination,  which  means  the  falling  of 
tiny  particles  into  the  peritoneal  cavity  (carcinoma  seed,  as  it  were) 
and  their  attachment  in  suitable  places  (at  first  in  the  deepest  por- 
tions of  the  peritoneum,  in  the  rectovesical  and  rectouterine  pouch). 
It  is  evident  that  gravity  is  an  element  in  the  spreading  of  peritoneal 
carcinoma.  The  ulcerations  of  gastric  cancers  depend  partly  upon 
ichorous  degeneration  and  suppuration  and  partly  upon  the  digest- 
ive influence  of  the  gastric  juice,  which  occasionally  causes  perfora- 
tion of  the  stomach.  The  vessels  of  the  stomach  and  of  the  spleen 
may  be  affected  by  an  inflammatory  gangrenous  ulceration,  which 
may  lead  to  dangerous  hemorrhages,  but  these  cases  are  infrequent. 
Cancerous  ulcerations  are  very  similar  to  the  simple  peptic  ulcer, 
from  which  they  may  be  distinguished  only  by  the  presence  of  the 
tumor  wall,  which,  if  absent,  enhances  the  difficulty  of  distinction 
between  the  two.  If,  indeed,  cancer  masses  are  found  in  the  sur- 
roundings of  such  an  ulceration,  the  questions  may  be  asked,  Has 
the  ulceration  arisen  from  a carcinoma,  or  Has  a simple  gastric 
ulcer  been  secondarily  affected  by  cancer  transformation?  Here 


540 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


the  clinical  history,  as  well  as  the  examination  and  analysis  of  gas- 
tric contents,  may  give  the  desired  information.  Rosenheim  has 
shown  that  normal  or  supernormal  hydrochloric  acid  secretion 
persists  in  the  carcinoma  which  has  secondarily  developed  from  an 
ulcer ; but  when  the  carcinoma  is  the  primary  growth,  the  hydro- 
chloric acid  is  permanently  absent  at  an  early  stage  in  the  disease. 

Anatomically,  it  may  be  stated  that  when  the  ulceration  has  a 
regular  bowl-shaped  appearance,  and  is  on  every  side  surrounded 
by  tumor  masses,  even  where  no  cancer  masses  can  be  found  in  its 
base,  the  carcinomatous  tumor  was  undoubtedly  the  primary,  the 
ulceration  the  secondary,  object;  and,  reversely,  when  a simple 
ulcer,  accompanied  by  all  typical  peculiarities,  presents  a thicken- 
ing only  at  one  side,  the  latter  tumor  mass  must  be  regarded  as 
secondary  and  the  ulcer  as  primary.  The  remaining  gastric 
mucous  membrane  sometimes  shows  insignificant  alterations,  which 
agrees  with  clinical  observations  as  to  gastric  cancers  remaining 
latent.  In  other  cases  a pronounced  chronic  inflammation  is  pres- 
ent, particularly  in  the  immediate  vicinity  of  the  tumor  masses  or 
ulcerations.  A hypertrophy  of  the  musculature  is  frequently 
apparent,  which  partly  depends  upon  alterations  in  the  mucosa 
and  partly  upon  a pyloric  stenosis,  the  latter  being  responsible  for 
the  condition  of  the  gastric  contents,  because  it  provokes  dilatation 
and  its  consequences.  The  loss  of  secretion  and  the  admixture  of 
blood  with  the  gastric  contents  is  directly  traceable  to  the  cancer- 
ous infiltration  or  the  accompanying  gastritis,  or  both.  The  hemor- 
rhages may  arise  by  ulcerative  disintegration,  as  well  as  from  rupture 
of  the  small  vessels  in  the  villous  cancer  proliferations. 

What  is  the  source  or  basis  of  the  primary  development  of  can- 
cer formation  ? According  to  prevalent  views,  all  gastric  carcino- 
mata do  not  originate  from  the  connective  tissue  of  the  submucosa, 
as  was  formerly  believed,  but  from  the  mucosa,  and  particularly 
from  the  glandular,  or  surface,  epithelium  of  the  same,  the  cells  of 
these  carcinomata  having  great  similarity  to  the  various  cells  of  the 
mucosa.  All  gastric  carcinomata  are  therefore  epithelial  tumors. 
We  owe  to  Waldeyer  the  first  exact  investigations  concerning  the 
beginning  of  cancer  formation,  which  have  been  confirmed  later  by 
other  researches.  According  to  him,  the  process  begins  with  an 
enlargement  and  hypertrophy  of  a group  of  ten  or  twelve  glands, 
which,  breaking  through  the  muscularis  mucosae,  enter  the  sub- 
mucosa. The  cells  of  these  gland-ducts  react  differently  to  stain- 
ing reagents,  being  colored  much  deeper,  and  filling  the  lumen 


ORIGIN  OF  GASTRIC  CANCER. 


541 


of  the  gland  in  an  irregular  manner.  A further  step  is  that  the 
connective  tissue  of  the  mucosa,  and  particularly  of  the  submucosa, 
undergoing  a transformation  into  granulation  tissue,  advances  and 
is  pushed  up  against  the  aggregations  of  epithelial  cells,  which  are 
thus  forced  apart  and  inclosed  in  groups  by  the  connective  tissue, 
giving  rise  to  the  cancer  alveoli  and  cancer  bodies  (cancer  cells). 
Accepting  this  as  a general  rule,  the  question  arises,  What  causes 
this  gland  group  and  the  adjoining  connective  tissue  to  enter  upon 
this  abnormal  growth  ? Cohnheim  says  that  abnormal  conditions 
of  primitive  germinal  tissue  are  present  here,  a remnant  of  unused 
primitive  cells  from  which  the  proliferation  starts.  This  is  a 
hypothesis  which  can  admit  of  no  proof,  since  after  the  prolifera- 
tion has  occurred  it  is  impossible  to  obtain  any  knowledge  of  the 
condition  of  the  locality  that  existed  there  prior  to  the  prolifera- 
tion. But  even  admitting  Cohnheim’s  theory,  we  must  ask,  Why 
do  these  embryonic  cells  suddenly  begin  to  grow  after  many  years? 
There  must  evidently  be  some  other  incentives  to  growth. 

There  is  undoubtedly  some  disposition  toward  the  development 
of  gastric  cancers  with  advancing  age.  What  the  nature  of  this 
predisposition  is  we  do  not  know.  There  seems  to  be  no  predis- 
position of  sex,  for  both  sexes  are  attacked  with  equal  frequency. 
The  pronounced  tendency  which  the  structures  of  the  pylorus  ex- 
hibit toward  cancerous  infection  attracts  attention  to  the  mechani- 
cal relations  there  existing.  Hauser  has  made  some  interesting 
observations  on  the  development  of  cancers  from  simple  peptic 
ulcers.  He  has  shown  that  the  gastric  secretory  glands  at  the 
edges  of  healing  ulcers  undergo  a proliferation  which  may  be 
augmented  to  a cancerous  neoplasm,  and  he  seeks  the  explanation 
for  this  process  in  an  increased  supply  of  nutritive  material  to  the 
glands,  and  in  a reduction  of  the  resistance  of  the  adjoining  tissues 
in  consequence  of  an  ulcerative  and  cicatricial  process. 

As  frequent  as  primary  carcinomata  are,  just  so  rare  are  the 
secondary.  Secondary  cancers  may  arise  in  the  stomach  by  direct 
extension  from  the  immediate  surroundings.  In  this  manner  a 
cancer  might  extend  to  the  gastric  walls  from  the  pancreas,  liver, 
and  lymphatic  glands.  Clinically,  the  most  important  of  the  primary 
carcinomata  is  the  esophageal,  which,  when  it  is  located  at  the  car- 
dia,  may  invade  the  stomach.  Reversely,  the  extension  of  gastric 
cancer  into  the  esophagus  is  really  more  frequent.  There  is  another 
kind  of  extension  of  esophageal,  lingual,  and  facial  carcinomata  to 
the  stomach,  which  is  not  transmitted  by  the  lymph-  or  blood- 


542 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


channels,  but  by  a direct  implantation  of  cancer  cells  upon  the 
mucosa.  Klebs  was  the  first  to  report  three  of  such  cases,  and 
Beck  has  investigated  a case,  concerning  which  he  assumes,  on  the 
strength  of  his  microscopical  preparations,  that  the  loosened  parts 
of  the  esophageal  cancer  had  fastened  themselves  in  the  gastric 
glands.  The  new  nodules  which  were  thus  formed  were  flattened 
epithelium  carcinomata,  composed  of  the  typical  pavement-epithe- 
lium of  the  esophagus.  This  raises  the  interesting  question 
whether  the  new  tumors  arise  solely  and  exclusively  from  the  im- 
planted tumor  cells,  or  whether  these  cells  produce  a kind  of  infec- 
tion of  the  local  cells  upon  which  they  fall,  so  that  the  latter  are 
converted  into  pavement-epithelium  cancer  cells.  Klebs  assumes 
the  latter  view,  but  Beck  leaves  the  question  undecided.  In  the 
place  occupied  by  the  tumor  that  he  investigated,  no  gastric  cells 
were  observable,  and  also  no  transition  forms  to  pavement  cells. 
The  secondary  cancers  of  the  peritoneum,  already  described,  arise 
in  a similar  manner — namely,  by  the  falling  of  cancer  particles  into 
the  peritoneal  cavity.  Reversely,  it  has  been  observed  that  an 
implantation  carcinoma  may  arise  upon  the  gastric  serosa  from  a 
deeper  portion  of  the  abdominal  cavity.  Orth  describes  a case  in 
which  the  inner  mucous  membrane  of  the  pylorus  showed  a typical 
cylindrical  cell  carcinoma,  while  the  serosa  of  the  same  viscus 
revealed  a pronounced  colloid  nodule  as  large  as  a walnut,  which 
could  not  have  arisen  in  any  other  way  except  by  implantation 
from  a colloid  carcinoma  of  the  cecum.  Another  mode  of  second- 
ary cancer  formation  is  that  of  metastasis  by  way  of  the  blood- 
vessels, these  secondary  neoplasms  corresponding  to  the  primary 
tumors  in  structure,  and  being  recognizable,  according  to  Grawitz, 
as  secondary  by  their  circumscribed  character.  These  secondary 
forms  are  rare. 

The  theory  of  infection  for  the  origin  of  gastric  cancers  would 
not  explain  the  great  variety  of  the  histogenesis  of  the  carcinoma. 
In  accepting  the  existence  of  a “ cancer-producing  microbe,”  one 
would  have  to  assume  that  this  organism  could  produce  a trans- 
formation of  connective  tissue  into  epithelium,  or  that  it  regularly 
produced  proliferation  only  in  one  kind  of  tissue — namely,  the  epi- 
thelial. A pathogenic  micro-organism  with  these  qualities  is  un- 
known at  the  present  time.  In  the  formation  of  metastases  only 
the  transported  cancer  cells  keep  on  proliferating  in  the  new  organ, 
while  the  tissue  of  this  organ  either  does  not  participate  at  all,  or 
only  to  a small  degree,  in  the  formation  of  the  new  cancer  nodule. 


THEORY  OF  INFECTIOUS  ORIGIN  OF  CANCER.  543 

In  the  transportation  of  tuberculous  tissue,  however,  it  is  this  tis- 
sue which  breaks  down,  and  the  new  tuberculous  focus  develops 
from  the  invasion  of  the  transported  tubercle  bacilli,  which  not  only 
cause  a disease  of  the  epithelium,  but  also  of  the  remaining  tissues 
(connective  tissue,  bone,  etc.)  with  which  they  come  in  contact. 
Transplantation  of  carcinoma  into  animals  has  very  rarely  suc- 
ceeded, whereas  inoculations  of  infectious  diseases  are  generally 
successful.  Another  explanation  of  the  development  of  cancer  has 
been  attempted  in  the  so-called  “ irritation  theory,”  which  is  based 
upon  the  susceptibility  of  the  two  openings  of  the  stomach  to 
greater  irritation  during  digestion  than  other  parts;  these  portions 
are  consequently  most  frequently  affected  (sixty  to  seventy  per  cent, 
of  all  cases);  but  satisfactory  proof  that  this  irritation  may  cause 
cancer  per  se  is  wanting.  We  have  elsewhere  stated  the  percent- 
age of  cancers  occurring  at  various  decades  of  life : According  to 
the  statistics  of  Welch,  Brinton,  and  Lebert,  three-fourths  of  all 
cancers  occur  from  the  fortieth  to  the  seventieth  year,  and  from  the 
thirtieth  to  the  seventieth  year  ninety-five  per  cent,  of  all  gastric 
cancers  manifest  themselves.  So  far  as  we  know,  only  one  case  of 
congenital  cancer  that  was  limited  to  the  stomach  has  been  reported 
(Wilkinson).  There  has  been  one  case  of  congenital  cancer  com- 
bined with  carcinoma  of  other  organs  (Widerhofer):  We  found  in 

the  literature  on  this  subject  a case  of  gastric  cancer  in  a child  five 
weeks  old  (Cullingworth).  Three  other  cases  in  children  some- 
what older  are  reported  by  Scheffer.  (The  subject  of  the  etiology 
of  cancer  is  reviewed  in  an  interesting  article  by  Roswell  Park, 
“ N.  Y.  Med.  Record,”  vol.  lii,  No.  i,  July  3,  1897.) 

Heredity. — It  is  generally  accepted  that  the  predisposition  to 
cancer  may  be  inherited.  According  to  Fleischer,  the  life  insur- 
ance companies  in  Germany  have  increased  their  premiums  for 
candidates  in  whose  families  gastric  carcinoma  has  been  observed. 
Napoleon  I,  his  sister,  and  his  father  died  of  gastric  carcinoma. 

Geographical  Distribution. — The  geographical  distribution  of 
gastric  cancer  is  very  irregular,  for  while  it  is  very  rare  in  some 
countries, — as  in  Turkey,  Egypt,  and  the  tropics, — it  is  said  to  be 
very  frequent  in  Thuringen,  in  Suabia,  in  Normandy,  and  in  Swit- 
zerland. The  causes  of  this  unequal  distribution  are  unknown. 
In  Egypt  gastric  cancers  are  unknown  (Griesinger),  but  gastritis 
and  enteritis  are  of  common  occurrence.  This  seems  to  show  that 
a genetic  relation  between  gastritis,  enteritis,  and  carcinoma  does 
not  exist.  According  to  Eichhorst  and  Haeberlin,  two  per  cent. 


544 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


of  all  deaths  in  Switzerland  are  caused  by  gastric  cancer.  From 
mortuary  statistics,  Tanchou  (“  Rech.  sur  le  Traitement  Med.  des 
Tumeurs  du  Sein,”  Paris,  1844)  estimates  the  frequency  of  gastric 
cancer  as  compared  with  that  of  all  the  causes  of  death  at  0.6 
per  cent.;*  Virchow,  at  1.9  per  cent.;  Wyss,  at  2 per  cent.;  and 
D’Espine,  at  2)/2  per  cent.  In  8468  autopsies,  chiefly  from  English 
hospitals,  Brinton  found  gastric  cancer  recorded  in  1 per  cent,  of 
the  cases.  Gussenbauer  and  von  Winniwarter  found  gastric  cancer 
recorded  in  1 y2  per  cent,  of  the  61,287  autopsies  in  the  Patholog- 
ical Anatomical  Institute  of  the  Vienna  University.  From  an 
analysis  of  11,175  autopsies  in  Prague,  Welch  found  gastric  cancer 
in  3 y2  per  cent,  of  the  cases. 

Welch  has  collected  and  analyzed,  with  reference  to  this  point, 
the  statistics  of  death  from  all  causes  in  the  city  of  New  York  for 
the  fifteen  years  from  1868  to  1882  inclusive,  and  reported  that 
of  444,564  deaths  during  this  period,  cancer  of  the  stomach  was 
assigned  as  the  cause  in  1548  cases,  and  cancer  of  the  liver  in  867 
cases.  Some,  at  least,  of  these  so-called  cancers  of  the  liver 
may  be  reckoned  gastric  cancers.  This  would  make  the  ratio  of 
gastric  cancer  to  all  causes  of  death  about  0.4  per  cent.,  and 
nearly  1 per  cent.  (0.93  per  cenf.)  if  only  the  deaths  from 
twenty  years  of  age  upward  be  taken,  gastric  cancer  hardly  ever 
occurring  under  that  age.  It  is  a fair  presumption,  also,  that  in 
New  York  not  over  1 in  200  of  the  deaths  occurring — at  all  ages 
and  from  all  causes — is  due  to  cancer  of  the  stomach,  and  that 
about  1 in  100  of  the  deaths  from  twenty  years  of  age  upward  is 
due  to  this  cause. 

The  following  table  (by  William  H.  Welch,  loc.  cit .)  gives  the  age 
in  2038  cases  of  gastric  cancer,  obtained  from  trustworthy  sources 
and  arranged  according  to  decades  : 


Age,  . . . 

10-20 

20-30 

30-40 

40-50 

50-60 

60-70 

70-80 

80-90 

90-100 

Over 

10 

No.  of  Cases, 

2 

55 

271 

499 

620 

428 

140 

20 

2 

■ 

Per  cent.,  . 

0. 1 

2.7 

13-3 

24.5 

3°-4 

21 

6.85 

1 

0. 1 

0.05 

From  this  analysis  we  may  conclude  that  three-fourths  of  all 


* Tanchou’s  statistics  are  based  upon  an  analysis  of  382,851  deaths  in  the  Department 
of  the  Seine  (see  Welch,  loc.  cit .,  p.  532). 


AGE  AND  LOCATION. 


545 


gastric  cancers  occur  between  forty  and  seventy  years.  The 
absolutely  largest  number  is  found  between  fifty  and  sixty 
years;  but,  taking  into  consideration  the  number  of  those  living, 
the  liability  to  gastric  cancer  is  as  great  between  sixty  and 
seventy  years.  Nevertheless,  the  number  of  cases  between  thirty 
and  forty  years  is  considerable,  and  the  occurrence  of  gastric  cancer 
even  between  twenty  and  thirty  is  not  so  exceptional  as  is  often 
represented,  and  is  by  no  means  to  be  ignored.  The  liability  to 
gastric  cancer  seems  to  lessen  after  seventy  years  of  age,  but  here 
the  number  of  cases  and  the  number  of  those  living  are  so  small 
that  it  is  hazardous  to  draw  positive  conclusions. 

Location. — The  following  table  gives  the  situation  of  the 
tumor  in  1300  cases  of  cancer  of  the  stomach  (from  article  by 
William  H.  Welch,  loc . cit.) : 


Pyloric 

Region. 

Lesser 

Curva- 

ture. 

Cardia. 

Pos- 

terior 

Wall. 

Whole  or 
Greater 
Part  of 
Stomach. 

Mul- 

tiple 

Tumors. 

Greater 

Curva- 

ture. 

An- 

terior 

Wall. 

Fundus. 

791 

148 

104 

68 

6l 

45 

34 

30 

19 

60.8 

11 -4 

8 

5-2 

4-7 

3-5 

2.6 

2-3 

i-5 

per  cent. 

per  cent. 

per  cent. 

per  cent. 

per  cent. 

per  cent. 

per  cent. 

per  cent. 

per  cent. 

From  this  table  it  appears  that  three-fifths  of  all  gastric  cancers 
occupy  the  pyloric  region  ; but  it  is  not  to  be  understood  that  in 
all  of  these  cases  the  pylorus  itself  is  involved.  In  four-fifths  of 
the  cases  the  comparatively  small  segment  of  the  stomach  repre- 
sented by  the  cardia,  the  lesser  curvature,  and  the  pyloric  region, 
is  the  part  affected  by  gastric  cancer.  The  lesser  curvature  and  the 
anterior  and  posterior  walls  are  involved  more  frequently  than  ap- 
pears from  the  table,  inasmuch  as  many  cancers  assigned  to  the 
pyloric  regions  extend  to  these  parts.  The  fundus  is  the  least 
frequent  seat  of  cancer.  In  the  cases  classified  as  involving  the 
greater  part  of  the  stomach  the  fundus  often  escapes. 

Frequency. — Malignant  disease  is  on  the  increase  in  this  country  . 
The  death-rate  from  cancer  in  New  York  city  was  1.82  per  cent,  from 
1874  to  1884,  but  from  1884  to  1894  the  death-rate  from  cancer  was 
2.17  per  cent,  of  the  total  mortality  (Jos.  D.  Bryant,  the  “Wesley 
M.  Carpenter  Lecture,”  “ New  York  Med.  Journal,”  May  18,  1895). 
Haeberlin  (“  Deutsches  Archiv  f.  klin.  Med.,”  1889,  Heft,  in  und 
iv)  gives  the  percentage  of  cancer  of  the  stomach  from  1877  to 
1886  as  4.1  per  cent.  This  writer  has  called  attention  to  the  fact 
36 


546  MALIGNANT  TUMORS  OF  THE  STOMACH. 

that  in  Switzerland  also  gastric  cancer  is  on  the  increase;  his 
figures,  showing  the  death-rate  from  cancer  of  the  stomach  for 
1000  inhabitants,  are  the  following:  1877,  0.61  per  cent.;  1878, 
0.66  per-cent.;  1879,  0.72  per  cent.;  1880,  0.77  percent.;  1881, 
0.85  per  cent.;  1882,  0.87  per  cent.;  1883,0.85  per  cent.;  1884, 
0.84  per  cent.;  1885,  0.90  per  cent.;  1886,  0.99  per  cent.  In 
England  the  proportion  of  deaths  from  cancer  to  the  total  mortality 
rate  was  1 in  129  in  1840.  This  had  risen  to  I in  28  in  1880.  The 
death-rate  from  cancer  is  now  about  four  times  as  great  in  England 
as  it  was  fifty  years  ago.  The  published  figures  of  the  Registrar- 
General’s  report  indicate  that  the  mortality  from  cancer  in  the  years 
from  1870  to  1890  has  increased  53  per  cent,  in  England.  These 
facts  are  alarming  and  should  stimulate  the  most  diligent  search 
for  the  cause  of  this  disease.  (For  more  complete  statistics  from 
various  States  and  cities  in  this  country  see  J.  C.  Hemmeter,  “New 
York  Med.  Record,’’  Oct.  21,  1899,  P-  577*) 

(B)  SARCOMATA. 

The  sarcomata  of  the  stomach  are  also  classified  into  two  groups 
according  to  their  origin — namely,  primary  and  secondary.  The 
latter  are  by  far  the  more  rare.  A single  exception  to  this  rule  is 
the  lymphosarcoma.  The  primary  sarcoma  of  the  gastric  wall 
may  develop  from  any  place  within  the  organ,  but  the  greater 
curvature  seems  to  be  preferred,  at  least  by  such  development  as 
that  in  which  tumor  nodules  (myosarcoma  and  fibrosarcoma)  are 
formed,  and  in  which  no  extensive  lateral  infiltrations  are  met  with. 

There  is  a disposition  on  the  part  of  some  authors  (H.  Schle- 
singer,  “ Zeitschrift  f.  klin.  Med.,”  Bd.  xxxn,  Supplement-Heft,  S. 
179)  to  separate  the  lymphosarcomata,  on  account  of  their  different 
anatomical  relations,  from  the  other  sarcomata.  The  point  of  issue 
of  the  latter  group  is  either  the  muscularis  or  the  submucosa,  the 
mucosa  not  being  diseased  primarily.  It  may,  however,  become 
injured  in  the  further  progress  by  the  arching  forward  of  the  tumor 
toward  the  interior  of  the  stomach,  resulting  in  lesions  of  the 
mucosa;  in  a purely  mechanical  way,  from  pulling  and  stretching; 
or  it  may  become  ulcerated  toward  the  inner  gastric  cavity.  In 
some  cases  the  tumor  may  arch  toward  the  peritoneal  cavity.  In 
the  center  of  the  sarcomatous  nodules,  particularly  in  the  center 
of  myosarcomata,  processes  of  softening  and  disintegration,  even 
of  a purulent  nature,  may  occur  and  give  rise  to  septic  peritonitis. 
These  tumors  possess  a spherical  or  an  irregularly  knotty  form, 


SARCOMA  OF  THE  STOMACH. 


547 


and  are  attached  by  either  a broad  or  narrow  basis ; they  some- 
times attain  vast  dimensions  (Brodowski  described  a myosarcoma 
weighing  twelve  pounds).  Metastases  in  neighboring  organs,  par- 
ticularly in  the  lymphatic  glands,  greatly  modify  the  anatomical 
picture,  duplicating,  as  to  appearances,  the  original  tumor.  The 
tumors  that  have  been  observed  so  far  are : Spindle-celled  sarcoma 
(Hardy,  Weissblum,  Habershon,  Tilger,  Malvoz);  angiosarcoma 
(Bruch);  myosarcoma  (Virchow,  Kosinski,  Kolisko,  Brodowski); 
and  fibrosarcoma  (Tilger,  Ewald,  Dreyer).  The  majority  of  the 
round-celled  sarcomata  that  have  been  described  (Virchow,  Cayley, 
Legg,  Berry,  Shaw,  Drost,  Rasch)  are  properly  classed  with  the 
lymphosarcomata.  W.  Fleiner  (“  Lehrbuch  der  Krankheiten  der 
Verdauungsorgane,”  Theil  \,vide  Magensarcom,  S.  295  und  31 1) 
has  clinically  observed  one  case  of  lymphosarcoma  and  one  case  of 
round-celled  sarcoma,  and  made  histological  studies  of  the  same 
from  the  autopsies;  and  H.  Schlesinger  has  given  the  clinical  his- 
tory and  undertaken  the  histological  study  of  two  cases  of  lym- 
phosarcoma and  one  of  round-celled  sarcoma  of  the  stomach 
(Joe.  cit.). 

The  primary  lymphosarcomata  of  the  stomach  seem  to  be  rarer 
than  the  secondary  form.  In  some  cases  the  infiltration  is  limited 
mostly  to  the  pyloric  region,  causing  a rigid  thickening  of  this 
part  (Torok).  In  other  cases  it  occurs  in  enormous  infiltrations 
extending  over  the  whole  stomach,  giving  to  the  inner  surface  the 
appearance  of  a coarse  swelling ; it  may  also  have  the  appearance 
of  a uniform  infiltration.  The  mucous  membrane  may  be  pre- 
served for  a long  time  in  lymphosarcomata,  but  ulceration  is  not 
impossible.  The  spreading  of  the  disease,  as  is  usual  with  a 
lymphosarcoma,  occurs  by  the  lymphatic  channels,  those  lymphatic 
glands  that  are  nearest  becoming  diseased  first,  then  the  adjacent 
organs,  and,  lastly,  the  peritoneum.  Sometimes  no  metastases 
occur,  as  in  one  case  of  Fleiner’s ; more  frequently  lymphosarco- 
mata are  found  as  secondary  neoplasms  in  the  stomach  after  pri- 
mary tumors  in  other  organs.  In  the  cases  of  Kundrat  (“  Ueber 
Lymphosarcomatose,”  “Wien.  klin.  Wochenschr.,”  1893,  No.  12) 
the  original  infected  areas  were  the  neck,  pharynx,  gums,  and  even 
the  rectum. 

Symptomatology. — What  is  said  here  on  symptomatology  has 
reference  to  all  neoplasms  of  the  stomach.  In  a small  number  of 
cases  the  development  of  malignant  growth  of  the  stomach  remains 
entirely  latent,  because  every  typical  gastric  symptom  is  wanting 


548  MALIGNANT  TUMORS  OF  THE  STOMACH. 

until  death.*  As  far  as  we  have  had  occasion  to  observe,  the  first 
symptoms  of  a gastric  carcinoma  are  those  of  chronic  gastritis. 

Most  of  these  patients  state  that,  up  to  the  time  of  their  disease, 
they  enjoyed  a very  good,  sound  stomach.  The  first  dyspeptic 
complaints  are  those  of  pressure  and  fullness  in  the  gastric  region, 
eructations,  anorexia,  nausea,  vomiting,  cardialgia,  and  coated 
tongue.  Disturbances  of  sensibility  are  not  felt  until  the  neoplasm 
has  reached  a certain  size,  thereby  exerting  pressure  on  the  sensory 
nerves  of  the  stomach  ; or  when,  by  its  ulcerations,  or  by  the  irrita- 
tion of  the  digestive  juices,  these  nerves  have  been  exposed.  The 
patient  has  a sensation  as  if  a stone  were  lying  in  his  stomach,  some- 
times complaining  of  unpleasant  feelings  of  emptiness,  which  come 
both  at  a varying  time  after  eating  as  well  as  on  an  empty  stomach, 
and  not  rarely  continue  an  entire  day,  so  that  the  patient  is 
constantly  reminded  of  his  stomach,  which  he  was  not  aware  of 
formerly,  and  is  placed  in  that  characteristic  despondent  and  mel- 
ancholic mood  frequently  met  with  in  gastric  sufferers.  These  sen- 
sations may  increase  to  actual  pain,  which,  however,  is  not  so 
severe  as  in  ulcer.  Eructations  are  present  in  the  beginning  of 
gastric  ulcer  as  well  as  later  on,  either  bringing  up  air  or  small 
particles  of  the  gastric  contents,  which  have  a bitter  taste ; but, 
later  on,  when*  in  consequence  of  achylia,  the  stagnating  gastric 
ingesta  ferment  more  and  more,  the  eructated  gas  may  have  a dis- 
gusting, decomposed  odor  and  taste. 

Pyrosis  may  be  present,  and  is,  as  a rule,  accompanied  by  excess 
of  organic  acids.  Singultus  occasionally  accompanies  the  eructa- 
tions, and  is  observed  most  frequently  with  carcinoma  of  thecardia. 
In  rare  cases  (Ebstein  and  Eichhorst)  there  may  be  a tetany  of  the 
constrictor  muscles  of  the  pharynx,  which  is  said  to  be  caused 
reflexly  from  the  stomach,  and  may  prevent  ingestion  of  food. 
The  frequency  of  nausea  and  vomiting  depends  upon  the  location 
of  the  tumor  in  the  stomach;  they  are  never  absent  when  the 
neoplasm  is  located  at  the  cardia  or  pylorus.  The  nature  and 
chemical  condition  of  the  vomited  matter  depend  upon  the  time  of 
the  emesis  and  the  degree  of  secretory  disturbance  as  well  as  upon 
the  extent  of  the  gastritis,  and  may  consist  of  more  or  less  altered 
ingesta,  decomposed  food  remnants,  mucus,  blood,  or  bile.  Ad- 


*Friedenwald  and  Hotaling,  “ N.  Y.  Med.  Rec. Sept.  24,  1898,  have  collected 
the  literature  of  a large  number  of  such  cases.  Osier,  “ Principles  and  Practice  of 
Med.,”  refers  to  several  that  were  observed  at  the  Johns  Hopkins  Hospital. 


PERISTALSIS,  SECRETION,  AND  ABSORPTION  IN  CARCINOMA.  549 

vanced  decomposition  is  not  observed  until  a late  period  of  the 
growth.  The  vomited  masses  are  rich  in  bacteria,  and  contain  the 
Oppler-Boas  bacilli,  which  are  characteristic  of  lactic  acid  fermen- 
tation, though  not  pathognomonic  of  cancer  (p.  129).  The  tongue 
nearly  always  has  a brownish-yellow  or  grayish-white  coating,  but 
may  be  quite  clean  after  profuse  vomiting.  The  taste  is  said  to  be 
pasty,  bitter,  or  offensive  in  the  last  stages,  and  salivation  and  thirst 
are  increased.  The  loss  of  appetite  belongs  to  the  earliest  symp- 
toms, with  particular  dislike  for  meat  at  all  stages  of  the  disease. 
In  some  patients  complete  anorexia  alternates  with  bulimia.  As  a 
rule,  appetite  remains  fair  as  long  as  there  is  any  gastric  secretion, 
or  as  long  as  the  motility  remains  fairly  good. 

Thirst  is  an  annoying  symptom  in  pyloric  cancers,  because 
they  prevent  the  passage  of  water  into  the  intestines — the  stomach 
being  incapable  of  absorbing  water. 

Constipation  and  Diarrhea. — In  the  literature  in  which  any  refer- 
ence to  these  points  was  made,  I found  that  in  75  per  cent,  of  gas- 
tric cancers  there  is  constipation,  in  20  per  cent,  there  is  diarrhea, 
and  only  in  5 per  cent,  does  the  stool  remain  normal.  The 
greater  frequency  of  constipation  is  due  to  mechanical  stenosis  by 
tumor  or  to  motor  insufficiency  due  to  carcinomatous  invasion  of 
the  muscularis. 

Disturbances  of  Peristalsis , Secretion , and  Absorption .« — These  are 
caused  by  chronic  gastritis,  anemia,  or  direct  extension  of  the  neo- 
plasm into  the  mucosa  and  muscularis  of  the  stomach.  The  dis- 
turbances of  motility  are  either  due  to  destruction  of  the  muscularis 
or  invasion  of  the  gastric  neoplasm,  or  to  stenosis  at  the  pylorus. 
We  do  not  believe  that  they  are  traceable  solely  to  the  induced  gas- 
tritis, because  in  chronic  gastritis,  according  to  very  careful  obser- 
vations, the  motility  in  the  majority  of  cases  is  not  very  seriously 
interfered  with.  Accordingly,  we  find  that  in  from  three  to  four 
hours  after  the  test-breakfast,  or  eight  to  ten  hours  after  a full  test- 
dinner,  when  the  stomach  normally  should  be  empty,  an  abundance 
of  food  remnants  is  contained  in  it.  In  cases  where  the  neoplasm 
is  not  located  at  either  orifice  of  the  stomach,  the  motility  remains 
good  for  a long  time,  and  even  in  the  absence  of  secretion  of  HC1, 
the  vicarious  digestion  of  the  intestines  is  sufficient  to  make  up  for 
the  loss  of  gastric  digestion  and  to  avoid  emaciation. 

If  it  is  desired  to  test  motility  in  gastric  carcinoma  by  means  of 
our  method, — that  is,  by  the  “ deglutable,  india-rubber  stomach- 
shaped bag,” — it  is  wise  not  to  distend  the  bag  too  much ; in  fact, 


550 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


in  cases  of  advanced  cancer,  the  use  of  any  intragastric  instrument 
except  the  stomach-tube  for  this  purpose  is  unjustifiable,  because, 
in  our  experience,  the  stomach-tube,  with  the  help  of  previous 
test-meals,  has  been  found  perfectly  sufficient  to  ascertain  the  con- 
dition of  the  motility  in  this  disease.  The  peristalsis  may  be 
studied  in  hospitals  by  means  of  the  X-rays  and  capsules  of  bis- 
muth subnitrate  swallowed  by  the  patient  (Boas  and  Levy  Dorn, 
“ Deutsch.  med.  Wochenschr.,”  1898,  2).  The  course  of  the  capsule 
can  be  readily  observed  by  the  fluoroscope.  The  loss  of  secretion 
in  gastric  cancer  was  first  discovered  by  von  der  Velden  (“  Deutsch. 
Arch.  f.  klin.  Med.,”  Bd.  xxm,  S.  369,  1879).  The  diagnostic 
value  of  the  absence  of  free  HC1  in  the  gastric  contents  in  malig- 
nant neoplasm  is  to-day  universally  admitted.  There  are  other 
diseases  (chronic  gastritis  and  achylia  gastrica)  in  which  free  HC1 
is  absent,  but  it  is  one  of  the  most  constant  symptoms  of  gastric 
cancer.  Only  in  the  carcinoma  that  arises  from  an  ulcer  do  we 
find  HC1  present,  and  this  is,  in  our  opinion,  explained  by  the  fact 
that  ulcus  carcinomatosum  is,  in  the  great  majority  of  cases,  re- 
ported a very  localized  affection  with  little  or  no  disseminating 
infiltration,  and  consequently  does  not  destroy  the  glandular  appa- 
ratus extensively.  We  should  not  conclude  our  study  of  the  secre- 
tory function  by  merely  testing  for  free  HC1.  In  all  cases  an  arti- 
ficial-digestion experiment  should  be  made  with  egg-albumen  discs, 
as  described  in  the  first  part  of  this  work,  and  the  amount  of  the 
HC1  deficit  determined. 

I do  not  advocate  this  step  as  an  accurate  method  of  deter- 
mining the  amount  of  combined  HC1  present;  if  information  on 
this  point  is  required,  I recommend  the  methods  of  von  Noor- 
denand  Honigman,  or  the  method  of  Martius  and  Luttke.  Fortu- 
nately, the  necessity  for  these  analyses  is  very  rare  in  practice. 
What  is  essential  to  know  is  how  far  behind  the  normal  the  HC1 
secretion  is  in  suspected  cancer  cases,  and  for  this  purpose  the 
determination  of  the  HC1  deficit  is  sufficient.  The  absence  of  free 
HC1  in  a large  majority  of  cancer  cases,  when  taken  in  conjunction 
with  other  signs  and  symptoms,  has  a high  diagnostic  significance. 
Although  absence  of  free  HC1  occurs  in  chronic  or  atrophic  gas- 
tritis and  achylia  gastrica,  in  progressed  cardiac  and  pulmonary 
diseases  and  nervous  anacidity  these  conditions  are  not  easily  mis- 
taken for  carcinoma.  Riegel  formerly  suggested  that  the  HC1  was 
destroyed  by  the  carcinomatous  tissue  itself,  or  a product  of  it; 
later  he  inclined  to  the  opinion,  now  generally  accepted,  that  the 


STATE  OF  BLOOD  AND  URINE  IN  CARCINOMA. 


551 


loss  of  secretion  is  due  to  the  accompanying  gastritis  or  actual 
carcinomatous  invasion  of  the  secretory  glands.  As  the  stomach 
does  not  secrete  HC1  uniformly, — i.  e.,  over  all  its  surface, — it  is 
conceivable  that  a carcinoma  may  occur  in  a portion  where  no  HC1 
is  secreted  normally,  and  in  such  a case  HC1  might  continue  un- 
disturbed as  long  as  the  neoplasm  does  not  extend.  The  accom- 
panying gastritis  may  in  other  cases  be  limited,  and  therefore  the 
glandular  apparatus  remain  largely  intact.  We  have  observed  six 
cases  in  which  the  presence  of  free  HC1  continued  to  the  end  of 
life.  In  two  the  neoplasm  was  seen  during  operation,  and  in  the 
remaining  four  at  autopsy.  These  six  cases  had  not  originated  on 
the  basis  of  an  old  gastric  ulcer,  but  were  rather  circumscribed 
cancer  masses  in  the  pyloric  antrum.  Absence  of  accompanying 
gastritis,  limited  carcinomatous  invasion  of  the  acid-producing 
glandular  portion,  or  location  in  the  portion  which  normally 
secretes  HC1,  may  serve  to  explain  the  cases  of  gastric  cancers  in 
which  free  HC1  is  still  detected.  They  are  so  rare,  however,  that 
they  can  hardly  invalidate  the  importance  of  the  sign.  Rosen- 
heim, Ewald,  Hammerschlag,  and  the  author  have  examined  the 
mucosa  from  stomachs  presenting  carcinoma  originating  from 
ulcers ; previous  test-meal  analysis  had  revealed  an  amount  of 
free  HC1  equal,  on  the  average,  to  0.12  per  cent.  No  structural 
changes  in  the  secretory  glands  were  observed. 

The  Jaworski  method  should  not  be  neglected  in  testing  for  the 
prozymogens  of  the  gastric  ferments.  About  200  c.c.  of  a 5 : 1000 
solution  of  HC1  are  poured  into  the  stomach,  after  it  has  been 
previously  cleansed,  and  a quantity  redrawn  in  twenty  minutes;  if 
this  does  not  digest  egg-albumen  after  a further  addition  of  HC1, 
and  no  rennin-zymogen  is  contained  in  it,  then  the  glandular  activ- 
ity is  completely  extinguished.  The  state  of  the  resorption  is  very 
much  reduced,  according  to  Eichhorst,  Zweifel,  Wolff,  and  others. 
Capsules  of  three  to  five  grains  of  iodid  of  potash,  which  should 
give  the  iodin  reaction  in  the  saliva  fifteen  minutes  after  they  are 
swallowed,  do  not,  as  a rule,  give  this  reaction  before  one  hour  to 
one  and  a half  hours  have  expired. 

With  the  progressive  cachexia,  the  color  of  the  face  and  of  the 
external  mucous  membrane  becomes  pale  or  yellowish.  There  is 
persistent  insomnia,  and,  as  a consequence  of  the  hydremia  and 
the  impoverished  condition,  the  vessel  walls  become  more  per- 
meable, producing  the  frequent  edema  at  the  ankles  and  other 
dependent  parts,  which  sometimes  invokes  suspicion  of  nephritis. 


552  MALIGNANT  TUMORS  OF  THE  STOMACH. 

The  body  weight  may  be  reduced  thirty  to  forty  pounds  in  from 
one  to  two  months.  The  urine  is  greatly  diminished  in  quantity, 
concentrated,  and  highly  colored,  as  a result  of  the  impaired 
absorption,  frequent  emesis,  and  edema.  The  reaction  is  neutral 
or  even  alkaline,  particularly  if,  by  methodical  lavage,  the  acids  and 
acid  salts  have  been  largely  removed.  An  excess  of  indican  is 
found  in  the  urine. 

Von  Jaksch  demonstrated  the  presence  of  acetone  in  the  urine, 
and  Maixner  discovered  peptone  in  the  urine  of  twelve  cases  he 
examined,  and  his  results  were  confirmed  by  Parganowski.  Maix- 
ner attributes  the  peptonuria  to  impairment  of  the  ability  of  the 
gastric  membrane  to  change  peptone  back  into  albumin,  while 
Parganowski  believes  that  the  formation  of  the  peptone  takes  place 
in  the  disintegrating  cancerous  tissue.  The  urine  also  gives  a 
Burgundy-red  color  with  chlorid  of  iron,  which  is  probably  due  to 
diacetic  acid.  The  feces  frequently  contain  undigested  muscle- 
fibers  and  egg-albumen  taken  in  the  food.  There  is  pronounced 
constipation  in  seventy-five  per  cent,  of  cases,  caused  principally  by 
stenosis  of  the  pylorus,  and  in  other  cases  by  the  greater  amount 
of  work  that  the  intestine  is  called  upon  to  perform  and  the  im- 
paired peristalsis.  In  twenty  per  cent,  of  cases  there  is  diarrhea, 
and  regular  evacuation  in  only  five  per  cent. 

Special  Symptoms. — Hematemesis. — The  hemorrhages  from 
gastric  carcinoma  are,  as  a rule,  not  abundant,  although  they  are 
quite  frequent.  They  are  most  frequently  observed  in  carcinoma 
of  the  pylorus  and  of  the  lesser  curvature.  As  hemorrhages 
which  are  not  copious  do  not  easily  lead  to  emesis,  there  is  suffi- 
cient time  for  changing  of  the  blood  pigments  into  hematin,  which 
is  uniformly  mixed  with  the  gastric  contents,  so  that  when  they 
are  eventually  vomited,  they  present  the  appearance  of  coffee 
grounds  or  dark  chocolate,  which  is,  according  to  Brinton,  a vomit 
that  is  observed  in  about  forty-two  per  cent,  of  the  cases,  and  is, 
therefore,  an  important  sign  in  gastric  cancer.  This  kind  of  vomit 
may  also  occur  in  chronic  passive  congestion  of  the  stomach  and 
in  ulcer.  In  chronic  gastritis  one  rarely  meets  with  even  small 
hemorrhage  ; there  is  no  diffuse  staining  of  the  ingesta,  which 
simply  shows  streaks  or  points  of  blood.  If  the  coffee-ground  ad- 
mixture in  vomit  occurs  frequently  or  daily  for  weeks,  then  it 
becomes  an  important  pathognomonic  symptom  of  gastric  malig- 
nant neoplasm. 

The  Occurrence  and  Determination  of  Tumor. — In  all  cases 


DIAGNOSIS  OF  GASTRIC  TUMORS. 


553 


of  suspected  carcinoma  of  the  stomach  the  examining  physician 
should  carefully  and  systematically  go  through  the  routine  of  in- 
spection, palpation,  percussion  of  the  entire  abdomen,  and  artificial 
distention  of  the  stomach  by  air  or  gas.  When  an  abdominal 
tumor  is  formed  by  the  dilated  stomach  itself,  the  diagnosis,  in  the 
majority  of  cases,  can  be  made  by  a simple  inspection.  To  deter- 
mine the  presence  of  peristalsis  in  dilated  stomachs,  rarely  anything 
else  than  close  inspection  is  necessary. 

There  are  two  conditions  in  which  the  stomach  itself  may  form 
a palpable  tumor  by  chronic  contraction:  one  is  where  the  organ 
shrinks  in  consequence  of  occlusion  of  the  esophagus,  and  can  be 
felt  as  a narrow,  firm  ridge  lying  below  the  left  lobe  of  the  liver; 
the  other  condition  is  known  as  cirrhosis  ventriculi , and  is  the  result 
of  chronic  hyperplasia  of  the  walls,  with  subsequent  contraction 
of  the  lumen.  In  very  rare  instances  it  may  be  caused  by  diffuse 
carcinomatous  infiltration.  The  infiltrating  scirrhous  carcinoma  of 
the  stomach,  even  at  the  autopsy,  may  not  be  distinguishable 
microscopically  from  cirrhosis  of  the  organ,  the  author  having 
observed  two  such  cases  in  which  the  nature  of  the  gastric  indura- 
tion was  not  discoverable  from  microscopical  study  of  the  sections 
from  the  stomach  but  only  from  the  metastases.  In  this  instance  we 
are  concerned  most  directly  with  the  nodular  and  massive  tumors 
of  the  stomach. 

As  three-fifths  of  all  tumors  occupy  the  pyloric  region,  they 
should  not  escape  diagnostic  palpation,  because  in  the  majority 
of  cases  they  displace  the  pylorus  downward  and  render  it 
palpable.  When  the  stomach  is  filled  with  stagnating  food  or 
water,  distended  by  gas,  or  in  a state  of  atony,  the  pylorus  is  gen- 
erally below  the  edge  of  the  liver.  In  some  cases  where  the 
abdominal  walls  are  not  too  thick,  it  is  possible  to  feel  and  recog- 
nize the  normal  pylorus  as  a small,  transversely  placed  ridge,  which 
varies  its  position  with  respiration.  Personally,  I have  occasionally 
been  able  to  grasp  the  normal  pylorus  between  the  fingers  of  the 
left  hand,  and,  by  massage  and  compression  of  the  fundus  by  the 
right  hand,  been  able  to  recognize  the  escape  of  air  and  liquid 
ingesta  through  the  pyloric  ring.  The  detection  of  the  location 
of  the  pylorus  is  easier  in  dyspeptic  patients  than  in  the  normal 
state,  because  in  cases  in  which  it  becomes  important  to  recognize 
the  pylorus  there  is  generally  considerable  emaciation  of  the 
abdominal  walls,  thus  facilitating  palpation.  Alternating  relaxation 
and  contraction  of  the  pylorus  may  sometimes  be  felt,  but  this 


554 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


phenomenon  is  very  rare.  Osier,  in  his  “ Practical  Monograph  on 
the  Diagnosis  of  Abdominal  Tumors”  (D.  Appleton  & Co.,  1894), 
sums  up  the  leading  points  concerning  the  solid  tumors  of  the 
stomach  in  the  following  terms : “ Though  only  a small  section  of 
the  stomach  is  available  for  palpation,  a very  large  proportion  of 
all  tumors  of  the  organ  may  be  felt,  owing  in  part  to  their  greater 
frequency  at  the  pyloric  portion,  and  in  part  owing  to  the  frequent 
depression  of  the  organ.”  He  gives  an  account  of  twenty-four 
cases,  in  all  of  which  a tumor  or  induration  was  detected.  In  the 
majority  of  the  cases  no  trouble  was  experienced  in  determining 
whether  or  not  a tumor  was  in  the  stomach.  Excessive  mobility 
of  a pyloric  growth  and  extensive  infiltrating  masses  in  the  epigas- 
tric region  were  the  only  conditions  causing  trouble  in  any  of  the 
cases  of  his  series.  As  other  forms  of  tumor  of  the  stomach  (those 
that  have  I referred  to  in  the  sections  on  Malignant  and  Benign 
Tumors)  are  rare,  a palpable  tumor  in  the  stomach  may,  as  a rule, 
be  considered  a carcinoma.  One  can  not  exclude  carcinoma  even 
when  a palpable  tumor  is  absent,  because  twenty  per  cent,  of  all 
cases  escape  objective  demonstration  during  their  entire  clinical 
history  (Fleischer).  Among  these  cases  we  must  reckon  the  can- 
cers affecting  the  cardia,  the  lesser  curvature,  and  part  of  those 
affecting  the  posterior  wall.  In  order  to  instruct  ourselves  con- 
cerning the  typical  peculiarities  of  a tumor,  and  to  avoid  confound- 
ing it  with  neoplasms  of  adjacent  organs,  repeated  and  thorough 
examinations  are  necessary.  The  patient  should  be  placed  in  a 
horizontal  position,  his  knees  should  be  flexed,  and  his  mouth  kept 
open,  and  palpation  should  be  careful  and  gentle,  because  energetic 
and  rapid  palpation  does  more  harm  than  good,  as  it  produces  an 
annoying  tension  of  the  abdominal  muscles.  We  are  in  the  habit 
of  evacuating  the  stomach  by  lavage,  and  also  the  entire  intestinal 
tract  by  a purge,  prior  to  palpation,  in  order  to  bring  about  the 
most  favorable  conditions  for  this  examination. 

Occasionally,  a tumor  will  be  evident  upon  simple  inspection  as 
a round  or  oval  prominence,  but  the  results  of  palpation  are'  more 
reliable.  The  cancer  can  be  felt  as  a hard,  uneven,  sharply  circum- 
scribed, nodular  tumor.  When  the  growth  has  extended  more 
toward  the  interior  of  the  stomach  and  brought  about  diffuse  infil- 
trations, one  feels  a more  uniform,  and  frequently  only  an  indistinct, 
resistance  toward  the  depths  of  the  epigastrium  or  right  hypochon- 
drium.  In  the  beginning  of  a carcinomatous  growth  at  the  pylorus 
its  smooth  contour  will  not  permit  of  a positive  differentiation  from 


POSITION  AND  MOVABILITY  OF  TUMORS.  555 

benign  hypertrophy,  especially  as  the  consecutive  symptoms  of 
stenosis,  gastritis,  and  dilatation  are  coincident  with  both.  In  this 
case  the  only  means  of  reaching  a decision  is  by  watching  the 
further  progress  of  the  tumor.  When  the  stomach  is  filled  with 
food  and  gases,  the  tumor  is  less  distinct  on  palpation.  Per- 
sistent and  stubborn  reflex  cramp  of  the  pylorus  may  give 
the  impression  of  carcinoma.  In  a case  reported  from  Leube’s 
clinic,  in  a man  aged  ’thirty-six  years,  who  had  a dilatation 
and  a distinctly  palpable  tumor  in  the  umbilical  region,  an  opera- 
tion was  decided  upon,  but  when  von  Heinecke  and  Leube  reex- 
amined the  man  under  chloroform  anesthesia,  the  tumor  had 
disappeared  ; the  patient  was,  consequently,  not  operated  upon, 
and  was  reported  living  in  good  health  twelve  years  after  this 
experience. 

In  two  cases  at  my  clinic  gastric  tumors  were  mimicked  by  sub- 
epidermic  neoplasms  of  the  skin.  One  was  a negress  with  an  elon- 
gate keloid  tumor  beneath  the  skin  of  the  epigastrium,  and  the 
other  was  a white  male  who  had  been  presented  for  operation  for 
gastric  cancer.  On  examination  he  was  found  to  have  a subcellu- 
lar  lipoma  in  the  abdominal  walls  over  the  epigastrium.  Disten- 
tion of  the  stomach  will  prevent  errors  of  diagnosis  in  such  cases. 

Position  and  Movability  of  the  Tumor. — Three-fourths  to 
five-sixths  of  the  normal  stomach  is  located  in  the  left  half  of  the 
abdomen ; therefore  one  would  expect  that  gastric  tumors  are 
generally  palpable  in  the  epigastrium  a little  to  the  left — rarely  to 
the  right — of  the  median  line,  and  above  the  umbilicus.  But  as 
pyloric  neoplasms  are  the  most  frequent  (sixty  per  cent.,  Welch), 
these  will  be  found  to  the  right  of  the  median  line.  Later  on,  the 
tumor  sinks  downward  more  and  more  and  can  be  demonstrated 
below  the  umbilicus,  particularly  if  it  is  a pyloric  neoplasm.  If 
no  adhesions  exist,  it  may  even  sink  down  into  the  pelvis. 
When  there  are  adhesions  near  the  locality  of  the  tumor,  it 
is  immovable;  but  if  they  are  absent,  the  tumor  may  be  moved 
to-and-fro  to  some  extent.  Osier  ( loc . cit.)  gives  some  clear  illus- 
trations of  the  positions  into  which  gastric  tumors  can  be  moved. 
Changing  the  position  of  the  body  brings  about  a moderate  move- 
ment in  the  growth.  In  order  to  ascertain  whether  a tumor 
belongs  to  the  stomach  proper,  the  changes  in  form  and  position 
of  the  organ,  which  are  caused  by  filling  the  same  with  water  or 
distending  it  with  air,  are  very  helpful.  If  on  filling  the  stomach 
with  water  the  tumor  lies  within  the  area  of  dullness  thus  artifi- 


556  MALIGNANT  TUMORS  OF  THE  STOMACH. 

cially  produced,  and  if  on  subsequent  distention  of  the  stomach  with 
C02  a tympanitic  resonance  can  be  made  out  above  and  below  the 
tumor,  it  belongs  to  the  stomach.  On  filling  the  colon  with  one 
to  two  liters  of  water  the  gastric  tumors  rise  upward,  and  may  hide 
behind  the  liver  and  sternum.  It  is  generally  stated  that  gastric 
tumors,  in  the  majority  of  cases,  do  not  move  with  respiration,  but 
that  tumors  of  the  liver  do.  There  are  many  exceptions  to  this 
rule.  If  there  are  any  adhesions  to  the  liver,  spleen,  or  diaphragm, 
stomach  neoplasms  participate  in  the  respiratory  movements  of 
these  organs.  If  the  tumor  is  of  considerable  size,  it  moves  down- 
ward with  respiration,  because  it  can  not  get  out  of  the  way  of  the 
descending  diaphragm.  The  percussion-note  over  the  tumor  is 
most  frequently  of  a dull,  tympanitic  character.  It  has  been  stated 
that  only  hepatic  tumors  give  a dullness  on  percussion,  and  that 
this  may  serve  to  differentiate  them  from  the  stomach  tumors  ; 
this,  however,  is  a misleading  sign,  because  large  gastric  tumors 
will  give  dullness  on  percussion,  and  if  a hepatic  tumor  is  located 
at  the  margin  of  the  liver,  or  if  a few  loops  of  intestine  or  the  colon 
lie  between  it  and  the  abdominal  wall,  a tympanitic  percussion- 
note  will  result.  Pulsations  may  be  evident  in  tumors  that  are 
adjacent  to  the  celiac  axis  or  superimposed  upon  the  aorta.  If  the 
latter  is  compressed  by  the  tumor,  the  tonicity  of  the  crural  pulse 
is  diminished,  and  the  epigastric  growth  may  mimic  an  aneurysm. 

Differentiation  of  Gastric  Tumors  from  Those  of  Adjoining 
Organs. — 1.  From  Splenic  Tumors . — As  gastric  cancers  rarely 
occur  at  the  fundus,  their  differentiation  from  splenic  tumors  is 
rarely  called  for  and  is  seldom  difficult.  The  spleen  is  movable 
with  respiration  ; the  stomach,  only  exceptionally.  In  splenic  tumor 
we  have  dullness  on  percussion  and  absence  of  dyspeptic  symptoms. 
In  gastric  tumor  we  have  a tympanitic  resonance  on  percussion 
and  disturbances  of  secretion  and  motility.  Splenic  tumors  can 
be  very  often  mapped  out  and  found  to  be  ascending  back  of  the 
ribs. 

2.  From  Tumor  of  the  Liver. — Hepatic  tumors  move  with  respira- 
tion, and  frequently  it  is  possible  to  grasp  the  gastric  tumor  and 
separate  it  from  the  liver.  The  contours  of  the  liver  should  be 
determined,  if  possible  ; for  with  hepatic  tumors,  the  liver  is  gener- 
ally enlarged  and  sensitive  to  pressure,  and  the  surface  is  frequently 
uneven.  Phenomena  of  disturbance  of  hepatic  circulation,  such  as 
icterus  and  ascites,  denote  liver  tumor.  It  is  true  that  dyspeptic 
symptoms  may  be  secondarily  caused  by  malignant  disease  of  the 


DIFFERENTIATION  OF  ABDOMINAL  TUMORS.  557 

liver,  but  then  they  present  themselves  later  in  the  disease  ; with 
gastric  cancer  dyspeptic  symptoms  are  among  the  very  first.* 

3.  From  Malignant  and  Other  Tumors  of  the  Gall-bladder. — Car- 
cinoma of  the  gall-bladder  and  accumulations  of  gall-stones  may 
be  confounded  with  pyloric  carcinoma.  The  latter  brings  on  gas- 
tric dilatation  and  grave  anomalies  of  function,  which  are  absent  in 
affections  of  the  gall-bladder.  Cancers  of  the  gall-bladder  are  not 
secondary  to  cancers  of’  the  stomach,  as  a rule.  If,  however,  the 
gall-bladder  tumor  presses  upon  the  pylorus,  and  also  causes 
stenosis  and  dilatation,  as  we  had  occasion  to  observe  at  an 
autopsy  in  the  Maryland  General  Hospital,  the  differentiation  from 
gastric  neoplasm  is  practically  impossible.  The  assertion  that 
hydrochloric  acid  is  still  secreted  when  the  carcinoma  is  in  the 
gall-bladder  and  not  in  the  stomach,  is  not  supported  by  sufficient 
evidence,  because  passive  congestion  of  the  stomach  concomitant 
with  gall-bladder  and  hepatic  tumors  often  brings  about  loss  of  gas- 
tric secretion. 

4.  Carcinoma  of  the  pancreas  has  frequently  deceived  clinicians 
in  the  diagnosis  of  abdominal  tumors.  Its  immovability  during 
respiration  and  palpation  might  suggest  pyloric  carcinoma;  pan- 
creatic tumors,  however,  frequently  cause  stasis  in  the  portal  vein 
and  pronounced  icterus  ; while  dyspeptic  disturbances  and  loss  of 
HC1,  which  are  early  and  prominent  symptoms  of  gastric  cancer, 
are  absent. 

5.  Tumors  of  the  Omentum  and  Peritoneum. — The  differentiation 
of  these  tumors  from  gastric  carcinoma  is  difficult  when  symptoms 
of  disturbed  gastric  digestion  are  present  and  the  tumor  does  not 
exceed  the  limits  of  the  stomach.  As  a rule,  these  tumors,  being 
secondary,  are  not  so  sharply  circumscribed  as  are  gastric  tumors. 
Ascites  is  rarely  absent.  The  original  source — the  primary  tumor 
in  some  other  organ — should,  if  possible,  be  discovered.  Sometimes 
disease  of  the  stomach  may  be  excluded  by  chemical  and  micro- 
scopical methods,  and  then  the  diagnosis  becomes  possible. 

6.  Tumors  of  the  colon , as  a rule,  sink  downward,  because  the 
colon  is  very  movable,  unless  (very  rarely)  adhesions  form  with 
the  abdominal  wall.  By  alternately  filling  the  stomach  with  water 
and  air,  and  subsequently  evacuating  it  again,  it  may  be  demon- 
strated that  the  tumor  is  independent  of  the  stomach.  When  the 


* The  liver  itself  may  give  the  signs  and  symptoms  of  a tumor  (see  chapter  on  Enter- 
optosis) . 


558 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


colon  is  filled  with  one  to  two  liters  of  water,  the  tumor  rises  but 
very  slightly,  if  at  all ; while  tumors  of  the  stomach,  on  filling  the 
colon,  generally  ascend,  and  may  disappear  behind  the  liver  or 
sternum.  Tumors  of  the  anterior  wall  of  the  colon  become  more 
distinct  when  it  is  filled  with  water,  while  those  of  the  posterior 
wall  become  less  distinct.  A stenosis,  as  a rule,  appears  promptly, 
and  the  colon  becomes  tremendously  expanded  in  front  of  the  con- 
striction. Osier  (loc.  cil.)  has  reported  a carcinoma  of  the  cecum 
and  colon,  with  enormous  secondary  enlargement  of  the  liver,  and 
extensive  secondary  nodules  were  scattered  through  the  lungs. 
His  case  is  very  instructive,  as  the  intestinal  symptoms  were  ab- 
sent, thus  illustrating  the  difficulty  in  making  a correct  diagnosis. 

7.  Duodenal  carcinoma  can  scarcely  be  separated  from  pyloric 
carcinoma.  The  occurrence  of  a tumor  in  the  vicinity  of  the  um- 
bilicus, the  cachexia,  the  consecutive  gastric  dilatation,  and  (if  the 
duodenal  carcinoma  should  ulcerate)  the  coffee-ground  vomit — all 
these  signs  may  be  present  in  cancers  of  either  locality.  If  free 
HC1  can  be  demonstrated  in  the  gastric  contents,  or  its  secretion 
can  be  caused  after  methodical  lavage,  the  other  symptoms  of  neo- 
plasm might  possibly  be  referred  to  the  duodenum.  Carcinoma  of 
the  duodenum,  as  Ewald  and  Riegel  have  observed,  may  be  com- 
bined with  atrophic  gastritis,  so  that  absence  of  HC1  may,  in  these 
cases,  occur,  which  absence  is  not  directly  caused  by  a gastric  car- 
cinoma ; hence,  the  diagnosis  is  largely  a matter  of  chance.  The 
author’s  method  of  duodenal  intubation  may  be  available  in  deter- 
mining a duodenal  stenosis.  It  is  evident  that  a thorough  knowl- 
edge of  gastric  cancer  and  the  application  of  all  physical  and 
chemical  methods  of  diagnosis  is  necessary  if  we  wish  to  be 
approximately  correct  in  our  diagnosis.  In  all  cases  of  doubtful 
differential  diagnosis  exploratory  laparotomy  should  not  be  de- 
ferred until  the  loss  of  strength  of  the  patient  contraindicates 
operation. 

Cachexia. — As  the  gastric  cancer  progresses,  anemia  and  ema- 
ciation increase  to  a pronounced  cachexia.  The  color  of  the  skin 
becomes  grayish-white  or  yellow;  it  may  appear  wrinkled,  atrophic, 
and  exfoliating.  Frequently  an  annoying  pruritus  is  present.  The 
body  weight  becomes  less  and  less  the  more  digestion  is  disturbed  ; 
the  severer  the  vomiting,  the  more  the  passage  of  chyme  into 
the  intestine  becomes  obstructed.  The  blood  grows  more  and  more 
deficient  in  red  blood-corpuscles  and  in  hemoglobin,  and  a state 
similar  to  pernicious  anemia  may  result.  Pronounced  diminution 


CARCINOMATOUS  ULCKK. 


559 


of  the  hemoglobin  is  so  constant  an  accompaniment  of  gastric 
cancer  that  it  can  almost  be  excluded  in  case  the  amount  of  hemo- 
globin is  equal  to  sixty  per  cent,  or  more  (Haberlin-Eichhorst). 
The  amount  may  sink  to  forty  and  thirty  per  cent.  In  one  case 
of  Eichhorst’s  it  sank  to  ten  per  cent.  Accidental  sounds  about 
the  heart  and  signs  of  cerebral  anemia  or  of  moderate  edema  have 
been  observed.  Ascites  is  a consequence  of  secondary  metastases 
in  the  liver  or  peritoneum,  or  of  thrombosis  in  the  portal  vein; 
but  toward  the  end  of  life  it  may  be  caused  by  great  cardiac 
asthenia  and  hydremia.  Thrombosis  of  the  main  vessels  of  one 
leg  has  been  observed,  and  constitutes  a very  fatal  sign.  The 
pulse  is  mostly  accelerated,  and  the  body  temperature  is  subnormal. 
Fever  is  a rare  occurrence  in  gastric  cancer;  if  it  does  occur,  it  is 
traceable  to  autointoxication  with  septic  products  formed  in  the 
ulceration  or  degeneration  of  the  cancer. 

Coma  carcinomatosum  is  a complication  of  symptoms  similar 
to  the  coma  of  diabetics,  and  is  accompanied  by  a peculiar,  dyspnea. 
The  respirations  are  strong  and  deep,  and  generally  attended  with 
a groaning  sound  in  expiration.  The  rate  of  respiration  is  either 
normal  or  moderately  increased.  The  temperature  is  either  nor- 
mal or  subnormal.  There  is  no  evidence  of  disease  of  the  lungs  or 
air-passages.  It  does  not  usually  appear  until  anemia  is  far  advanced. 
This  kind  of  coma  was  first  described  by  Petters  and  Kaulich,  and 
later  by  von  Jaksch  (“Wien.  med.  Wochenschr.,”  1883,  p.  473), 
and  is  probably  a consequence  of  autointoxication.  (See  litera- 
ture of  this  subject  in  Albu,  “ Autointoxicationen  des  Intestinal- 
tractus,”  Berlin,  1895,  p.  105.) 

As  we  have  stated  in  the  pathology  of  carcinoma,  swellings  of 
the  peripheral  lymph-glands  are  not  rare  at  autopsies.  A hard 
swelling  of  the  supraclavicular  glands  was  considered  typical  by 
Friedreich  and  Henoch.  I find  that,  clinically,  swelling  of  the 
cervical  lymph-glands  is  a rare  sign,  and  occurs  only  toward  the 
end  of  the  disease,  by  which  time  the  diagnosis  is  generally  clear. 
If  severe  vomiting  ceases  suddenly,  a breaking  down  of  the  can- 
cerous infiltration  of  the  pyloric  region  may  be  inferred, — by  which 
communication  with  the  intestines  may  be  restored, — or  it  may 
be  due  to  excessive  muscular  insufficiency. 

Carcinomatous  Ulcer  (Ulcus  Carcinomatosum). — We  have 
already  stated,  in  the  section  on  the  Pathology  of  Gastric  Ulcer,  that 
atypical  cell-proliferation  may  develop  from  a benign  gastric  ulcer, 
which  thereafter  entirely  assumes  the  character  of  a carcinoma. 


560  MALIGNANT  TUMORS  OF  THE  STOMACH. 

Rokitansky  and  Dittrich  were  the  first  to  describe  this  condition, 
but  Hauser  (“  Das  chronische  Magengeschwiir,”  Leipzig,  1883) 
gave  the  most  accurate  histological  description  of  it.  In  1891 
Kollmann  (“Berlin,  klin.  Wochenschr.,”  1891,5  und  6)  reported 
fourteen  cases,  to  which,  up  to  the  present  time,  as  far  as  we  know, 
about  fourteen  more  can  be  added  from  literature.  In  this  form  of 
carcinoma  the  gastritis  is,  at  the  beginning  at  least,  limited  to  the 
immediate  neighborhood  of  the  ulcer,  or  it  may  be  entirely  absent. 
Accordingly,  the  functional  disturbances  are  less,  and  secretion 
may  be  normal,  or  we  may  even  find  hyperchylia.  Very  late  in 
the  course  of  this  type  the  remainder  of  the  mucosa  may  suffer 
from  cancerous  infiltration  or  gastritis,  just  as  is  the  case  with  the 
ordinary  gastric  carcinoma,  and  then  the  functional  disturbances 
become  more  pronounced.  The  diagnosis  of  carcinomatous  ulcer 
can  be  made  if  a tumor  can  be  recognized,  together  with  normal  or 
excessive  secretion  of  HC1  and  a progressive  cachexia.  Of  course, 
the  previous  history,  which  gives  an  account  of  years  of  gastric 
pain, — whereas  cancer  patients  have,  as  a rule,  when  they  present 
themselves  not  suffered  so  long, — is  a valuable  factor  in  the  diag- 
nosis. If  vomiting  of  blood  or  melena  occurs  in  the  clinical  his- 
tory, the  diagnosis  becomes  probable,  but  it  is  difficult  to  distin- 
guish between  carcinomatous  ulcer  and  the  tumor-like  induration 
of  a large  simple  ulcer.  It  is  also  difficult  to  distinguish  the 
carcinomatous  ulcer  from  hypertrophic  stenosis  of  the  pylorus. 
Sometimes  the  recognition  of  secondary  metastases  in  the  liver,  or 
other  signs  of  cancerous  dissemination,  such  as  ascites  and  peri- 
toneal carcinosis,  may  be  deciding  factors.  In  one  of  our  cases 
there  was  no  tumor  to  be  felt,  only  symptoms  of  cachexia  and  of 
gastric  ulcer.  For  literature,  see  Rosenheim,  “ Zur  Kenntniss  des 
mit  Krebs  complicirten  runden  Magengeschwurs,”  “ Zeitschrift  f. 
klin.  Medicin,”  Band  xvn,  Seite  1 16 ; also  Boas  ( loc . cit),  second  edi- 
tion, 1895,  pages  188  and  189,  and  Hemmeter,  “New  York  Med. 
Record,”  volume  lii,  No.  i i,  September  1 1,  1897,  page  365.  D.  D. 
Stewart  has  reported  a case  in  which  two  isolated  carcinomatous 
ulcers  occurred  in  the  stomach  (“Am.  Jour.  Med.  Sciences,”  Nov., 
1898). 

Perforations. — When  a carcinoma  perforates  into  other  hollow 
organs,  or  exteriorly,  life  may  be  maintained  for  a short  time, 
but  perforation  into  the  pleural  or  pericardial  cavities,  or  into  the 
lungs,  rapidly  leads  to  death.  Gastrocolic  fistulae  cause  very  rapid 
emaciation,  because  the  ingesta  pass  directly  into  the  colon,  in 


FRAGMKNTS  SHOWING  MITOSIS. 


56 


which  very  little  digestion  and  resorption  occur.  With  this  kind 
of  perforation,  portions  of  excrement  may  be  vomited.  Bronchitis, 
traumatic  pneumonia,  and  pericarditis  may  accompany  the  disease. 
Tuberculosis  may  be  combined  with  gastric  carcinoma. 

Diagnosis. — The  majority  of  authors  say  that  fragments  of  the 
cancer  rarely  occur  in  the  vomit  or  are  rarely  brought  up  in  the 
tube.  In  fact,  it  appears  that  the  finding  of  carcinomatous  parti- 
cles is  considered  an  accident.  It  is  probable  that  this  occurrence 
is  said  to  be  so  rare,  not  because  these  fragments  do  not  occur  in 
the  vomit  or  wash-water,  but  because  they  are  not  methodically 
and  systematically  looked  for.  The  great  importance  of  an  early 
diagnosis  of  carcinoma  justifies  the  clinician  in  going  to  some  trou- 
ble in  order  to  find  these  fragments.  We  are  in  the  habit  of  feed- 
ing all  suspected  cases  for  forty-eight  hours  by  th^  rectum. 
Thereafter,  the  stomach  is  washed  out  with  normal  salt  solution  ; 
for  this  purpose  we  use  a stomach-tube,  which,  though  quite  soft, 
is  provided  with  an  edge  of  the  usual  firmness  around  the  lower 
opening.  This  tube,  on  being  moved  about  in  the  stomach,  is  very 
likely  to  dislodge  surface  particles  of  the  neoplasm.  There  is 
every  reason  why  we  should  intentionally  attempt  to  secure  cancer 
particles  from  the  stomach  just  as  they  are  secured  by  cureting 
from  the  uterus.  We  have  been  able,  in  this  manner,  to  find  parti- 
cles of  the  neoplasm  in  the  wash-water  after  it  has  been  permitted 
to  settle  in  a conical  glass  for  about  six  hours,  or  after  the  solid 
particles  were  brought  down  with  the  centrifuge.  When  the  sedi- 
ment in  the  bottom  of  the  glass  is  first  examined  by  a low  power, 
and  afterward  by  the  higher  power  of  the  microscope,  cells  in  a 
state  of  atypical  mitosis  can  frequently  be  found.  Previous  to  the 
rectal  feeding,  we  wash  out  the  stomach  thoroughly  in  order  to  avoid 
confounding  cancer  particles  with  particles  of  meat,  etc.,  retained 
with  the  ingesta.  If  this  method  is  systematically  followed,  we 
believe  that  cancer  particles  will  be  more  frequently  found ; nor 
should  we  always  deny  the  existence  of  carcinoma  when  we  find 
no  fragment  giving  the  typical  histological  structure  of  these 
neoplasms,  as  described  under  their  pathology. 

Whenever  we  find  pieces  of  mucosa  in  which  the  glandular 
ducts  are  elongated  and  dilated,  and  the  cells  present  numerous 
karyokinetic  figures,  and  when  asymmetrical  and  hypochromatic 
forms  are  found,  the  possibility  of  the  existence  of  carcinoma 
should  suggest  itself,  even  when  typical  carcinoma  cells  are  absent ; 
particularly  when  the  interstitial  tissue  is  considerably  increased 
37 


562 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


and  broadened,  showing  much  small,  round-cell  infiltration  when 
numerous  eosinophilic  cells  are  present  and  the  parietal  or  oxyntic 
cells  have  disappeared,  and  are  replaced  by  cylindrical  or  cuboidal 
epithelial  cells,  which  proliferate  down  into  the  peptic  ducts  from 
the  vestibular  alveoli. 

Whenever  cancer  is  suspected,  the  wash-water  should  be  ob- 
tained from  the  fasting  stomach  in  the  morning,  before  any  food  is 
taken ; preferably,  the  contents  should  be  drawn  by  the  expression 
method  without  dilution,  and  any  cellular  detritus  brought  down 
by  the  centrifuge.  In  speaking  of  Rieder’s  pioneer  work  in  this 
direction,  George  Dock  (“  Cancer  of  the  Stomach  in  Early  Life,” 
“Am.  Jour,  of  the  Med.  Sciences,”  June,  1897,  p.  655)  expresses 
himself  as  follows : “ It  was  therefore  a matter  of  great  interest 
when  Rieder  (‘  Deutsches  Archiv  fur  klin.  Med.,’  Bd.  liv,  H.  6, 
S.  544)  reported  a case  in  which  he  made  a diagnosis  of  malignant 
disease  of  the  peritoneum  and  pleura  from  finding  numerous  cells 
in  the  exudates,  showing  indirect  nuclear  division.”  The  patient 
was  a woman  of  forty  years.  “ Section  showed  sarcoma  (carci- 
noma?) of  the  peritoneum,  probably  secondary  to  malignant  dis- 
ease of  the  ovaries.”  In  the  fluids  obtained  during  life,  cells  were 
found  which  were  remarkable,  “ in  the  first  place,  on  account  of  the 
differences  in  size  and  shape  of  the  individual  cells.  Often  there 
were  indentations  and  constrictions,  sometimes  buddings.  In  many 
cells  there  were  one  or  many  vacuoles,  often  so  large  that  the 
nucleus  was  pushed  to  one  side,  sometimes  hardly  visible.  The 
nuclei  varied  in  size  and  number.”  The  examination  of  the  stained 
cells  showed  large  numbers  of  cells  in  a state  of  indirect  division, 
and  especially  cells  with  atypical  mitoses. 

“The  most  remarkable  features  of  the  sediment  are  presented  by 
the  great  number  of  karyokinetic  figures.  These  are  especially 
common  in  cells  from  twelve  to  eighteen  micromillimeters  in  diam- 
eter. The  protoplasm  of  these  cells  is  usually  more  homogeneous 
than  that  of  others.  Vacuoles  sometimes  occur,  and  in  rare  cases 
the  protoplasm  may  be  very  much  degenerated.  Mitoses  are  so 
numerous  that  every  field  contains  one  or  more.  Often  two  to  five 
can  be  seen  in  a small  field.  Various  stages  of  nuclear  and  cell-divi- 
sion are  present.  The  most  common  is  that  of  the  equatorial  plate. 
The  spirem  and  the  monaster  are  uncommon.  The  metaphase  is 
not  so  easily  recognizable,  partly  on  account  of  the  obscurity  of 
many  of  the  figures.  The  anaphase  is  common.” 

Cells  containing  more  than  one  nucleus,  and  with  the  nuclei  in 


THE  EARLY  DIAGNOSIS  OF  GASTRIC  CANCER. 


563 


different  stages,  are  also  common.  In  these  cells  one  or  more  of  the 
nuclei  are  in  the  resting  stage,  and  one,  or  sometimes  more,  in  vari- 
ous stages  of  indirect  division  and  sometimes  showing  an  atypical 
figure. 

The  mitoses  found,  so  far  as  they  can  be  studied  by  the  chro- 
matin alone,  show  all  the  common  abnormalities.  Thus,  we  find 
hypo-  and  hyperchromatic  nuclei,  the  latter  being  rare.  Giant 
mitosis  may  be  represented  by  the  tripolar  figure.  Asymmetrical 
mitosis  is  not  easy  to  recognize,  on  account  of  the  imperfect  preser- 
vation of  the  chromosomes  in  many  cases.  The  examples  of 
mitosis  in  multinuclear  cells  resemble  often  the  figures  given  by 
Krompecher  (“  Ueber  die  Mitose  mehrkerniger  Zellen,  und  die 
Beziehung  zwischen  Mitose  und  Amitose,”  “ Archiv  f.  path.  Anat.,” 
Bd.  cxlii,  S.  447). 

The  interesting  history  of  atypical  mitosis  can  only  be  touched 
on  here.  Eberth  (“  Archiv  f.  path.  Anat.  und  Physiol.,”  Bd.  lxvii) 
was  the  first  to  describe  division  into  four  parts,  but  his  statements 
were  at  first  discredited  by  Flemming  and  Strassburger.  Later, 
however,  Arnold  (ibid.,  Bd.  lxxxiii)  found  multiple  karyokinesis 
in  carcinoma.  He  thought  the  process  might  result  in  polynuclear 
cells.  Since  then  a great  deal  of  work  has  been  done  on  this  sub- 
ject, much  of  it  being  excited  by  the  ingenious  speculations  of 
Hansemann.  From  an  examination  of  the  work  done  so  far  it 
appears  that  atypical  mitoses  are  found  in  various  pathological 
conditions,  not  only  in  new  growths,  like  cancer  and  sarcoma,  but 
also  in  benign  tumors  and  in  regenerations;  in  short,  “in  all  tis- 
sues of  strong  reproductive  activity  and  when  there  is  active 
mitosis”  (Strobe).  They  are  also  found  in  tissues  irritated  by 
various  poisons,  such  as  quinin,  chloral,  nicotin,  etc.,  or  in  tissues 
exposed  to  high  temperature  (Galeotti).  In  cancer  all  observers 
find  them  in  great  richness  and  variety,  but  the  view  that  the  pres- 
ence of  even  a large  number  of  pathological  mitoses  in  a tissue 
justified  the  diagnosis  of  cancer  is  gradually  being  abandoned.  As 
the  literature  is  quoted  in  the  works  of  Hansemann  (“  Archiv  f. 
path.  Anat.,”  Bd.  cxix,  S.  299,  Bd.  cxxm,  S.  356,  Bd.  cxxix,  S.  436  ; 
“ Studien  fiber  die  Specificitat  den  Altruismus  und  die  Anaplasis 
der  Zellen,”  Berlin,  1893),  Strobe  (“  Beitrage  zur  path.  Anat.,” 
Bd.  xi,  xiv,  Cornil  (“  Journal  de  ’1  Anat.  et  de  la  Physiol.  Norm,  et 
Path.,”  1891,  tome  xxvn,  p.  97),  and  Galeotti  (“  Beitrage  zur  path. 
Anat.,”  Bd.  xiv,  xx),  it  is  not  necessary  to  give  a complete  bib- 
liography here  (George  Dock,  loc.  citi). 


564 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


Dock’s  studies  (Joe.  cit .)  concern  only  the  exudates  and  transu- 
dates in  suspected  carcinoma  of  pleura  and  peritoneum.  The 
author,  in  applying  the  method  to  examination  of  particles  from 
carcinomatous  stomachs,  concludes  that  although  the  presence  of 
a large  number  of  cells  in  stomach-contents  showing  atypical 
mitosis  is  not  pathognomonic  of  carcinoma,  nevertheless  it  is  very 
significant,  and  should  stimulate  further  clinical  investigation  toward 
positive  demonstration  of  existence  of  malignant  gastric  neoplasm. 

We  have  found  in  one  case,  four  weeks  before  the  tumor  at  the 
pylorus  was  palpable,  portions  of  gastric  mucosa,  in  which  the 
glandular  ducts  were  very  closely  packed,  containing  numerous 
leukocytes  and  showing  a marked  atypical  appearance  of  the  gland- 
ular epithelia,  differing  from  the  normal  gland-cells  by  intense  pig- 
mentation of  the  nuclei  and  much  darker  staining  of  the  proto- 
plasm, together  with  marked  increase  of  the  connective  tissue, 
small,  round-cell  infiltration,  and  in  portions  disappearance  of  the 
peptic  cells,  cylindrical  epithelial  cells  having  replaced  them. 
In  a second  case  an  abundance  of  cells  showing  atypical  mitosis 
were  found  after  cureting  the  stomach,  and  the  diagnosis  of  cancer 
made  three  months  before  a tumor  became  palpable,  which  at  opera- 
tion proved  to  be  a carcinoma  of  the  posterior  wall.  There  was 
no  marked  Uffelmann  reaction  for  lactic  acid  in  this  case,  but  HC1 
free  and  combined  was  absent  at  every  test-meal.  Such  appear- 
ances in  fragments  should  stimulate  further  careful  and  frequent 
examinations.  Sooner  or  later,  in  our  experience,  a fragment  will 
be  obtained  which  will  give  the  typical  structure  of  carcinoma. 

Concerning  the  significance  of  the  Oppler-Boas  bacillus  we  have 
already  spoken  in  the  first  part  of  this  work.  We  can  confirm  the 
opinions  of  the  authors  quoted,  that  this  organism  is  a very  impor- 
tant diagnostic  sign  in  this  disease.  My  associate,  Dr.  Harry 
Adler,  and  myself  have  thus  far  examined  fifty-five  cases  of  gastric 
carcinoma,  and  found  the  organism  present  in  fifty-two.  Lactic 
acid  is  a valuable  sign  of  intragastric  fermentation,  due  to  stagna- 
tion from  dilatation  and  stenosis.  It  is  not  pathognomonic  of  gas- 
tric cancer,  because  it  may  not  be  present  in  excess  even  in  cancer, 
provided  the  gastric  peristalsis  is  unimpaired  ; and,  again,  it  may 
be  present  when  the  pyloric  stenosis  is  due  to  a benign  obstruction. 
However,  as  the  majority  of  gastric  cancers  destroy  the  motility 
and  cause  obstruction,  lactic  acid,  notwithstanding  the  exceptions 
reported  (William  S.  Thayer),  is  a valuable  diagnostic  sign.  See 
“A  New  Test  for  Lactic  Acid  in  Gastric  Contents,”  J.  P.  Arnold, 


THE  EARLY  DIAGNOSIS  OF  GASTRIC  CANCER.  565 

“The  Journal  of  the  American  Med.  Association,”  August  21, 
1897.  This  is  a modification  of  the  chlorid  of  iron  test,  but  not 
so  accurate  as  that  given  on  page  169.  Lactic  acid  is  formed  in 
the  stomach  by  the  action  of  lactic  acid  bacilli  on  carbohydrates. 
Sticker  has  proved  that  the  simple  passage  of  carbohydrates 
through  the  mouth  causes  the  formation  of  more  or  less  lactic 
acid  without  exception  ; the  amount  formed  in  this  way  is  too  small 
to  be  discovered  by  the  Uffelmann  test. 

Four  conditions  are  necessary  to  effect  excessive  formation  of 
lactic  acid  in  the  stomach  ; these  are:  (1)  Impaired  gastric  peris- 
talsis, which  means  stagnation  ; (2)  absence  of,  or  great  reduction 
of,  HC1  secretion ; (3)  reduction  of  albumin  digestion,  and  (4)  im- 
paired absorption.  Although  there  may  be  stagnation  and  reduc- 
tion or  absence  of  HC1  secretion,  lactic  acid  will  not  form  in  the 
stomach  if  the  proteid  digestion  is  fairly  good  and  does  not  fall 
below  seventy-five  per  cent.  Whenever  there  is  much  lactic  acid 
in  the  stomach,  the  proteid  digestion  will  usually  be  below  fifty 
per  cent,  or  entirely  absent.  The  importance  of  impaired  albumin 
digestion  as  a factor  in  the  formation  of  lactic  acid  has  been  first 
emphasized  by  Hammerschlag  and  confirmed  by  Lindner  and 
Kuttner.  It  is  indispensable  to  investigate  the  combining  power 
that  proteids  have  for  free  lactic  acid  in  this  connection,  for  this 
organic  acid  can,  to  a certain  extent,  replace  HC1  in  proteolysis. 
If,  as  Hammerschlag  points  out,  lactic  acid  is  absent  when  albu- 
min digestion  is  perfect,  or  rather  above  seventy-five  per  cent., 
although  the  other  conditions  may  exist,  the  question  arises,  How 
much  of  the  already  formed  lactic  acid  may  have  entered  into  com- 
bination with  the  albumin  of  the  food  (in  the  absence  of  HC1)  and 
thus  escaped  detection  ? 

(1)  In  the  progress  of  gastric  carcinoma  the  secretion  of  HC1 
suffers  first  (destruction  of  oxyntic  cells) ; then  (2)  the  formation  of 
pepsin  and  rennin  becomes  impaired — the  loss  of  pepsin  brings  on 
the  defective  albumin  digestion  ; (3)  lactic  acid  fermentation  fol- 
lows as  a third  step,  requiring,  in  addition  to  the  other  two  condi- 
tions, the  factor  of  stagnation. 

The  accuracy  of  the  diagnosis,  upon  which  the  success  of  any 
possible  operation  must  depend,  is  based  on  : (1)  The  recognition 
of  tumors  ; (2)  the  finding  of  cancerous  particles  in  the  wash- 
water;  (3)  demonstration  of  the  Oppler-Boas  bacillus;  (4)  the 
excess  of  lactic  acid;  (5)  the  absence  of  HC1  and  ferments, 
reduced  or  absent  albumin  digestion — by  the  filtrate  of  the  gastric 


566 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


contents;  (6)  the  occurrence  of  hematemesis  and  melena ; (7)  the 
loss  of  motility  and  presence  of  gastrectasia ; (8)  the  general  symp- 
tomatology and  anamnesis. 

The  early  diagnosis  is  possible  only , as  far  as  I can  judge  at 
present,  by  frequent  microscopical  examinations  of  curetings  from 
the  gastric  mucosa  which  are  very  significant  if  they  give  evidence 
of  numerous  atypical  mitoses.  In  any  case,  showing  absence  of  HC1 
together  with  any  one  single  sign  of  the  others  just  enumerated, 
that  does  not  improve  under  three  weeks  of  treatment,  exploratory 
laparotomy  should  be  advised.  (Hemmeter,  “The  Early  Diag- 
nosis of  Cancer  of  the  Stomach,”  “New  York  Medical  Record,” 
October  21,  1899,  p.  577.) 

Carcinoma  of  the  Cardia. — Signs  and  Symptoms. — Complaints 
of  an  uncomfortable  feeling,  as  of  a foreign  body,  and  of  pressure 
above  the  gastric  region,  particularly  after  the  ingestion  of  food. 
Sensations  of  pain  are  not  contemporaneous  with  swallowing  of 
food,  but  occur  independently.  On  ingestion  of  food  a sensation 
as  if  the  same  becomes  clogged,  or  is  caught  before  it  reaches  the 
stomach  ; patients  imagine  that  copious  drafts  of  water  give  relief, 
most  likely  because  this  can  pass  through  the  stenosis  caused  by 
the  neoplasm.  Another  important  symptom  is  vomiting,  which  is 
not  actual  gastric  vomit,  but  the  retching  up  of  mucus  and  a few 
food  particles  containing  no  HC1.  The  cause  of  these  regurgita- 
tions of  masses  of  mucus  is  the  formation  of  a large  dilatation  of 
the  esophagus  above  the  stenotic  carcinoma  of  the  cardia.  In  this 
esophageal  diverticulum  or  dilatation  the  food  is  caught,  retained, 
putrefies,  and  is  eventually  vomited  up  again.  There  is  also  a 
septic  catarrhal  esophagitis  present  at  this  place.  Liquid  or  semi- 
liquid substances  may  for  a long  time  be  able  to  pass,  while  rela- 
tively solid  substances  give  rise  to  the  difficulties  stated.  Later 
on,  as  the  stenosis  increases,  liquids  can  not  pass  either,  and  loss 
of  appetite  and  strength  goes  on  uninterruptedly. 

If  an  obstacle  to  the  passage  of  the  sound  can  be  ascertained  at 
the  entrance  to  the  stomach  in  a person  over  thirty  years  of  age, 
the  diagnosis  of  cancer  of  the  cardia  becomes  certain.  In  all  such 
suspected  cases  only  a soft  elastic  tube  should  be  used  for  explora- 
tive sounding.  In  a number  of  cases  in  private  practice  I was 
enabled  to  establish  the  diagnosis  by  microscopical  examination  of 
small  portions  of  the  carcinoma  that  were  brought  up  with  the 
sound.  These  neoplastic  fragments  are  occasionally  found  in  the 
eye  of  a lower  opening  of  the  sound,  and  they  constitute  a definite 


DIAGNOSIS  OF  CARCINOMA  OF  THE  CARDIA.  567 

criterion.  In  one  of  the  foregoing  cases  the  diagnosis  was  con- 
firmed by  Dr.  M.  Einhorn,  and  in  the  other  by  autopsy.  In 
addition  to  the  sounding  and  the  cancerous  fragments,  the  follow- 
ing signs  are  of  diagnostic  importance : 

1.  Percussion  of  the  region  over  xiphoid  cartilage  is  very  painful. 

2.  On  the  sound  blood  will  frequently  be  found  mixed  with  the 
extremely  fetid  mucus,  and  at  times  nests  of  cancer  cells. 

3.  On  placing  a stethoscope  over  the  epigastrium,  normally  two 
deglutition  sounds  can  be  heard.  One  is  synchronous  with  the 
beginning  of  the  act  of  swallowing,  and  the  other  is  heard  from 
seven  to  twelve  seconds  later.  In  carcinoma  of  the  cardia  the 
second  deglutition  sound,  which  signifies  the  entrance  of  liquid 
into  the  stomach,  may  be  much  delayed  or  absent  entirely;  this 
sign  is  of  importance  per  se. 

4.  Supraclavicular  swelling  of  the  lymph-glands,  if  palpable,  sup- 
ports the  diagnosis,  but  this  is  a rare  sign  in  my  experience. 

5.  Lauenstein  asserts  that  there  is  a systolic  murmur  audible  in 
the  epigastrium,  due  to  pressure  of  the  tumor  upon  the  aorta. 
According  to  Boas  this  is  an  inconstant  sign. 

Duration  of  the  disease  is  six  to  nine  months  after  the  first 
symptoms  are  manifested  ; death  occurs  as  a result  of  gradual 
exhaustion,  marasmus,  aspiration  pneumonia,  secondary  carcino- 
mata in  the  liver  and  other  organs,  and  intercurrent  hemorrhages. 

Differential  diagnosis  from  chronic  gastritis  is  difficult  in  the 
beginning  of  cancer  of  the  cardia,  as  in  both  the  presence  or  absence 
of  hydrochloric  acid  is  no  criterion  ; but  as  the  cancer  progresses, 
the  sound  will  settle  the  doubt  in  locating  the  stenosis.  From  eso- 
phageal ulcer  the  cardia  carcinoma  is  differentiated  by  the  fact 
that  pain  is  immediately  associated  with  deglutition  of  food,  by  the 
age  of  patient  (see  tables  of  ages  at  which  ulcer  and  cancer  are 
most  frequent),  by  the  hematemesis  and  the  bloody  stools  of 
ulcer.  Ulcer  of  the  esophagus  is  extremely  rare  in  comparison  to 
cancer. 

From  diverticulum  the  cardia  carcinoma  is  differentiated  by  the 
following  facts  : Diverticulum  is  frequent  in  the  upper  third,  rare 
in  the  lower  third,  of  the  esophagus.  The  permeability  of  the 
gullet  will  be  more  variable  than  in  cancer,  because  the  sound  will 
often  skip  the  diverticulum.  In  the  latter  there  will  rarely  be  pain, 
and  the  marasmus  will  not  be  so  progressive  and  rapid.  From 
cardiospasm,  or  cramp  of  the  cardia,  the  carcinoma  is  differentiated 
by  the  occasional  free  passage  of  the  thickest  tubes  in  the  neurosis, 


568  MALIGNANT  TUMORS  OF  THE  STOMACH. 

which  occurs  almost  exclusively  in  neurasthenics.  Nutrition  is 
not  so  much  damaged  as  in  cancer. 

If  tuberculosis  or  syphilis  is  present,  one  must  think  of  .the  pos- 
sibility of  the  neoplasm  being  caused  by  these  diseases. 

Syphilis  may  be  excluded  or  diagnosed  by  the  effect  or  non- 
effect of  specific  treatment,  and  tuberculosis  by  the  effect  of  hypo- 
dermic injection  of  minute  doses  of  tuberculin. 

Treatment  of  Cardia  Carcinoma. — So  long  as  there  is  no  cure 
possible,  this  must  be  palliative.  During  the  time  that  deglutition 
still  brings  liquid  food  into  the  stomach,  the  sufferer  must  be  care- 
fully fed  on  highly  nutritious  liquid  diet — liquid  eggs  and  wine,  as 
described  in  the  diet  of  gastritis,  beef-tea,  soups  of  fluid  potato  or 
pea  puree  in  bouillon,  Leube-Rosenthal  beef-solution,  von  Mehr- 
ing’s  “ Kraft  ” chocolate,  egg'-nog.  When  pain  was  great,  I have 
found  that  chloral  hydrate  (15  grains,  three  times  daily)  not  only 
relieved  it,  but  acted  as  a local  disinfectant  in  the  diverticulum 
above  the  stenosis.  Boas  recommends  iodid  of  potassium  in  doses 
of  15  grams,  three  times  daily,  as  aiding  in  keeping  the  esophagus 
from  closing  up  as  soon  as  it  would  otherwise.  Arsenic  is  said  to 
effect  the  same  prolonged  permeability.  I have  had  no  success 
with  these  drugs  in  my  cases.  In  one  case  I succeeded  in  keep- 
ing the  esophagus  open  for  six  months  by  intubating  with  an  in- 
elastic tube  four  inches  long  and  as  wide  as  an  ordinary  Ewald 
tube.  The  tube  was  removed  every  ten  days  and  replaced.  Patient 
lost  no  weight  in  those  six  months,  but  even  gained.  Death  was 
caused  by  aspiration  pneumonia,  during  a period  in  which  the  tube 
was  left  out  in  order  to  wrest  the  esophagus  from  the  stout  cord  by 
which  the  tube  was  connected  with  the  mouth,  and  which  was 
usually  tied  around  the  patient’s  neck. 

When  deglutition  is  impossible,  the  only  thing  left  to  be  done  is 
gastrostomy.  If  the  patient  can  be  persuaded  to  undergo  this 
operation,  it  should  be  done  before  marasmus  proceeds  too  far, 
as  it  then  prolongs  life  and  the.  shock  of  the  operation  is  better 
borne. 

This  operation  consists  in  making  an  opening  into  the  stomach 
for  the  purpose  of  feeding  the  patient  by  passing  food  directly  into 
the  organ.  F.  Kaiser  (in  Czerny,  “ Beitr.  z.  operativ  Chirurg.”) 
collected  31  gastrostomies;  of  these,  28  died  from  the  immediate 
results  of  the  operation.  Zesas  (“  Archiv  f.  klin.  Chirurg.,”  Bd. 
xxxii,  S.  188)  reported  13 1 cases  from  literature,  mostly  esophageal 
cancers,  which  in  their  stenosing  effects  are  identical  with  those  of 


SIGNS  IN  CARCINOMA  OF  THE  BODY  OF  STOMACH.  569 

the  cardia.  Among  these  only  19.5  percent,  recovered  sufficiently 
from  the  operation  to  call  this  a success. 

Carcinoma  of  the  Body  of  the  Stomach  and  of  the  Pylorus. 

— ( Cancer  of  the  Fundus , Anterior  or  Posterior  Walls , the  Curva- 
tures, and  Pylorus .) 

Subjective  Signs. — 1.  Sudden  abrupt  beginning  of  the  disease, 
striking  an  apparently  healthy  organ. 

2.  Loss  of  appetite  in  90  per  cent,  of  cases. 

3.  Aversion  to  meat. 

4.  In  stenosing  pyloric  cancer  there  is  much  thirst. 

5.  Frequent  eructations,  which,  when  there  is  dilatation,  can  be 
very  offensive. 

6.  Pressure  in  the  beginning,  pain  later  on. 

7.  There  is  frequent  vomiting,  which  is  more  copious  in  pyloric 
cancers  because  of  the  accumulations  from  the  dilatation. 

Frequently  the  vomit  has  a coffee-ground  appearance,  and  the 
hemin  test  (referred  to  in  part  1)  proves  the  presence  of  blood. 
The  state  of  the  bowels  is  variable,  but  constipation  occurs  in  75 
per  cent.  The  vomit  contains,  as  a rule,  no  hydrochloric  acid,  but 
excess  of  lactic  acid  and  Oppler-Boas  bacilli. 

Objective  Signs. — On  inspection,  palpation,  and  percussion  a 
tumor  can  be  made  out  in  at  least  50  per  cent,  of  the  cases. 

Tumors  of  the  pylorus  do  not  move  with  the  respiratory  move- 
ments unless  attached  to  the  liver  ; tumors  of  the  curvatures  gen- 
erally show  distinct  respiratory  movements. 

Examination  of  Stomach- Contents. — The  results  will  be  character- 
istic in  most  cases,  and  evince — 

1.  Grave  interference  with  the  motility. 

2.  Suppression  of  secretion. 

3.  Reduced  or  absent  albumin  digestion. 

4.  Products  of  stagnation  dependent  upon  these. 

5.  Fragments  of  neoplasm  or  mucosa  showing  characteristics 
previously  described. 

The  disturbances  of  peristalsis  are  due  most  likely  to  a direct 
invasion  of  the  muscularis  by  cancerous  proliferation.  The  simplest 
way  of  testing  the  motor  disturbance  is  to  cleanse  the  stomach 
thoroughly  by  lavage  in  the  evening,  giving  a test-supper  thereafter 
and  examining  the  following  morning,  when,  normally,  the  stomach 
should  be  empty;  but  in  carcinoma  much  food  and  mucus,  with 
absence  of  hydrochloric  acid  and  presence  of  lactic  acid,  are  found 
in  88  percent,  of  the  cases  in  our  experience.  In  carcinomata  that 


570 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


have  arisen  from  old  ulcers,  a secretion  of  hydrochloric  acid  per- 
sists until  the  last  stages  of  the  disease.  This  assertion  of  Rosen- 
heim’s is  not  always  correct;  if  the  glandular  layer  is  invaded, 
secretion  must  cease,  no  matter  whether  the  carcinoma  arose  from 
an  ulcer  or  not.  The  fact  that  carcinomatous  ulcers  do  not 
destroy  the  secretion  of  HC1,  as  a rule  is  due  to  their  anatomical 
location — they  occurring  mostly  in  the  pyloric  region,  which  does 
not  contain  the  oxyntic  cells  in  abundance.  Lactic  acid  is  tested  for 
by  Uffelmann’s  reaction ; in  carcinoma  there  is  an  excess  in  from  78 
to  90  percent,  of  the  cases.  Demonstration  of  the  long,  base-ball- 
bat-shaped  Oppler-Boas  bacillus  is,  according  to  Kaufman,  Schle- 
singer,  and  Riegel,  a very  important  sign.  There  should  always 
be  a careful  lookout  for  histological  evidences,  such  as  bits  of  the 
growth  in  the  wash-water  and  vomit ; this  clinches  the  diagnosis. 

Secondary  symptoms  are  anemia,  cachexia,  and  edema  of  the 
ankles  in  15  to  20  per  cent,  of  the  cases.  The  urine  contains 
excess  of  nitrogen  excretion,  indican,  and  peptone.  Latent  cancers 
may  occur  ; they  are  very  rarely  observed,  however,  at  the  autopsy. 

Ulcus  Carcinomatosum. — The  diagnosis  is  made  from  a history  of 
ulcer,  with  years  of  gastric  pain, — not  a sudden  and  abrupt  begin- 
ning,— and  the  presence  of  hydrochloric  acid,  even  hyperacidity. 
A previous  history  of  hematemesis  and  blood  in  the  stools  points 
to  origin  of  the  carcinoma  from  ulcer.  Simple,  uncomplicated  ulcer 
may  cause  a tumor-like  thickening,  simulating  cancer ; here  the 
analysis  of  gastric  contents  may,  in  rare  cases,  even  show  excess  of 
lactic  acid,  owing  to  motor  insufficiency  and  cicatricial  stenosis,  and 
the  diagnosis  then  becomes  difficult,  as  is  also  the  differential  diag- 
nosis of  ulcus  carcinomatosum  from  simple  hypertrophic  stenosis 
of  the  pylorus.  Fortunately,  such  states  without  any  other  impor- 
tant signs  are  rare. 

Treatment. — There  is  no  successful  medicinal  treatment  for  this 
disease.  Life  may  be  prolonged  by  a suitable  diet,  as  nutritious  as 
possible  and  adapted  to  the  individual  conditions.  A highly  nutri- 
tious proteid,  carbohydrate,  and  fatty  diet  should  not  be  interdicted 
so  long  as  the  motility  is  good  and  the  patient’s  strength  can  be 
upheld  by  intestinal  digestion.  When  there  is  stagnation  owing  to 
pyloric  obstruction,  the  carbohydrates  and  fats  must  be  diminished. 
The  best  tonic  for  the  stomach  is  daily  lavage,  even  when  there  is 
not  much  stagnation ; but  when  the  latter  is  marked  and  accom- 
panied by  fermentation,  antiseptics  may  advantageously  be  added 
— such  as  boric  acid,  20  to  30:  1000  H20  ; salicylic  acid,  3 : 1000 


TREATMENT  OF  GASTRIC  CANCER. 


571 


H20;  sodium  benzoate,  10  to  30:  1000  H20;  resorcin,  10  to  30:  1000 
H20;  thymol,  5 : 1000  H20 ; lysol,  I to  2 : 1000  H20  ; hydrochloric 
acid,  4 to  5 : 1000  H20.  It  is  always  well  to  get  the  stomach 
clean  by  simply  using  warm  salt  solution,  and  to  finish  the  lavage 
by  a last  irrigation  with  one  of  the  disinfectants,  of  which  we  pre- 
fer hydrochloric  acid. 

A tonic  which  has  been  serviceable  in  my  experience  and  which 
will  arouse  appetite  and  promote  digestion  in  the  invaded  organ,  if 
this  is  at  all  possible,  is  the  following : 


K • Extract,  condurango, 45  ° c.c.  f^xij 

Strychnin,  sulph., 0.021  c.c.  gr. 

Acid,  hydrochloric,  dil. , 12.0  c.c.  f^iij 

Elixir  gentianse, q.  s.  180.0  c.c.  f;|vj. 


M. 


SlG. — Take  one  tablespoonful  in  two  ounces  of  water,  after  meals,  through  a tube. 


When  there  is  much  anemia,  the  following  formulae  has  my 
preference  in  this  disease  as  well  as  in  ulcer : 

1£  . Solution  of  iron  and  manganese,  . . . 186.60  grams 

Liquor  potassi  arsenit., 3.0  grams 

SlG. — One  tablespoonful  three  times  daily. 

Or — 

H.  Strychnin,  sulph.,  0.02  grams 

Elix.  gentian,  cum  ferri  chloridi,  . q.  s.  186.60  grams 
SlG. — One  tablespoonful  three  times  daily. 

Constipation  is  best  met  by  large  colon  irrigations  or  with  the 
fluid  extract  or  active  syrup  of  cascara  sagrada  (Clinton). 

Diarrhea  must  be  met  by  salol,  bismuth  salicylate,  or  benzo- 
naphthol.  Opiates  are  not  advisable  for  this  symptom  unless  there 
is  pain. 

For  pain  hot  external  cataplasms  and  20  to  30  drops  of  com- 
pound spirit  of  ether  should  be  first  tried.  If  severe,  codein  (gr. 

extract,  belladonnse  (gr.  in  f§j  of  peppermint  water,  gener- 
ally relieves  it,  and  may  be  repeated  if  requisite.  The  pain  is  rarely 
so  intense  as  to  require  hypodermic  injections  of  morphin.  Lavage 
systematically  and  scientifically  employed  seems  to  prevent  pain ; 
it  certainly  prolongs  life,  and  sometimes  apparently  works  wonders 
for  these  patients. 

For  the  diet  in  gastric  carcinoma  we  refer  to  the  chapter  on 
Dietetics,  pages  203  and  240. 

Fifty  grams  of  rich  milk  or  a glass  of  tokay,  a few  crackers,  and 
chocolate  are  permissible  foods;  also  young  pigeon,  partridge,  and 


f.lvj 

rr^xlviij.  M. 


gr-  lA 

Svj-  M. 


5;2 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


prairie-hen.  If  the  motility  is  good,  one  must  not  be  too  severe 
on  the  patient’s  desire  for  food ; many  cases  can  live  and  gain 
strength  on  an  ordinary  nourishing  diet  when  it  is  not  retained  too 
long  in  the  stomach  ; under  these  circumstances  mutton  chops  and 
broiled  beefsteak,  finely  minced,  may  be  allowed. 

Surgical  Treatment. — As  already  mentioned,  gastrostomy  is  a 
palliative  operation  for  malignant  tumor  of  the  cardia  and  esopha- 
gus, to  permit  of  direct  introduction  of  food  by  establishing  an 
opening  between  the  stomach  and  the  abdominal  wall.  In  carcinoma 
of  the  pylorus  another  palliative  operation  is  practised — when  it  is 
impossible  or  inexpedient  to  remove  the  growth — under  the  name 
of  gastro-enterostomy.  This  consists  in  the  establishment  of  a new 
communication  between  the  stomach  and  the  small  intestine,  thus 
allowing  the  chyme  to  reach  the  intestines  without  passing  the 
pylorus. 

The  radical  operations  are  resections  of  the  pylorus  or  excision 
of  the  tumor,  no  matter  where  it  may  be  situated  in  the  stomach. 
These  operations  are  contraindicated  if  metastases  are  detectable 
in  other  organs,  by  the  presence  of  great  anemia  or  cachexia, 
by  the  large  size  of  the  tumor,  or  if  there  are  adhesions  to  other 
organs.  The  detailed  descriptions  of  these  operations  belong  to 
text-books  on  abdominal  surgery  : 

See  “ Surgery  of  the  Alimentary  Canal,”  by  A.  Ernest  Maylard  ; P.  Blakis- 
ton’s  Son  & Co.,  Philadelphia,  1896. 

“The  Cartwright  Lectures  on  Gastric  Surgery,”  by  W.  W.  K'een,  “ Phila. 
Med.  Jour.,”  volume  1,  1898. 

“ Abdominal  Surgery,”  by  J.  Grieg  Smith,  published  by  P.  Blakiston’s  Son  & 
Co.,  Philadelphia,  1896. 

“ Surgery  by  American  Authors,”  by  Roswell  Park,  volume  11,  chapter  viii, 
published  by  Lea  Brothers,  Philadelphia. 

“System  of  Surgery,”  by  Fred.  S.  Dennis,  volume  IV,  page  217. 

“ Abdominal  Surgery,”  by  M.  H.  Richardson  and  Farrar  Cobb. 

“ A Text-book  of  Abdominal  Surgery,”  by  Skene  Keith  and  G.  S.  Keith. 

Frederick  Treve’s  “ Manual  of  Operative  Surgery,”  volume  11,  page  405. 

Franz  Koenig,  “ Lehrbuch  d.  speciel.  Chirurg.,”  Band  11,  Seite  281. 

Penzoldt  and  Stintzing’s  “ Handbuch  d.  speciel.  Therapie,”  volume  iv,  page 
444.  (“  The  Operative  Treatment  of  Gastric  Disorders,”  by  Professor  von 

Heinecke,  Erlangen.) 

The  Course  to  Pursue  in  Practice. — Occurrence  and  Detection. 
— With  the  exception  of  the  cases  that  arise  from  ulcer,  cancer  of 
the  stomach,  as  a rule,  develops  gradually.  Among  the  phenomena 
are  symptoms  of  more  or  less  severe  dyspepsia,  gradually  ranging 


THE  COURSE  TO  PURSUE  IN  PRACTICE. 


573 


to  the  most  decided  ones  of  chronic  gastritis,  which,  almost  with- 
out exception,  accompany  every  carcinoma  of  the  stomach.  Therein 
lies  a great  hindrance  to  timely  detection.  If,  however, — and  this 
especially  in  older  individuals, — the  symptoms  of  chronic  gastritis 
appear  without  any  distinct  cause,  and  in  a stomach  previously 
entirely  sound,  and  get  worse  constantly,  even  with  a mild  diet, 
and  are  increased  by  pains  and  vomiting  even  before  food  is  taken 
(with  a jejune  stomach),  so  that  in  a few  weeks  rapid  emaciation, 
with  an  extraordinary  sallow  complexion,  become  pronounced 
features,  carcinoma  of  the  stomach  should  be  suspected. 

What  are  the  characteristic  and  most  important  diagnostic  signs 
of  gastric  carcinoma?  Examination  with  the  stomach-tube  is  to 
be  made,  and  the  reaction  for  free  acid  in  the  contents  of  the 
stomach  which  have  been  brought  up  one  hour  after  the  test- 
breakfast  is  to  be  tried.  In  any  case  the  treatment  with  lavage  is 
to  be  instituted,  and  with  it  the  most  frequent  repetition  of  the  test 
for  free  acid.  In  this  connection  it  is  well  to  make  examination  of 
the  juices  after  several  test-meals,  and  eventually  with  means  stim- 
ulating the  secretion  of  acids  (orexin) ; but,  of  course,  always  at  a 
time  when,  under  normal  circumstances,  free  acid  ought  to  be 
present.  Protracted  absence  of  free  hydrochloric  acid,  even  though 
it  may  occur  in  other  diseases  of  the  stomach,  speaks,  in  the 
method  of  procedure  indicated,  with  great  probability  for  cancer, 
since  in  more  than  ninety  per  cent,  of  the  cases  HC1  was  found 
absent.  Frequent  presence  of  hydrochloric  acid  argues  against 
cancer.  Repeated  examination  with  the  tube  brings  us  other  signs 
of  carcinoma,  which  by  other  observations  are  not — or,  at  any  rate, 
not  so  easily — obtained.  Occasionally  a particle  of  the  cancer  is 
found  in  the  vomited  masses,  and  the  diagnosis  is  made  sure. 
This  may  happen  more  easily  with  lavage  in  the  wash-water  from 
carcinoma  of  the  cardia,  when  it  may  also  be  found  in  the  eye  of 
the  tube.  During  methodical  lavage,  coffee-ground  vomit  is 
seen  earlier  and  more  frequently  than  if  we  depend  upon  the 
vomiting.  In  the  latter  case  it  is  often  poured  away  before  the 
physician  gets  a chance  to  examine  it.  In  case  of  carcinoma  one 
does  not  need  to  fear  hemorrhage  in  using  the  tube,  provided  it 
is  done  carefully.  Finally,  one  may  also  use  the  contents  of  the 
stomach  obtained  with  the  tube  for  the  quantitative  and  qualita- 
tive determination  of  the  lactic  acid. 

An  approximately  simple  method  for  this  purpose  has  been 
recently  published  by  H.  Strauss,  of  Riegel’s  Klinik  (“  Berlin,  klin. 


574  MALIGNANT  TUMORS  OF  THE  STOMACH. 

Wochenschr.,”  1895,  No.  37).  Excess  of  lactic  acid  has  been 
found  in  eighty-two  per  cent,  of  my  cases.  It  is  true  that  it  has 
also  been  shown  to  exist  with  gastritis  and  hypertrophic  benign 
stenosis  of  the  pylorus,  which  somewhat  diminishes  its  value. 
It  is  not  an  early  sign  in  this  disease.  But  still,  as  it  appears  at 
present,  in  connection  with  other  signs  it  is  valuable  for  the 
diagnosis,  even  though  its  absence  does  not  argue  against  carci- 
noma and  was  especially  observed  in  carcinomatous  ulcer.  It 
will  therefore  be  possible  in  many  cases  to  fix  the  diagnosis  with 
a great  degree  of  probability,  even  before  a tumor  is  palpable, 
when  elderly  persons  previously  sound  grow  rapidly  worse  in 
spite  of  suitable  treatment,  and  when  cachectic  symptoms  ap- 
pear quickly,  when  the  absence  of  free  hydrochloric  acid  con- 
tinues, or  when  there  is  vomiting  of  coffee-ground  masses.  Since, 
ordinarily,  the  tumor  can  only  be  felt  when  the  cancer  has 
reached  a certain  size  and  lies  in  an  especially  favorable  posi- 
tion, the  diagnosis  by  recognition  of  a tumor  is  generally  no  longer 
an  early  diagnosis.  The  examination  in  chloroform  narcosis  must 
be  brought  in  at  a comparatively  early  date  to  facilitate  pal- 
pation, and  with  a sufficient  degree  of  insensibility  it  will  indeed 
very  much  facilitate  the  detection.  Distention  with  air  through 
the  stomach-tube  renders  a tumor  at  the  front  wall  or  at  the 
pylorus  more  distinctly  recognizable,  and  gives  information  con- 
cerning the  size  of  the  stomach.  Distention  of  the  intestine  in 
narcosis  by  means  of  air  is  also  brought  in  as  an  aid  to  the  diag- 
nosis. If  it  is  not  possible  to  feel  a tumor,  and  if,  in  spite  of  this, 
one  is  convinced  that  a neoplasm  does  exist,  one  should  propose  an 
exploratory  incision,  with  eventual  further  operative  procedures  if 
the  prospects  warrant  immediate  good  results.  If  carcinoma  should 
follow  apparently  in  the  course  of  gastritis  or  ulcer,  the  diagnosis 
becomes  more  difficult  than  if  it  is  developed  in  an  apparently 
healthy  stomach,  for  then  the  symptomatology,  the  state  of  the 
secretions,  and  the  proof  of  the  presence  of  lactic  acid  or  hemor- 
rhage are  of  much  less  value.  Then  the  diagnosis  requires  the 
greatest  circumspection.  Since  the  detailed  description  of  all  the 
possibilities  does  not  suit  the  compass  of  the  work,  we  will  here 
only  refer  again  to  the  fact  that,  with  rapidly  increasing  emacia- 
tion of  the  patients,  the  physician  must  not  rest  until  he  has 
found  the  causes  in  a carcinoma,  or  in  another  factor,  such  as 
stenosis  of  the  pylorus.  In  all  chronic  cases  with  the  chemical 
and  physical  signs  described,  exploratory  laparotomy  is  urged  if 
improvement  does  not  follow  in  three  weeks  of  appropriate  treat- 


TREATMENT  OF  INDIVIDUAL  SYMPTOMS. 


575 


ment.  In  cases  in  which  the  carcinoma  causes  no  symptoms,  or 
only  very  indefinite  ones  as  regards  the  stomach  (for  instance,  in 
the  case  of  people  advanced  in  age),  the  diagnosis  is,  of  course, 
impossible,  and  active  treatment  not  so  important.  If  there  is  a pal- 
pable tumor  in  the  region  of  the  stomach,  we  have  the  problem  of 
determining  that  the  same  is  really  a new  formation  belonging  to 
the  stomach.  From  the  therapeutic  standpoint,  one  is  to  avoid  con- 
founding it  with  tumors  which  either  need  not  be  or  can  not  be 
operated.  Among  the  former  are  to  be  mentioned  the  normal 
head  of  the  pancreas,  which  with  severe  emaciation  might  be  mis- 
taken for  a carcinoma;  lymphatic  glands,  which  are  felt  as  small 
smooth  nodules  alongside  of  the  spinal  column,  and  may  be  quite 
harmless  (Leube);  tumor  of  the  spleen,  which  can  not  be  grasped 
from  above;  movable  kidney,  which  is  smooth,  and  which  gives 
the  kidney  shape.  Of  the  nonoperable  tumors,  or  only  exception- 
ally operable,  we  should  exclude  cancer  of  the  liver,  which,  with- 
out the  characteristic  gastric  symptoms  of  the  stomach,  causes  the 
liver  to  appear  enlarged  and  much  distended,  or  causes  nodules  to 
appear  on  the  palpable  lower  edge  (see  the  extension  of  the  cancer 
from  the  stomach  to  the  liver).  Gall-bladder  and  omental  carci- 
nomata are  chiefly  to  be  excluded  from  diagnosis  by  the  absence  of 
the  conspicuous  stomach  symptoms,  and  the  latter  by  the  want  of 
respiratory  movability  and  by  the  presence,  generally,  of  ascites. 
Carcinoma  of  the  mesenteric  glands  is,  under  some  circumstances, 
not  to  be  distinguished  from  that  of  the  stomach.  Penzoldt 
recently  observed  a case  which  had,  in  addition,  violent  hemat- 
emesis  and  stomach  symptoms.  The  differential  diagnostic  points 
from  tumors  of  the  duodenum,  colon,  and  neighboring  organs  have 
already  been  considered  (pp.  556  to  558). 

DIET  FOR  GASTRIC  CARCINOMA. — {Rosenheim.) 

8 a.  m. — One  cup  of  tea  with  milk  or  a farinaceous  soup,  eventually  with  a 
little  wheat  bread. 

10  A.  m. — Toast,  sardels,  caviar,  perhaps  also  oysters,  with  good  claret,  sherry, 
or  Madeira. 

1 P.  m. — Bouillon  or  soup  (flour,  rice,  sugar,  and  tapioca  soups),  eventually 
with  addition  of  peptone,  or  Leube-Rosenthal’s  meat-solution.  White 
meat  or  game,  or  beefsteak  from  finely  scraped  beef,  or  jellies  with  gravy, 
or  calves-feet.  Vegetables.  Potato  puree,  finely  chopped  spinach,  well 
cooked  asparagus. 

Stews  : Stewed  apples,  pears,  prunes  (without  hulls). 

Drinks  : Red  wine,  water  with  cognac. 

4 p.  m. — Meat  peptone,  chocolate  or  cocoa  with  cakes. 

7 p.  m. — Bouillon  and  soup  from  leguminous  flour. 


576 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


For  further  diet  for  gastric  carcinoma  see  chapter  on  Dietetics. 

Treatment  of  Loss  of  Appetite. — Of  the  so-called  stomachic 
remedies,  condurango  is  useful  in  this  disease.  We  prefer  the 
officinal  fluid  extract  of  condurango.  The  other  stomachics  and 
bitter  tonics  used  are  the  tinctures  of  calumbo,  gentian,  cinchona, 
etc. ; likewise  hydrochloric  acid,  which,  however,  does  not  always 
agree  with  the  patient.  Orexin  generally  has  no  effect,  but  an 
attempt  with  0.2  to  0.3  gm.  of  orexin  basicum  should  be  made. 
Also,  lavages  of  the  stomach  with  decoctions  of  hops  and  quassia 
wood,  according  to  Kussmaul  and  Fleiner,  may  be  used  with  ad- 
vantage. Washing  the  stomach  remains  the  best  means  for  excit- 
ing the  appetite. 

Treatment  of  Vomiting. — Against  vomiting  we  recommend  : 
Small  quantities  of  ice,  ice-cold  water  containing  carbonic  acid  or 
champagne,  a few  drops  of  chloroform,  tincture  of  iodin,  creasote, 
morphin  subcutaneously  or  as  a suppository,  cold  bandages  on  the 
epigastrium.  If  it  is  a consequence  of  stagnation  of  foods  in  the 
stomach,  lavage  is  the  most  efficacious  treatment.  If  the  vomited 
matter  has  a foul  smell,  and  foul  belching  is  present,  one  may  add 
thymol  (0.5  per  cent.),  boric  acid  (two  to  three  per  cent.),  salicylic 
acid,  resorcin,  chloroform  (0.5  per  cent.),  to  the  wash-water.  The 
treatment  of  hemorrhages  is  the  same  as  for  gastric  ulcer. 

Treatment  of  the  Pain. — Steam  vapor,  bandages,  and  poultices, 
hot  cloths,  or  plates  have  only  a temporary  success.  If  the  pains 
are  very  violent,  one  can  not  avoid  the  subcutaneous  injection  of 
morphin,  but  care  must  be  exercised  to  avoid  starting  the  morphin 
habit. 

Treatment  of  Constipation. — This  very  frequent  and  troublesome 
symptom  must  be  eliminated,  if  possible,  by  large  colon  irrigations 
(one  liter),  by  injections  of  water  with  the  addition  of  soap,  turpen- 
tine, castor  oil,  etc.,  which  increase  their  effect,  or  by  the  injection 
of  glycerin.  Only  when  this  is  of  no  avail  must  recourse  be  had 
to  the  vegetable  purgatives — e.  g.,  Extr.  aloe,  Extr.  rhei  comp.,  aa 
3.0;  addeSucc.  liq.,  q.  s.  ft.  pil.  30.  M.  One  or  two  pills  at  bedtime. 
Saline  purgatives  are  justly  objected  to,  since  they  weaken  the 
patient  to  a remarkable  degree.  For  the  same  reason  Penzoldt, 
Ewald,  and  Lebert  declare  that  drinking  cures  at  Carlsbad  and 
other  saline  springs  are  not  advisable.  This  prohibition  is  gen- 
erally very  hard  for  those  patients  who  have  placed  all  their  hope 
on  a sojourn  at  the  springs.  The  advice  of  Lebert  (quoted  by 
Ewald),  to  let  them  drink  small  quantities  of  the  mineral  water 


LITERATURE  ON  CANCER  OF  THE  STOMACH. 


5 77 


at  home,  is  very  practical,  for  generally  it  is  without  success,  and 
the  patient  will  then  willingly  give  up  a trip  to  the  springs.  If  the 
constipation  is  due  to  stenosis  of  the  pylorus,  medicines  by  the 
mouth  are  useless.  So  the  treatment,  briefly,  is  lavage,  tonics, 
rest,  the  most  highly  concentrated  and  nutritious  food,  whenever 
it  is  too  late  or  impossible  to  operate. 

Prognosis. — If  the  diagnosis  can  be  made  early,  and  operative 
treatment  gives  fair  prospects  of  immediate  good  results,  there  is, 
as  we  have  seen  from  the  statistics  given  in  the  chapter  on  Surgical 
Operations  (p.  348),  some  hope  of  prolonging  life.  But  if  an  opera- 
tive interference  is  impossible  (see  the  contraindications,  p.  366) 
or  refused,  the  disease  must  prove  fatal.  Careful  dietetic  and 
mechanical  treatment  may,  in  individual  cases,  prolong  life  for 
several  months.  In  cancerous  neoplasms  that  do  not  affect  the 
orifices  the  immediate  danger  is  not  so  great.  I have  reported  a 
case  in  which  a positive  diagnosis  of  malignant  tumor  could  be 
made  from  a cancer  particle  that  came  up  in  the  wash-water  and 
in  which  a tumor  was  diagnosed  by  Da  Costa  and  Musser  sixteen 
months  before  the  author  examined  the  patient.  This  patient  lived 
two  years  and  two  months  after  the  tumor  was  first  recognized. 


LITERATURE  ON  CANCER  OF  THE  STOMACH. 

1.  Aaron,  C.  A.,  “ The  Early  Diagnosis  of  Cancer  of  the  Stomach,”  “ Canada 
Lancet,”  i897-’98,  xxx,  395-398. 

2.  Acker,"  Zur  Pathogenese  der  Geschwulstmetastasen,”  “ Deutsche  Archiv 
f.  klin.  Med.,”  xi. 

3.  Aisberg,  " Casuistik  zur  Chirurgie  der  Magencarcinoms  ” ; "Drei  Falle 
von  Gastro-enterostomie,  im  dritten  Verlangerung  des  Lebens  um  drei  Jahre 
und  fiinf  Monate,”  " Miinch.  med.  Wochenschr.,”  No.  50  und  51,  1896. 

4.  Arnold,  J.,  “ Ueber  Theilungsvorgange  in  den  Wanderzellen  : ihre  pro- 
gressive und  regressive  Metamorphose,”  "Archiv  f.  mikr.  Anatomie,”  XXX, 

1887. 

5.  Arnold,  J.  P.,  “ Colloid  Cancer  of  the  Stomach,”  " Proc.  Path.  Soc.,” 
Phila.,  1897-98,  1,  305. 

6.  Badaloni,  N.,  "Del  cancero  dello  stomaco,”  " Gazz.  de.  osp.  Milano,” 
1897,  xviii,  705-740. 

7.  Bazy,  " Cancer  de  l’estomac,  gastro-enterostomie  ; avec  le  bouton  de 
Murphy,”  " Bull,  de  la  Soc.  de  chirg.,”  xix,  1896. 

8.  Benedict,  A.  L.,  "Some  so-called  Diagnostic  Points  of  Gastric  Carci- 
noma,” “ Int.  Med.  Magazine,”  Phila.,  i897~’98,  vi. 

9.  Billroth,  "Wiener  klin.  Wochenschr.,”  1891,  No.  34. 

10.  Boas,  J.,  "Ueber  das  Vorkommen  von  Milchsaure  im  gesunden  und 
kranken  Magen,  nebst  Bemerkungen  zur  Klinik  des  Magencarcinoms,”  "Zeit- 
schrift  f.  klin.  Med.,”  Bd.  xxv,  1894. 

38 


578 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


11.  Bousquet,  “ Du  chimisme  gastrique  dans  le  cancer  d’estomac,”  “ These 
de  Paris,”  1896. 

12.  Bosquier,  “ Coexistance  d’une  cirrhose  de  Laennec  et  d’un  cancer  latent 
de  l’estomac,”  “Journal  de  med.de  Lille,”  18,  1,  1896. 

13.  Brechoteau,  “Du phlegmon  peri-ombilical et des  fistulesgastro-cutanese 
dans  le  cancer  de  l’estomac,”  “ These  de  Paris.” 

14.  Bret,  “ Adenopapillare  de  l’estomac,”  “ Soc.  anat.  de  med.  de  Lyon,”  16. 
mars,  1898. 

15.  Brinton,  W.,  “British  and  Foreign  Medico-Chirurgical  Review,”  Jan- 
uary, 1857. 

16.  Brooks,  H.,  “ A Case  of  Primary  Multiple  Sarcoma  of  the  Stomach,  Fol- 
lowing Gunshot  Wound,”  “Med.  News,”  N.  Y.,  1898,  lxxxii,  pp.  617-620. 

1 7.  Bryant,  Jos.  D.,  “The  Wesley  M.  Carpenter  Lecture,”  “ N.  Y.  Med. 
Jour.,”  May  18,  1895. 

18.  Buhre,  B.,  “Die  Bedeutung  der  Milchsaure  Reaction  fur  die  Diagnose 
des  Magenkrebses,”  “ Hygiea,”  1897,  Heft  1 (Schwedisch). 

19.  Cahn  und  von  Mehring,  “ Berl.  klin.  Wochenschr.,”  1885. 

20.  Capello,  P.,  “ A propositio  di  un  raro  caso  di  mio  sarcoma  cistico 
dello  stomaco,”  “Bull.  d.  s.  Accad.  med.  di  Roma,”  1898-99,  xxiv,  321- 
342. 

21.  Capps,  J.  A.,  “ Digestion  Leukocytosis  as  an  Aid  in  Diagnosis  of  Cancer 
of  the  Stomach,”  “ Boston  Med.  and  Surg.  Jour.,”  1897,  cxxxvii,  468,  1. 

22.  Cardarelli,  “Carcinoma  dello  stomaco  svil  uppato  sulfondo  di  ulcera,” 
“ Clin,  mod.,”  Pisa,  1897,  ill,  173. 

23.  Carter,  J.  M.  G.,  “ The  Treatment  of  Carcinoma  of  the  Stomach,”  “ In- 
ternat.  Clin.,”  Phila.,  1897,  in,  45-50. 

24.  Caussade  et  Renon,  “ Cancer  du  pylore,  suppressive  de  la  function 
pylorique,  atrophie  de  l’estomac,  atrophie  generalisee  de  tours  les  organes,” 
“ Presse  med.,”  1 Janvier,  1898. 

25.  Chaine,  “ Cancer  du  pylore  sans  hematemese  ni  melaena  ; Cancer  du 
foie,”  “Jour,  de  med.  de  Bordeaux,”  31  Janvier,  1896. 

26.  Chaput,  “ Ulcere  gastrique  avec  degenerescence  cancereuse  au  debut 
presentation  du  malade,”  “ Soc.  med.  des  hop.,”  15  Octobre,  1897. 

27.  Chiaruttini,  E.,  “ Sul  valore  dell  acido  lattico  gastrico  per  la  diagnosi 
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28.  Clarke,  J.  M.,  “ A Case  of  Cancer  of  the  Pylorus  Presenting  some  Un- 
usual Features,”  “ Lancet,”  London,  1898,  11,  866-868. 

29.  Coley,  “ Amer.  Jour,  of  the  Med.  Sciences,”  1894. 

30.  Comte,  “ Neoplasme  du  pylore,  pyloro-plastic,  gastro-enterostomie,” 
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31.  Cook,  G.  W.,  “ Adeno-carcinoma  of  the  Stomach,”  “ Nat.  Med.  Rev.,” 
Wash.,  i898-’99,  viii,  197. 

32.  Coyon,  “ Cancer  du  pylore  avec  generalisation,”  “ Soc.  anat.,”  10  Juni, 
1898. 

33.  Cuony,  “ Un  cas  de  guerison,  sans  intervention  chirurgicale,  d’une  affec- 
tion cancereuse  de  l’estomac,”  “ Rev.  med.  de  la  Suisse  Rom.,”  Geneve,  1897, 
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34.  Davison,  C.,  “ Carcinoma  of  the  Stomach,”  “ Chicago  Clinic,”  1898,  xi 
213-216. 


LITERATURE  ON  CANCER  OF  THE  STOMACH. 


579 


35.  Debove,  “ Societe  med.  des  hopit.,”  November,  1889. 

36.  Deguy,  “ Cancer  latent  de  la  face  posterieuse  de  l’estomac,”  " Presse 
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37.  Deguy,  “ Diagnostic  du  cancer  d’estomac,”  “Journal  des  Practice,”  16 
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38.  Deutschlander,  “ Ueber  die  diagnost.  Bedeutung  des  Magenchemismus 
bei  Carcinoma  ventriculi,”  Dissert.,  Graefewald,  i895-’96. 

39.  Dieulafoy,  “Transformation  de  l’ulcere  stomacal  en  cancer  (abstr.),  ” 
“ Presse  med.,”  Par.,  1897,  11,  289-293. 

40.  Dock,  Geo.,  “Airier.  Jour,  of  the  Med.  Sciences,”  June,  1897,  p.  655. 

41.  Dock,  Geo.,  “ Cancer  of  the  Stomach  in  Early  Life,  and  the  Value  of 
Cells  in  Effusions  in  the  Diagnosis  of  Cancer  of  the  Serous  Membranes,” 
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42.  Dreyer,  “Ueber  das  Magencarcinom,”  Diss.,  Berlin,  1894. 

43.  Ebstein,  “ Ueber  Magenkrebs,”  “ Volkmann’s  Sammlung  klin.  Vor- 
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44.  Eichhorst,  “ Lehrbuch  der  spec.  Pathol,  und  Therapie.” 

45.  Eisenlohr,  “ Deutsches  Archiv  f.  klin.  Med.,”  1895. 

46.  Ekehorn.  G.,  “ Some  Further  Cases  of  Cancer  of  the  Stomach,  with 
Special  Reference  to  the  Lactic  Reaction,”  “Upsala  Lakaref.  Forh,”  i896-’97, 
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47.  Ely,  J.  S.,  “ A Study  of  Metastat.  Carcinoma  of  the  Stomach,”  “ Ameri- 
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48.  Emmerich,  “ Deutsche  med.  Wochenschr.,”  1895. 

49.  Ewald,  “ Krebs  der  Cardia  Metastase  im  rechten  Leberlappen  ; Gastros- 
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50.  Falk,  Fritz,  “Ueber  einen  Fall  von  Netz  echinokokkus  mit  Magencar- 
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51.  Feirtag,  “ Ueber  das  Verhalten  des  gesunden  und  kranken  Magens  be- 
ziichlich  der  Milchsaurebildung  wahrend  der  Kohlenhydratverdauung,” 
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52.  Fenwick,  N.  S.,  “ The  Early  Diagnosis  of  Cancer  of  the  Stomach,” 
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53.  Fick,  W.,  “ Ein  Endotheliom  und  ein  Carcinom  des  Magens,” 
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54.  Fischl,  “ Die  Gastritis  bei  Carcinom  des  Magens,”  “ Prager  Zeitschr.  f. 
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55.  Fitz  (R.  H.),  Conant  (W.  M.),  and  Porter  (C.  B.),  “ Successful  Resection 
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56.  Flatow,  “ Ueber  die  Entwickelung  des  Magenkrebses  aus  Narben  des 
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57.  Forneau,  Richard,  “ Ein  Beitrag  zur  Aetiologie  des  Magencarcinoms,” 
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58.  Fotheringham,  “Carcinoma  of  the  Stomach,”  “Canad.  Pract.,” 
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59.  Fox,  “The  Diseases  of  the  Stomach,”  London,  1872,  p.  184. 

60.  Frenoy,  “ Des  taux  cancers  de  l’estomac,”  “ These  de  Paris,”  1897. 

61.  Friedenwald,  J.,  “Latent  Cancer  of  the  Stomach,”  “Maryland  Med. 
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5 8o 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


62.  Friedreich,  “ Ein  Fall  von  Magenkrebs,”  “Berk  klin.  Wochenschr.,” 
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63.  Fussell,  M.  H.,  “Carcinoma  of  the  Stomach,”  “ Tr.  Path.  Soc.,”  Phila., 
1898,  xviii,  p.  46. 

64.  Gauthier,  “ De  l’etat  du  coeur  dans  le  cancer  primitif  d’estomac,”  “ These 
de  Lyon,”  1896. 

65.  Gockel,  M.,  “ Ueber  die  traumatische  Entstehung  des  Carcinoms,  mit 
besonderer  Beriicksichtigung  des  Intestinaltractus,”  “ Archiv  d.  Verd.- 
Krankh.,”  Bd.  II. 

66.  Godhardt-Danhieux,  “Sur  le  diagnostic  du  cancer  de  restomac,”  Poly- 
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67.  Golding-Bird,  “ Contributions  to  the  Chemical  Pathology  of  Some  Forms 
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68.  Gordon,  A.,  “ The  Semeiotic  Value  of  the  Different  Symptoms  in  Can- 
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69.  Griesinger,  “Archiv  f.  phys.  Heilkunde,”  1854,  p.  528. 

70.  Guinard,  Urbain,  “Cancer  du  pylore  sans  troubles  gastriques,  Pylorec- 
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7 1.  Haberlin,  “Ueber  neue  diagnostische  Hiilfsmittel  bei  Magenkrebs,” 
“ Deutsches  Archiv  f.  klin.  Med.,”  1889,  Bd.  xlv. 

72.  Hamilton,  H.  J.,  “Carcinoma  of  the  Stomach  with  Subcutaneous  Metas- 
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73.  Hampeln,  P.,  “ Zeitschr.  f.  klin.  Med.,”  Bd.  viii,  p.  232. 

74.  Hanau,  “ Erfolgreiche  experimentelle  Uebertragung  von  Carcinom,” 
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75.  Hanot,  “ Sur  une  forme  septicemique  du  cancer  de  l’estomac,”  “ Archiv 
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76.  Hauser,  “ Das  chronische  Magengeschwiir,  sein  Vernarbungs-Process 
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77.  Hauser,  “ Das  Cylinderepithelcarcinom  des  Magens  und  des  Dick- 
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78.  Hayem,  G.,  “ Forme  anemique  du  cancer  de  restomac,”  “ Presse  med.,” 
Paris,  1898,  11. 

79.  Hayem,  “ Diagnostic  du  cancer  du  pylore,”  “ Med.  moderne,”  11  Juni, 
1898. 

80.  Hechler,  F.  H.,  “Ueber  den  diagnostischen  Wert  der  Lymphdriisen- 
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81.  Heinemann,  “Virchow’s  Archiv,”  vol.  lviii,  p.  180. 

82.  Henry,  Fred  P.,  “ The  Diagnostic  Value  of  the  Blood  Count  in  Latent 
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83.  Hensen,  H.,  “Ueber  einen  Befundvon  Infusiorien  im  Mageninhalt  bei 
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84.  Herard,  “ Formes  septiques  du  cancer  restomac,”  These  de  Paris, 
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85.  Heresco,  “ Hernie  ombilicale  avec  phenomenes  d’estranglement,  cancer 
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86.  Hiltermann,  “Ueber  Metastase  eines  Gallertkrebses  des  Magens  in  die 
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LITERATURE  ON  CANCER  OF  THE  STOMACH.  58 1 

87.  Hirsch,  “ Handbuch  der  histologisch-geographischen  Pathologie,” 
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88.  Hirtz  et  Luys,  “ Ascite  chyliforme  an  cours  d’un  cancer  de  restomac,” 
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89.  Hofmann,  A.,  “ Die  Verdauungsleukocytose  bei  Carcinoma  ventriculi,” 
“ Zeitschr.  f.  klin.  Med.,”  Berlin,  1897,  xxxm,  pp.  460-475. 

90.  Honigmann  und  v.  Noorden,  “ Ueber  das  Verhalten  der  Salzsaure  in 
carcinomatosen  Magen,”  “ Zeitschr.  f.  klin.  Med.,”  xm. 

91.  Hosslin,  V.,  “ Ueber  den  Einfluss  ungeniigender  Ernahrung  auf  die 
Beschaffenheit  des  Blutes,”  “Munch.  med.  Wochenschr.,”  1890,  Nos.  38 
and  39. 

92.  Hiibner,  “ Untersuchungen  liber  44  Falle  von  Magencarcinom,  mit 
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93.  Hiiltl,  H.,  “ Ein  Fall  von  Gastro-enterostomie  bei  Carcinoma  pylori,’’ 
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94.  Israel,  O.,  “ Magenkrebs  mit  ungewohnlicher  secundarer  Ausbreitung 
im  Darmkanal,  Recurrenslahmung  und  Bemerkung  liber  klinstliche  Beleuch- 
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95.  Ivanhofif,  M.  N.,  “ Malignant  Tumor  of  the  Stomach  Treated  Success- 
fully by  the  Alkaloid  of  Chelidonium  majus,”  “ Med.  Obozr.,”  Mosk.,  1898,  L. 

96.  Jacobs,  “Ein  Fall  von  Magen-  und  Ovarialkrebs  mit  gleichzeitiger 
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97.  Jez,  V.,  “Ueber  die  Blutuntersuchung  bei  Magenerkrankungen,  beson- 
ders  bei  Ulcus  rotundum  und  Carcinoma  ventriculi,”  “ Wiener  med.  Wochen- 
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98.  Johnston,  J.  A.,  “Specimen  of  Carcinoma  of  the  Stomach,”  “Cincin. 
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99.  Johnston,  G.  W.,  and  Stewart,  A.,  “ The  Value  of  Certain  Chemical  and 
Microscopical  Procedures  in  the  Diagnosis  of  Cancer  of  the  Stomach,”  “Nat. 
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100.  Kaufmann,  E.,  “ Ein  seltenes  Praparat  von  Magencarcinom,”  " Jahresb. 
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101.  Katzenellenbogen,  “ Beitrage  zur  Statistik  des  Magencarcinoms,” 
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102.  Kellogg,  J.  H.,  “ Cancer  of  the  Stomach,”  “Tr.  Mich.  Med.  Soc.,” 
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103.  Kelynack,  J.  N.,  “ On  the  Occurrence  of  a Cancerous  Development  in 
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104.  Klebs,  “ Allgemeine  Pathologie”  : “ Ueber  das  Wesen  und  die  Erken- 
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105.  Klemperer,  “Ueber  den  Stoffwechsel  und  das  Koma  der  Krebs- 
kranken,”  “ Berl.  klin.  Wochenschr.,”  1889. 

106.  Koch,  “ Ueber  das  Carcinoma  ventriculi  ex  ulcero  rotundo,”  “ Petersb. 
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107.  Knickerbocker,  H.J.,  “The  Oppler-Boas  Bacilli  in  the  Diagnosis  of 
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582 


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109.  Kraske,  P.,  “ Erfahrungen  uber  den  Mastdarmkrebs,”  “ Samml.  klin. 
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in.  Kulneff,  N.,  “Ueber  basische  Zersetzungs-producte  im  Magen-  und 
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1 12.  Von  Kundrad,  R.,  irnd  Schlesinger,  H.,  “ Zur  Diagnose  der  Verwach- 
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1 13.  Laache,  S.,  “ Die  Anamie,”  Christiania,  1883. 

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1 16.  Laulie,  “ Squirrhe  du  pylore  et  rein  flottant,  pylorectomie  et  gastro-enter- 
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1 17.  Lebert,  “Ueber  Magenkrebs  in  atiologischer  und  pathogenetischer 
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1 18.  Lepine  cf.  Mouisset,  “Etude  sur  le  carcinome  de  l’estomac,”  “ Revue 
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1 19.  Letulle,  “ Carcinose  peritoneo-intestinale  secondaire  a un  cancer  de 
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120.  Letulle,  “Diagnostic  du  cancer  de  l’estomac,”  “ Prov.  med.,”  15,  vii, 
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121.  Letulle,  “ Cancer  multiples  du  tube  digestif,”  “ Presse  med.,”  19  Mai, 
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122.  Leyhdecker,  O.,  “ Ueber  einen  Fall  von  Carcinom  des  Ductus  thoracicus 
mit  chylosem  Ascites,”  Inaug. -Diss.,  Heidelberg,  1893,  “Virchow’s  Archiv,” 
1893,  Bd.  cxxxiv. 

123.  Limbeck,  V.,  “ Grundriss  einer  klinischen  Pathologie  des  Blutes,”  Jena, 
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124.  Lindh,  A.,  “Operationen  wegen  Magenkrebs  und  Magengeschwiir,” 
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125.  Lyonnet,  “ Linites  cancereuses,  ganglions  troisies,  ascite  chyleuse,  gen- 
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127.  Macdonald,  G.  C.,  “ Total  Removal  of  the  Stomach  for  Carcinoma  of 
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128.  Maillefert,  “ Zur  Lehre  vom  Carcinoma  ventriculi  ex  Ulcere  rotundo,” 
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129.  Malkoff,  G.  M.,  “Apropos  of  a Case  of  Cancer  in  the  Region  of  the 
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130.  Malkow,  G.,  “ Ueber  einen  Fall  von  Carcinom  des  Pylorus  mit  Ulcus 
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583 


132.  Matieu,  M.,  “ Du  cancer  prdcoce  de  l’estomac,”  “ Th£se  de  Lyon,”  1884. 

133.  Matieu,  M.,  “ Etat  dela  muqueuse  de  l’estomac  dans  le  cancer  de  cet 
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134.  Mathieu,  A.,  ” Etude  sur  trois  cas  de  cancer  succedant  a l’ulcere  simple 
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135.  Mathieu,  A.,  et  Lanier,  Nathan,  “ Cancer  du  canal  thoracique,  consec- 
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136.  McGraw,  T.  A.,  “ Pyloric  Cancer,”  “ Phys.  and  Surg.,”  Detroit  and 
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137.  McRae,  T.,  “Report  on  150  Cases  of  Cancer  of  the  Stomach  in  the 
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138.  Menetrier,  “ Arch,  de  Physiolog.,”  15  Fevr.,  1888. 

139.  Muller,  Fr.,  “ Stoffwechseluntersuchungen  bei  Krebskranken,”  “ Zeit- 
schr.  f.  klin.  Med.,”  1889,  xvi. 

140.  Noble,  Wm.  H.,  “ Report  of  an  Operation  for  the  Removal  of  the  Stom- 
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141.  Notthafft,  “ Ueber  die  Entstehung  der  Carcinome,”  “ Deutsches  Archiv 
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142.  Nothmann,  “ Ueber  Strahlennarben  des  Magens  und  Carcinoma  ven- 
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143.  Olivvier  et  Halipre,  “ Gastrite  sclereuse  hypertrophique  de  nature  can- 
cereuse,”  “Normandie  medicale,”  1,  iv,  1898. 

144.  O’Neil,  Wm.,  “A  case  of  Vomiting  Large  Masses  of  Cancerous  Mat- 
ter,” “ Lancet,”  London,  3,  x,  1896. 

145.  Pal,  J.,  “Carcinoma  ventriculi ; Anemia;  Tod,”  “Jahrb.  d.  Wien.  k. 
k.  Krankenanst.,”  1895,  Wien  u.  Leipzig,  1897,  iv,  pt.  2,42. 

146.  Pean,  Doyen,  etc.,  “ Traitement  chirurgical  du  cancer  de  l’estomac,” 
X.  Congr.  Frang.  de  chirurgie,  1897. 

147.  Perret,  “ Cancer  colloide  du  pylore  avec  propagation  aux  ganglions  de 
la  colonne,  au  rein  gauche,  au  cervelet,  etc.,”  “ Soc.  des  science  med.  de  Lyon,” 
Avril,  1897. 

148.  Phillippen,  J.,  “ La  valeux  du  signe  de  Boas  dans  le  diagnostic  du  can- 
cer de  l’estomac,”  “ Clinique,”  Brux.,  1898,  xil,  1-5. 

149.  Pianese,  “ Beitrag  zur  Histologie  und  Aetiologie  des  Carcinoms” 
(Deutsch  von  Teuscher),  Suppl.  zu  “ Ziegler’s  Beitrage,”  Jena,  1899. 

150.  Plitek,  V.,  “ Appunti  sulla  combinazione  del  carcinoma  con  l’ulcera 
dello  stomaco,”  Morgagni,  Milano,  1897,  xxxix,  53-64. 

1 5 1 . Porger,  “ Ein  Fall  von  Carcinoma  ventriculi  durch  Resection  geheilt 
seit  sechs  Jahren  ohne  Recidiv,”  “ Wien.  med.  Wochenschr.,”  No.  36,  1897. 

152.  Poth,  “Ein  Fall  von  beginnendem  Magencarcinom,”  Dissert.,  Miin- 
chen,  i895-*96. 

153.  Quenu,  “ Gastro-enterostomie  avec  bouton  de  Murphy  et  pylorectomie 
pour  cancer  de  l’estomac  ; mort  16  mos.  apres,”  " Bull,  de  la  Soc.  de  chir.,” 
xix,  1897. 

154.  Rabe,  “Cancer  du  coeur,  secondaire  a un  cancer  de  l’estomac,”  Soc 
anat.,  26  Novembre,.  1897. 


5 §4 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


155.  Rauzier,  “ De  la  diminution  de  1’uree  dans  le  cancer,  Hypazoturie  can- 
cereuse,”  “ These  de  Montpellier,”  Ref.  in  “Arch,  de  Med.  exp.,”  1890. 

156.  Reineboth,  “Die  Diagnose  des  Magencarcinoms  aus  Spiilwasser  und 
Erbrochenem,”  “ Deutsches  Archiv  f.  klin.  Med.,”  Bd.  lviii,  4. 

157.  Ribbert,  “ Beitrage  zur  Histogenese  des  Carcinoms,”  “Virchow’s 
Archiv,”  Bd.  cxxxv. 

158.  Ribbert,  “ Weitere  Beobachtungen  liber  die  Histogenese  des  Carci- 
rioms,”  “ Centralbl.  f.  allg.  Pathologie,”  V,  1894. 

159.  Richardson,  M.  H.,  “A  Successful  Pylorectomy,  with  Removal  of  a 
Portion  of  the  Pancreas,  for  Cancer  of  the  Pylorus,”  “ Boston  Med.  and  Surg. 
Jour.,”  Aug.  4,  1898. 

160.  Richardson,  M.  H.,  “A  Successful  Gastrectomy  for  Cancer  of  the 
Stomach,”  “ Boston  Med.  and  Surg.  Jour.,”  Oct.  27,  1898. 

161.  Riegel,  “ Ueber  die  therapeutische  Anwendung  der  Condurangorinde,’’ 
“ Berl.  klin.  Wochenschr.,”  1874. 

162.  Riegel,  “Ueber  den  Werth  der  Condurangorinde  bei  dem  Symptomen- 
bild  des  Magencarcinoms,”  “Berl.  klin.  Wochenschr.,”  1887. 

163.  Riesmann,  D.,  “Cancer  of  the  Stomach,”  “ Proc.  Path.  Soc.  Phila.,” 
1897,  1,  9-18. 

164.  Riess,  “ Ueber  den  Werth  der  Condurangorinde  bei  dem  Symptomen- 
bild  des  Magencarcinoms,”  “Berl.  klin.  Wochenschr.,”  1887. 

165.  Robin,  A.,  “ Traitement  medical  du  cancer  de  l’estomac,”  “Bull, 
med.,”  13,  xi,  1897. 

166.  Robert,  “ Hematemese  terminee  par  la  mort  due  a une  tumeur  de 
l’estomac  (sarcoma  plexiforme),”  “ Bull,  et  mem.,  Soc.  dechir.  de  Par.,”  1898, 
N.  S.,  xxiv,  294-296. 

167.  Rokitansky,  “Carcinoma  ventriculi,”  “Allg.  Wien.  med.  Ztg.,”  1897, 
xiii,  93, 105,  107,  129,  142,  152. 

168.  Rokitansky,  “ Secundares  Lebercarcinom  in  Folge  von  Magenkrebs,” 
“Allg.  Wien.  med.  Ztg.,”  1898,  xliii,  105. 

169.  Rommelaere,  “Journal  de  Med.,  de  Chir.,  et  de  Pharm.  de  Bruxelles,” 
i883-’86. 

170.  Rorig,  “ Primares  Cancroid  des  Magens,”  Dissert.,  Wurzburg,  1895- 
’96. 

171.  Rosenbach,  “ Ueber  eine  eigenthiimliche  Farbstoff bildung  bei  schweren 
Darmleiden,”  “Berlin,  klin.  Wochenschr.,”  1889. 

172.  Rosenheim,  “Ueber  atrophische  Processe  an  der  Magenschleimhaut  in 
ihrer  Beziehung  zum  Carcinom  und  als  selbstandige  Erkrankung,”  Discus- 
sion, “Berlin,  klin.  Wochenschr.,”  1888. 

173.  Rosenheim,  “ Zur  Kenntniss  des  mit  Krebs  complicirten  runden  Ma- 
gengeschwiirs,”  “ Zeitschr.  f.  klin.  Med.,”  1890. 

174.  Sabrazer  et  Cabauner,  “ Des  gangrenes  des  extremities  d’origine  arte- 
rielle  dans  le  cancer  l’estomac,”  “ Arch.  gen.  de  med.,”  Paris,  1898,  1,  pp. 
99-i  11. 

175.  Sailer,  Jos.,  and  Taylor,  A.  E.,  “The  Condition  of  the  Blood  in  the 
Cachexia  of  Carcinoma,”  “ Internat.  Med.  Magaz.,”  July,  1897. 

176.  Scheuerlen,  “ Verhandl.  d.  Ver.  f.  innere  Medicin,”  “ Deutsche  med. 
Wochenschr.,”  1887,  No.  48. 

177.  Schlesinger,  H.,  “ Klinisches  liber  Magentumoren  nicht  carcinoma- 


LITERATURE  ON  CANCER  OF  THE  STOMACH.  585 

toser  Natur  (Magensarkom),”  “Zeitschr.  f.  klin.  Med.,”  Bd.  xxxii,  Suppl., 
Heft  8. 

178.  Schneider,  G.,  Inaugural-Dissertation,  Berlin,  1888. 

179.  Schneyer,  “Zeitschr.  f.  klin.  Med.,”  1895. 

180.  Schoenborn,  “ Ueber  traumatische  Entstehung  eines  Magenkrebses,” 
“ Aerztl.  Vereinsbl.  f.  Deutschl.,”  1897,  xxvi,  509. 

181.  Scholz,  F.,  “Beitrage  zur  Statistik  des  Magenkrebses,”  Dissert., 
Gottingen,  i896-’97. 

182.  Schule,  “ Beitrage  zur  Diagnostik  des  Magencarcinoms,”  “ Munch, 
med.  Wochenschr.,”  1894. 

183.  Schule,  “Ueber  die  Friihdiagnose  des  Carcinoma  ventriculi,”  “ Munch, 
med.  Wochenschr.,”  No.  37,  1897. 

184.  Senator,  “Ueber  Selbstinfection  durch  abnorme  Zersetzungsvorgange 
und  dadurch  bedingtes  dyskrasisches  Coma  (Kussmaul’s  Symptomencomplex 
des  diabetischen  Comas),”  “Zeitschr.  f.  klin.  Med.,”  1884,  vn. 

185.  Von  Sohlern,  “ Der  Einfluss  der  Ernahrung  auf  die  Entstehung  des 
Magengeschwiirs,”  “ Berl.  klin.  Wochenschr.,”  1889,  Nos.  13  and  14. 

186.  Soupalt,  M.,  “ Cancer  de  l’estomac,  stase  gastrique  sans  dilatation,” 
“ Presse  med.,”  Paris,  1898,  1,  217. 

187.  Soupalt,  M.,  “ Epithelioma  du  corps  de  Pestomac,  gastrectomie  partielle  ; 
guerison,”  Soc.  anat.,  24  Dec.,  1898. 

188.  Steinhaus,  “Ueber  Carcinomzelleneinschliisse,”  “Virchow’s  Archiv,” 
1891,  Bd.  cxxvi. 

189.  Stempfle,  L.,  “ Ein  Fall  von  Leberabscess  im  Anschluss  an  ein  Carci- 
nomatos  entartetes  Ulcus  ventriculi,”  Dissert.,  Erlangen,  i896-’97. 

190.  Stewart,  D.  D.,  “A  Case  of  Two  Isolated  Carcinomatous  Gastric 
Ulcers ; Apparent  Recovery  after  Exploratory  Celiotomy ; Death  eighteen 
months  later,  following  a Second  Operation  ; Hyperchlorhydria  to  the  end,” 
“ Tr.  Assoc.  Amer.  Physic.,”  Phila.,  1898,  xm,  272-299. 

191.  Strauss,  “ Sarkomatosis  der  Haut  und  des  Magens,”  Dissert.,  Wurz- 
burg, i895~’96. 

192.  Strube,  Geo.,  “Trichomonas  hominis  in  the  Gastric  Contents  in  Carci- 
noma of  the  Cardia,”  “Berl.  klin.  Wochenschr.,”  Aug.  8,  1898. 

193.  Strube,  Geo.,  “ A Case  of  Cancer  of  the  Pylorus  Presenting  Some 
Unusual  Features,”  “Lancet,”  Oct.  1,  1898,  vol.  11. 

194.  Stucky,  T.  H.,  “Malignant  Disease  of  the  Pylorus,”  “ Internat.  Clin.,” 
Phila.,  1898,  8,  3.  s.  159-163. 

195.  Szekacs,  B.,  “ Ein  Fall  von  Magenkrebs  mit  intermittierendes  Fieber,” 
Budapest,  koz  korhazak  eokonyve,  1894,  rol  Budapest,  1896. 

196.  Thayer,  W.  S.,  “Johns  Hopkins  Hosp.  Bullet.,”  1893,  No.  31. 

197.  Thoma,  “Ueber  eigenartige  parasitare  Mikroorganismen  in  den  Epi- 
thelzellen  der  Carcinome,”  “ Fortschritte  der  Medicin,”  1889,  No.  2. 

198.  Tuffier  et  Dujarier,  “ Perigastrite  gangreneuse  anterieure  suite  de  can- 
cer gastrique,”  Soc.  Anat.  de  Paris*,  14.  Janv.,  1898. 

199.  Uffelmann,  “ Ueber  die  Methode  der  Untersuchung  des  Mageninhalts 
auf  freie  Salzsaure,”  “ Deutsches  Archiv  f.  klin.  Med.,”  1880,  Bd.  xvi. 

200.  Ullman,  J.,  “ Gastric  Carcinoma  ; the  Presence  of  the  ‘ Faden  ’ (Oppler- 
Boas)  Bacillus  as  an  Important  Factor  in  Gastric  Carcinoma,”  “ Buffalo  Med. 
Jour.,”  i898-’99,  N.  S.,  xxxviii,  18-23. 


586 


MALIGNANT  TUMORS  OF  THE  STOMACH. 


201.  Vedel,  “ Cancer  de  l’estomac  avec  perforation  et  abouchement  dans  une 
masse  ganglionnaise  peritonite  aigue  fibrineuse,”  “ Nouv.  Montpellier  med.," 
28  mai,  1898. 

202.  Von  den  Velden,  “ Ueber  Vorkommen  und  Mangel  der  freien  Salzsaure 
im  Magensafte  bei  Gastrectasie,”  “ Deutsch.  Archiv  f.  klin.  Med.,”  1879,  Bel. 

XXIII. 

203.  Verstraete,  “Deux  cas  de  cancer  de  l’estomac,”  “J.  d.  sc.  med.  de 
Lille,”  1898,  1. 

204.  Vickery,  H.  F.,  “A  Report  of  Three  Cases  of  Cancer  of  the  Stomach  in 
which  Hydrochloric  Acid  was  Present,”  “ Boston  Med.  and  Surg.  Jour.,”  1897, 
cxxxvii,  132. 

205.  Vilcog  et  Lancy,  “ Cancer  de  l’estomac,  pyemie  streptococcique  second- 
aire,”  Soc.  Anat.  de  Paris,  19,  vi,  1897. 

206.  Virchow,  “ Bemerkungen  fiber  die  Carcinomzelleneinschlusse,”  ‘‘Vir- 
chow’s Archiv,”  1892,  Bd.  cxxvu. 

207.  Virchow,  “ Krankhafte  Geschwiilste,”  1. 

208.  Volkmann,  R.,  “ Beitrage  zur  Chirurgie,”  Leipzig,  1875,  und 

“Deutsche  Zeitschr.  f.  Chirurgie,”  1880,  Bd.  xm. 

209.  Waldeyer,  “ Volkmann’s  Sammlung  klin.  Vortrage,”  I,  No.  13. 

210.  Walker,  J.  W.,  “A  Case  of  Pyloric  Carcinoma  and  Melancholia,  with 
Internal  Illusions,”  “ Amer.  Jour.  Insan.,”  1897,  liii,  510-512. 

21 1.  Wazoldt,  “Ueber  einen  Fall  von  Absonderung  eines  iibermassig  sauren 
Magensaftes  bei  Magencarcinom,”  “ Charite  Annalen,”  1888,  XIV. 

212.  Weber,  W.  C.,  “Early  Diagnosis  of  Carcinoma  of  the  Stomach  by 
Means  of  Chemical  Analysis  of  the  Gastric  Contents,”  “Jour.  Amer.  Med. 
Assoc.,”  11,  vii,  1896. 

213.  Welch,  Wm.  H.,  “American  System  of  Medicine,”  vol.  11,  “ Cancer  of 
the  Stomach,”  p.  53,  no  references. 

214.  West,  Charlotte  C.,  “ Report  of  Two  Cases  of  Cancer  of  the  Stomach,” 
“ Phila.  Polyclin.,”  1898,  vii,  107-110. 

215.  Willigk,  “ Prager  Vierteljahresschrift,”  vol.  x,  2,  1853. 

216.  Winterberg,  J.,  “ Zwei  Falle  von  Magencarcinom  mit  Perforation  durch 
die  vordere  Bauchwand,”  “Wien.  klin.  Rundschau,”  1898,  xn,  585,  607. 

217.  Witte,  W.  C.  F.,  “ Carcinoma  of  the  Stomach,  Retrogressive  Lymphatic 
Transport,  Multiple  Carcinomatous  Construction  of  the  Ileum,  and  Triple 
Simultaneous  Perforation,”  “ Phila.  Med.  Jour.,”  1898,  I,  846-848. 

218.  Witzel,  “ Centralbl.  f.  Chirurg.,”  1891,  No.  31. 

219.  Worthington,  N.,  “ Cancer  of  the  Stomach,”  “Montreal  Med.  Jour.,” 
1897-98,  xxvi,  601. 

220.  Wortmann,  Carl,  “Ein  Fall  von  Carcinoma  ventriculi  im  Anschluss  an 
chronisches  Magengeschwiir,”  Dissert.,  Wurzburg,  i896-’97. 

221.  Wyss,  “Blatter  f.  Gesundheitspflege,”  Zurich,  1872-74. 

222.  Yates,  H.  W.,  “ Cancer  of  the  Stomach,  with  Report  of  a Case,” 
“ Phys.  and  Surg.,”  Detroit  and  Ann  Arbor,  1898,  xx,  147— 1 55 ; Discus- 
sion, 179. 


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589 


590  STOMACH  DISEASES  CAUSED  BY  INFECTIOUS  GRANULOMATA. 


CHAPTER  V. 

STOMACH  DISEASES  CAUSED  BY  INFECTIOUS 
GRANULOMATA. 

These  affections  have,  almost  exclusively,  a purely  pathological 
significance.  Among  the  infectious  granulations  reported  as  affect- 
ing the  stomach  are  tuberculosis,  syphilis,  abdominal  typhus, 
glanders,  and  lymphadenoma.  We  shall  consider  gastric  tubercu- 
losis and  syphilis  separately. 

Typhoid  neoplasms  and  ulcerations  of  the  stomach  are  very 
rare;  even  more  unusual  than  tuberculous  ulcerations.  The 
medullary  swelling  of  lymph-glands,  however,  as  well  as  the 
ulcers  arising  therefrom,  have  been  described  as  occurring  in  the 
stomach  (Orth,  “ Specielle  pathol.  Anatomie,”  Bd.  i,  S.  714). 

Concerning  the  occurrence  of  glanders  in  the  human  stomach, 
only  one  observation  is  on  record — viz.,  Bollinger  (O.  Wyss), 
“ Rotz,”  “von  Ziemssen’s  Handb.,”  Bd.  in,  S.  482,  1876. 

Leukemic  and  aleukemic  lymphadenomata,  as  occurring  in  the 
human  stomach,  have  been  reported  several  times  (“  Lymphade- 
noma,“ Cornil  and  Ranvier,  “ Manuel  de  l’Histolog.  Patholog.,” 
p.  294).  This  neoplasm  occurs  in  the  deeper  part  of  the  true 
mucosa  and  in  the  submucosa,  but  sends  prolongations  into  the 
outer  layers.  Lymphadenomata  and  glanders  may  ulcerate  on  the 
inner  surface  of  the  stomach. 

TUBERCULOSIS  OF  THE  STOMACH. 

The  gastric  mucosa  has  almost  entire  immunity  from  bacterial  in- 
fection. As  the  intestines  are  the  seat  of  frequent  infection,  when 
there  can  be  no  doubt  that  bacteria  have  entered  through  the  esopha- 
gus and  stomach,  the  immunity  of  the  last-named  organ  must  depend 
upon  some  peculiarity  in  its  structure  or  secretions.  Tubercle 
bacilli  are  not  affected  by  the  acid  gastric  juice,  as  has  been  proved 
by  Falk  (loc.  cit .)  and  Frank  (loc.  cit .),  who  demonstrated  that  the 
growth  of  the  bacilli  could  not  be  retarded  by  the  gastric  secre- 
tion. This  does  not  imply,  however,  that  these  bacilli  can  grow 
in  the  gastric  juice.  The  normal  stomach,  as  a matter  of  fact,  is  not 
favorable  to  bacterial  development.  The  gastric  immunity  may 
further  be  accounted  for  by  the  scarcity  of  lymph-glands  in  the 


TUBERCULOSIS  OF  TIIE  STOMACH. 


5QI 


gastric  wall.  In  the  intestines 'lymphatic  nodules  are  abundant, 
and  they  bear  some  definite  relation  to  the  formation  of  tubercle. 
The  occurrence  of  smaller  and  larger  tuberculous  foci  in  the 
stomachs  of  adults  and  children  proves  that  the  gastric  immunity 
can  not  be  complete.  Undoubtedly  a number  of  conditions  must 
simultaneously  cooperate  to  bring  about  a tuberculous  invasion. 
Prominent  among  these  are  : (1)  A lessened  resistance  or  reduced 
vitality  of  the  gastric  mucous  membrane  ; (2)  a diminished  secre- 
tion or  absence  of  HC1 ; (3)  an  altered  state  of  the  blood  ; (4)  the 
presence  of  tubercle  bacilli. 

A number  of  the  tuberculous  gastric  ulcerations  that  are 
reported  have  developed,  not  from  a direct  invasion  of  the  bacilli 
into  the  mucosa,  but  from  an  invasion  into  the  serosa,  occurring 
from  circumscribed  or  diffuse  peritonitis. 

Gastric  tuberculosis  occurs  in  two  forms — (1)  miliary  tuberculosis 
of  the  wall  of  the  stomach,  a not  uncommon  type;  (2)  tubercu- 
lous ulceration  of  the  stomach,  an  extremely  rare  occurrence. 
Miliary  tuberculosis  of  the  stomach  occurs  simultaneously  with  the 
eruption  of  tubercle  throughout  the  organism.  It  is  usually  found 
to  exist  with  a miliary  tuberculosis  of  the  intestines  and  peritoneum. 
These  cases  may  strongly  resemble  severe  attacks  of  typhoid  fever. 
The  author,  while  physician-in-charge  of  Bay  View  Asylum,  Bal- 
timore, observed  two  cases  of  acute  miliary  tuberculosis  which 
were  diagnosed  as  typhoid  fever.  Even  the  characteristic  rose 
spots  were  present,  and  taken  for  such  by  the  author  and  other 
clinicians.  This  was  at  a time  when  microscopical  examination 
for  tubercle  bacilli  was  not  in  vogue,  and  the  Widal  test  not  yet 
discovered.  The  necropsies  were  made  by  Professor  William  T. 
Councilman,  revealing  acute  miliary  tuberculosis. 

The  immunity  of  the  stomach  from  tuberculosis  was  shown  in 
the  experiments  of  Orth  (loc.  cit.).  By  feeding  rabbits  with  tubercle 
bacilli  he  obtained  intestinal  tuberculosis  seven  times,  and  gastric 
tuberculosis  but  once.  In  a case  of  tuberculosis  of  the  esophagus 
reported  by  Dr.  S.  Flexner  (loc.  cit.),  although  extensive  destruc- 
tion of  the  esophagus  existed,  and  the  pleural  cavity  had  been 
opened,  and  though  millions  of  tubercle  bacilli  must  have  been 
taken  into  the  stomach,  this  observer  assured  us  that  no  gastric 
tuberculosis  was  detected. 

Clinically,  gastric  tuberculosis  is  without  much  significance.  It 
is,  as  a rule,  not  diagnosticated.  Tuberculous  ulcerations  are  found 
most  frequently  in  the  pyloric  part,  and  Orth  describes  isolated 


592  STOMACH  DISEASES  CAUSED  BY  INFECTIOUS  GRANULOMATA. 

miliary  tubercles  occurring  in  the  vicinity  of  ulcerations.  In  rare 
cases  tuberculous  ulcerations  have  produced  fatal  symptoms  by 
disintegrating  and  eroding  a gastric  artery,  or  by  perforating 
the  gastric  wall.  The  demonstration  of  the  tubercle  bacillus  in 
a gastric  ulcer  was  first  made  by  Coats  {loc.  cit .).  Matthieu  and 
Remond  {loc.  cit.),  Musser  {loc.  cit),  and  Serafini  {loc.  cit.),  in  their 
cases,  also  succeeded  in  proving  the  presence  of  tubercle  bacilli. 
Kiihl  examined  for  the  tubercle  bacillus  in  four  cases  from  the 
Pathological  Museum  of  the  University  of  Kiel,  but  could  demon- 
strate it  positively  in  only  two  of  these,  which  were  recent  cases. 
The  other  two  were  older  specimens,  having  been  in  the  museum 
a long  time.  A large  number  of  the  reported  cases  of  tubercular 
ulcers  are  doubtful,' either  because  no  microscopic  examination  was 
made  at  all,  or  the  authors  failed  to  stain  for  the  bacillus.  Such 
cases  are  those  of  Paulicky  {loc.  cit.),  Hebb  {loc.  cit),  Chvostek 
{loc.  cit.,  four  cases),  Lange  (loc.  cit),  Barlow  (loc.  cit),  Quenu  (loc.  cit), 
and  Bignon.  The  earliest  reported  case  of  tubercular  ulcer  is 
Litten’s  (loc.  cit),  which  showed  an  isolated  ulcer  on  the  anterior 
gastric  wall,  with  typical  giant  cells  and  caseating  tubercles. 
Letorey  (loc.  cit)  recently  reported  a case,  and  gave  an  analysis  of 
21  cases.  In  1887  Marfan  reviewed  the  subject,  and  collected  14 
authenticated  cases.  The  disease  is  most  frequently  found  in 
males.  In  19  cases  collected  by  Letorey,  in  which  the  sex  was 
stated,  it  occurred  16  times  in  males  and  3 times  in  females.  The 
ulcers  are  usually  single.  In  a case  from  Professor  Osier’s  clinic, 
however,  at  the  Johns  Hopkins  Hospital  (parts  of  this  stomach 
were  presented  to  the  author  for  examination  through  the  kindness 
of  Dr.  S.  Flexner,  who  performed  the  autopsy),  there  were  numer- 
ous ulcers  of  various  sizes.  In  this  case  the  intestines  were  also 
the  seat  of  numerous  ulcerations  penetrating  to  the  muscular  coat. 
The  stomach  showed  118  to  120  areas  of  loss  of  substance  over  the 
entire  organ,  but  most  thickly  on  the  anterior  surface  near  the 
greater  curvature.  Hermann  Durck  (loc.  cit)  observed  four  cases 
of  undoubted  tuberculous  ulcer  in  900  autopsies  at  Munich. 
Frerichs  and  Litten  have  reported  cases  in  which  the  a tuberculous 
ulceration  was  limited  to  the  stomach,  the  intestines  being  intact. 
The  sizes  of  the  ulcers  vary  from  a pin’s  head  to  five  centimeters 
in  diameter.  Musser  (loc.  cit)  has  reported  a case  of  a tuberculous 
ulcer  1x3  inches  in  extent ; and  in  one  of  the  cases  of  Durck  (loc. 
cit),  occurring  in  a child  ten  years  old,  there  existed  an  ulcer 
exceeding  in  size  that  of  a German  five-mark  piece  (somewhat 


TUBERCULOSIS  OF  THE  STOMACH. 


593 


larger  than  a silver  dollar).  Secondary  tuberculous  changes  may 
extend  to  the  stomach  through  perforation  resulting  from  caseat- 
ing  neighboring  lymph-glands.  This  is  generally  rapidly  followed 
by  purulent  processes  in  the  glands.  When  the  peritoneum  of  the 
stomach  becomes  involved  in  a general  peritoneal  tuberculosis,  the 
posterior  wall  of  the  organ,  which  is  probably  the  most  protected, 
is  either  entirely  free,  or,  at  any  rate,  is  much  less  affected  than  the 
anterior  wall. 

Habershon  {loc.  cit.)  assumes  that  infection  of  the  gastric  mucosa 
occurs  by  way  of  the  vascular  channels.  He  does  not  believe  in 
a direct  infection  of  the  mucosa  because  of  the  acidity  of  the  gastric 
juice.  Klebs  (“  Tuberculose,”  published  by  Leopold  Voss,  1894, 
p.  80)  assumes  that  tuberculous  new  formations  occur  on  the  basis 
of  preexisting  gastric  ulcers.  A critical  review  of  the  literature  is 
given  in  an  interesting  report  of  multiple  tuberculous  ulcers  of  the 
stomach  (three  cases,  by  Alice  Hamilton,  M.D.,  “ Johns  Hopkins 
Hospital  Bulletin,”  April,  1897). 

The  bibliography,  though  extensive,  is  not  quite  complete,  and 
we  have,  in  the  following,  added  cases  which  have  come  to  our 
notice.  In  these  three  cases  tubercle  bacilli  were  demonstrated  by 
the  Ziehl-Neelsen  method  of  staining.  Dr.  Hamilton  inclines  to  the 
opinion  of  Klebs,  that  gastric  erosions,  or  previously  existing  losses 
of  substance,  constitute  the  portals  of  entry  for  the  tubercle  bacillus. 
The  facts  in  the  second  case  indicate  that  many  small  erosions 
of  hemorrhagic  origin  preexisted  in  the  stomach,  some  of  which 
became  invaded  with  tubercle  bacilli  swallowed  with  the  sputum. 
Perforation  not  infrequently  occurs.  It  was  present  six  times  in 
the  fourteen  cases  reported  by  Marfan — three  times  through  a 
tuberculous  gland’.  In  eight  of  Letorey’s  cases  the  presence  of  a 
gastric  tuberculosis  was  suspected  during  life  and  confirmed  at  the 
necropsy.  Death  by  perforation  peritonitis  resulted  in  a case  re- 
ported by  Paulicky  (loc.  cit.).  Most  frequently  death  results  from 
advanced  tuberculosis  in  other  organs.  In  three  of  the  cases 
death  was  caused  by  severe  hemorrhage  following  an  erosion  of  a 
blood-vessel  through  the  ulcerative  process.  In  the  critical  con- 
sideration of  the  subject  by  Dr.  Hamilton  ( loc . cit.)  it  was  found 
that  the  authentic  literature  contained  fifteen  undoubted  cases,  and 
nine  more,  which  were  probable,  but  not  proved.  While  there  is 
a disposition  for  development  of  tuberculosis  in  the  intestine, 
there  are  numerous  cases  reported  where  ulcers  existed  in  the 
stomach,  the  intestines  being  wholly  exempt.  The  deepest  ulcers, 
39 


594  STOMACH  DISEASES  CAUSED  BY  INFECTIOUS  GRANULOMATA. 

when  found  multiple  in  the  stomach,  do  not  extend  beyond  the 
muscularis  mucosae,  and  the  infiltration  of  the  mucous  membrane 
extends  little  further  than  the  actual  ulceration.  These  facts  are 
very  evident  in  the  sections  kindly  presented  to  the  author  by  Dr. 
S.  Flexner,  and  which  were  taken  from  the  cases  reported  by 
Dr.  Hamilton.  Superficial  small  ulcerations  still  showed  vestiges 
of  glands,  but  without  any  recognizable  distinction  between  oxyn- 
tic  and  chief  cells.  Epithelioid  and  lymphoid  cells  were  pro- 
fusely scattered  throughout  the  remnants  of  mucous  membrane. 
The  free  surfaces  of  the  ulcers  were  in  a state  of  necrosis,  covered  at 
times  by  a homogeneous,  finely  granular  matter.  The  deeper  layers 
were  in  a state  of  comparative  preservation.  Tubercle  bacilli  were 
present  in  small  numbers,  both  on  the  free  surface  of  the  ulcers  and 
among  the  remnants  of  the  glands.  Letulle  (Anatom.  Societe 
Paris,  1893;  also  abstracted  in  “ Centralbl.  f.  allgem.  Pathologie,” 
Bd.  iv,  1893,  S.  760)  in  108  autopsies  on  undoubted  cases  of  pul- 
monary tuberculosis,  found  but  one  case  of  tuberculosis  of  the 
stomach.  The  organ  presented  ten  submucous  nodules  as  large 
as  peas,  containing  giant  cells  and  a few  tubercle  bacilli. 

Diagnosis. — The  diagnosis  of  the  possible  tuberculous  nature 
of  a gastric  ulcer  during  life  is  certainly  very  problematical. 
Tubercle  bacilli  that  may  be  found  in  the  gastric  contents  do  not 
serve  to  throw  light  on  the  subject.  They  may  have  been  swal- 
lowed, or  they  may  have  been  contained  in  the  food.  The  only 
possibility  would  be  to  use  a weak  hypodermic  injection  of  tuber- 
culin (one  milligram),  and  if  a temperature  reaction  follows  when 
all  signs  of  tuberculosis  in  the  lungs,  larynx,  and  other  organs  are 
absent,  then  the  diagnosis  of  a local  tubercular  ulcer  in  the  stomach 
would  be  justifiable.  J.  Petruschky  (“  Verhandlungen  d.  XVI.  Con- 
gress. f.  innere  Medicin,”  April,  1899,  S.  366)  reports  two  cases 
with  the  typical  clinical  history  of  gastric  ulcer  that  did  not  im- 
prove after  the  most  approved  treatment  for  this  disease.  An 
injection  of  one  milligram  of  tuberculin  was  followed  in  five  days 
by  five  milligrams,  and  in  six  days  by  ten  milligrams.  After  the 
third  injection  a violent  reaction  set  in,  particularly  an  intense  local 
reaction  of  the  stomach,  expressing  itself  in  vomiting  (without 
blood)  and  gastralgic  pains.  There  were  no  reactions  on  the  part 
of  the  lungs  or  other  organs.  After  every  injection  an  increased 
sensitiveness  of  the  gastric  region  was  evident.  The  diet  consisted 
mainly  of  milk,  and  no  internal  medication  was  given.  The  general 
condition  and  strength  of  the  patient  improved  visibly.  Toward 


LITERATURE  ON  GASTRIC  TUBERCULOSIS. 


595 


the  end  of  the  treatment  the  patient  received  injections  containing 
ioo  milligrams.  Recovery  was  complete  after  three  months.  The 
first  case  continued  well  without  a relapse  for  five  years.  The 
cure  of  the  second  case  was  not  complete  at  date  of  report.  This 
author  states  that  the  test-meals  from  these  cases,  a half-hour  after 
an  Ewald  test-breakfast,  showed  a distinct  reaction  for  free  HC1. 
This  evidence  might  be  useful  in  the  rare  cases  where  tubercular 
ulcer  might  be  confounded  with  carcinoma. 

LITERATURE  ON  GASTRIC  TUBERCULOSIS. 

1.  Anger,  in  Marfan’s  “ Thesis,”  Paris,  1887. 

2.  Barbacci,  “ Lo  Sperimentale,”  May,  1890. 

3.  Barlow,  Path.  Soc.,  London,  1887. 

4.  Beadles,  “ British  Med.  Jour.,”  1892,  11. 

5.  Bellrose,  N.  W.,  “ Gastric  Ulcer,  Probably  Tubercular,  Report  of  a Case,” 
44  Colorado  Med.  Jour.,”  1897,  in. 

6.  Birch-Hirschfeld,  “ Lehrbuch  d.  path.  Anat.,”  Bd.  ii,  S.  642. 

7.  Bias,  “Ueber  tuberculose  Geschwiire  des  Magens,”  Dissert.,  Munchen, 
1895-96. 

8.  Blumer,  G.,  “ Tuberculosis  of  the  Stomach,  with  a Report  of  a Case  of 
Multiple  Tuberculous  Ulcers  of  that  Organ,”  “ Albany  Med.  Ann.,”  1898,  xix. 

9.  Brechemin,  “ Proge’s  Medical,”  1879. 

10.  Cazin,  in  Fernet’s  article,  “Bull,  et  Mem.  d.  1.  Soc.  Med.  des  Hop.,” 
1880,  tome  xvii. 

11.  Chvostek,  “Wien.  med.  Blatter,”  1882,  v. 

12.  Coats,  “Glasgow  Med.  Jour.,”  1886. 

13.  Cordua,  “ Arbeiten  aus  dem  patholog.  Institut  in  Gottingen,”  Berlin, 
1893. 

14.  Duguet,  in  Spillman’s  “These,”  Paris,  1878. 

15.  Diirck,  Hermann,  “ Ergeb.  d.  allgem.  Path.”  (Four  Cases  of  Tubercu- 
lous Ulcer  in  Nine  Hundred  Autopsies). 

16.  Eppinger,  “ Prager  med.  Wochenschr.,”  1881. 

1 7.  Falk,  “Virchow’s  Archiv,”  Bd.  xciii,  S.  177. 

18.  Flexner,  S.,  “ Tuberculosis  of  Esophagus,”  “Bull.  Johns  Hop.  Hosp.,” 
No.  28,  1893. 

19.  Frank,  “ Deutsche  med.  Wochenschr.,”  1884,  No.  20. 

20.  Habershon,  S.  H.,  “ Trans.  Path.  Soc.,”  London,  vol.  xlv,  p.  7 3. 

21.  Hamilton,  Alice,  “Johns  Hopkins  Hospit.  Bulletin,”  April,  1897. 

22.  Hattute,  “ Gaz.  des  Hop.,”  1874. 

23.  Hebb,  G.,  “ Westminster  Hosp.  Reports,”  1888,  ill. 

24.  Kanzow,  “ Ein  Beitrag  zur  Casuistik  der  tuberculosen  Magenge- 
schwiire,”  Dissert.,  Munchen,  1893-96. 

25.  Kuhl,  “ Thesis,”  Kiel,  1889. 

26.  Labadie-Lagrave,  “ Bull.  Soc.  Anat.,”  1870. 

27.  Lange,  “ Memorabilien,”  Heilbronn,  1871,  XVI. 

28.  Lava,  “ Gazz.  Med.  di  Forino,”  1893. 


59 6 STOMACH  DISEASES  CAUSED  BY  INFECTIOUS  GRANULOMATA. 


29.  Letorey,  “These,”  Paris,  1895. 

30.  Litten,  “ Virchow’s  Archiv,”  1876. 

31.  Lorey,  “ Bull.  d.  1..  Soc.  Anat.,”  1874. 

32.  “ Lubarsch  und  Ostertag,”  vol.  11,  p.  336. 

33.  Marfan,  “ These,”  Paris,  1887. 

34.  Mathieu  and  Remond,  in  Letorey’s  “ Thesis,”  Paris,  1875. 

35.  Mathieu,  “ Bull.  d.  1.  Soc.  Anat.,”  1881. 

36.  Muller,  K.,  “ Ueber  Dyspepsia  praetuberculosa,”  “ Ungar.  med.  Presse,” 
Budapest,  1898,  ill. 

37.  Miisser,  “ Phila.  Hosp.  Reports,”  1890,  1. 

38.  Oppolzer,  in  Marfan’s  “ These,”  Paris,  1887. 

39.  Orth,  “ Exper.  Magengeschw.,”  “Virchow’s  Archiv,”  Bd.  lxxvi. 

40.  Packard,  F.  A.,  “ Tuberculous  Ulcer  of  the  Stomach,”  “ Tr.  Path.  Soc.,” 
Phila.,  1898,  xviii. 

41.  Paulicky,  “Berlin,  klin.  Wochenschr.,”  1867. 

42.  Pozzi,  “ Bull.  Soc.  Anat.,”  1868. 

43.  Prezewoski,  “Gastritis  Tuberculosa”  (five  cases),  “ Centralbl.  f. 
allgem.  Path.  u.  path.  Anat.,”  Bd.  vi,  S.  270. 

44.  Quenu,  in  Marfan’s  “ Thesis,”  Paris,  1887. 

45.  Serafini,  “ Annal.  clin.  del  Osp.  di  Napoli,”  1888. 

46.  Talamon,  “ Progres  Med.,”  1879. 

47.  Weinberg,  “Ulceration  Tuberculeuse  de  l’estomac,”  “Soc.  Anat.  de 
Paris,”  5,  vi,  1897. 

48.  Wilms,  M.,  “ Miliar  tuberculose  des  Magens,”  “ Centralbl.  f.  allg.  Path, 
u.  path.  Anat.,”  Jena,  1897,  vui. 

49.  Petruschky,“  Verhandlung.  d.  XVI.  Congress,  fur  innere  Medicin,”  Wies- 
baden, April,  1899. 


SYPHILIS  OF  THE  STOMACH. 

Pathological  changes  caused  by  syphilis  occur  in  the  stomach  in 
two  main  forms — (1)  the  syphilitic  ulcer  and  (2)  the  syphilitic  neo- 
plasms. In  addition  to  these  the  author  recognizes  a third  form — 
(3)  the  diffuse  syphilitic  gastritis  (chronic  form).  While  the  first 
two  forms  are  due  to  direct  syphilitic  disease,  the  third  form  may  be 
due  to  indirect  syphilis — for  instance,  to  the  formation  of  countless 
syphilitic  gummata,  forming  nodules  in  the  mucosa  and  submucosa 
barely  visible  to  the  naked  eye.  This  third  form,  in  the  majority 
of  cases,  is  probably  due  to  what  Chiari  terms  indirect  syphilis 
— that  is,  due  to  circulatory  disturbances,  passive  congestions, 
hemorrhages,  etc.,  produced  by  syphilitic  disease  of  other  organs, 
especially  of  the  liver. 

Gastric  disturbances  are  observed  in  individuals  affected  with 
syphilis,  even  at  an  early  prodromal  stage  of  cutaneous  eruptions. 
These  patients  may  develop  all  the  symptoms  of  acute  gastritis, 
with  a feeling  of  pressure,  fullness  in  the  stomach,  loss  of  appetite, 


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SYPHILIS  OF  THE  STOMACH. 


597 


nausea,  etc.  The  symptoms  of  acute  or  subacute  gastritis  may 
be  accompanied  by  gastralgia,  coated  tongue,  headache,  and  actual 
vomiting.  These  symptoms  can  not  be  pronounced  as  syphilitic, 
because  other  etiological  factors  can  not  be  excluded  ; one  is  there- 
fore disposed  to  assign  the  gastric  symptoms  to  better  known 
causes.  Allen  A.  Jones  has  reported  two  cases  of  gastralgia, 
which  were  undoubtedly  caused  by  syphilis  (“  Phila.  Med.  Jour.,” 
vol.  hi,  p.  958).  Acute  diseases  of  the  neighboring  organs  (liver, 
pancreas,  and  spleen)  are  not  so  rare  in  syphilis  as  was  assumed 
not  long  ago.  Jullien  {loc.  cit.)  describes  attacks  of  vomiting, 
colic,  and  diarrhea  in  the  course  of  recent  syphilis;  and,  according 
to  Fournier  {loc.  cit),  bulimia  is,  in  rare  cases,  a symptom  in  severe 
forms  of  lues.  This  condition  is  observed  more  frequently  in 
women  than  in  men,  and  occurs  between  the  third  and  sixth 
month  of  the  disease.  According  to  this  author,  it  is  sometimes 
associated  with  polydipsia.  In  a consideration  of  the  previous 
gastric  diseases  we  have  seen  that  the  nerves  react  in  a very  sensi- 
tive manner  to  certain  anomalous  states  of  the  blood — anemias, 
etc.  In  lues  we  have  characteristic  reduction  of  the  erythrocytes 
and  of  the  percentage  of  hemoglobin.  We  might  trace  the  symp- 
toms described  to  these  blood  conditions  in  preference  to  ascribing 
them  to  disease  of  the  gastric  mucosa. 

Chronic  Gastritis  Due  to  Syphilis. — This  is  a rather  frequent 
and  important  syphilitic  affection,  and  is  one  of  the  main  causes  of 
the  poor  state  of  nutrition  in  luetics.  It  is,  as  a rule,  associated 
with  characteristic  syphilitic  disease  in  other  digestive  organs 
(spleen,  pancreas,  and  liver).  Histologically,  it  may  be  found  to 
be  a simple  chronic  gastritis,  or  else  combined  with  gummata  or 
gummatous  ulcers,  and  is  then  a phenomenon  of  the  later  stages. 
Syphilitic  chronic  gastritis,  in  the  absence  of  gummata  or  gum- 
matous ulcers,  does  not  differ  pathologically  from  ordinary  chronic 
gastritis,  except  in  the  greater  frequency  of  small  round- cell 
accumulation,  especially  in  the  submucosa,  sometimes  appearing 
like  miliary  gummata.  The  cases  that  are  described  by  Virchow 
{loc.  cit)  were  due  to  chronic  passive  hyperemia  caused  by  circu- 
latory disturbances,  and,  in  our  opinion,  present  nothing  character- 
istic of  syphilitic  gastritis.  Chronic  syphilitic  gastritis  may 
develop  from  repeated  attacks  of  the  acute  form,  just  as  with 
non-specific  chronic  gastritis.  Relapses  are  not  necessarily  due 
to  syphilis. 

If  characteristic  syphilitic  lesions  exist  in  the  liver,  kidneys, 


598  STOMACH  DISEASES  CAUSED  BY  INFECTIOUS  GRANULOMATA. 

spleen,  pancreas,  or  intestines,  the  chronic  gastritis  should,  in  my 
opinion,  be  attributed  to  syphilis.  In  tertiary  syphilis  the  remark- 
able malnutrition  is  due  to  a chronic  luetic  gastritis.  The  clinical 
phenomena  of  luetic  gastritis  are  not  different  from  the  non-specific 
inflammations  of  the  stomach. 

Diagnosis. — It  is  conceded  by  gastro-enterologists  that  iodids 
and  salts  of  mercury  have  a deleterious  effect  upon  the  gastric 
functions  in  normal  individuals.  If,  therefore,  the  symptoms  of 
gastritis  develop  in  a confirmed  luetic,  and  improve  upon  the 
administration  of  iodid  of  mercury,  getting  worse  when  the  mer- 
cury is  discontinued  and  improving  again  when  the  drug  is  re- 
sumed, the  diagnosis  of  chronic  syphilitic  gastritis  is  logical. 

We  have  observed  symptoms  of  acute  gastritis  in  a child  eleven 
years  old,  daughter  of  a man  who  had  contracted  syphilis  while 
he  was  a soldier  in  the  German  army  in  the  Franco-Prussian  war, 
i870-’7I.  The  father  of  this  child  has  had  maniacal  attacks,  in 
which  he  had  to  be  restrained.  About  once  a month  he  has  typical 
epileptic  convulsions,  which  may  last,  with  short  intervals,  for  ten  to 
twelve  hours,  with  foaming  at  the  mouth,  involuntary  evacuations, 
etc.  He  admits  the  original  infection,  and  gives  a correct  history 
of  primary  and  secondary  syphilis.  The  child  recently  developed 
a huge  gumma  of  the  lower  jaw,  which  assumed  the  dimensions  of 
a goiter.  The  gastric  symptoms  were  incessant  vomiting  and  gas- 
tralgia.  By  treatment  with  mercurial  inunctions  the  stomach 
symptoms  disappeared  in  the  course  of  two  weeks ; the  child  was 
apparently  cured  after  six  weeks  of  this  treatment.  The  efficacy 
of  this  form  of  treatment  was  all  the  more  fortunate  since  the  child 
could  retain  nothing  on  its  stomach  and  medication  by  the  mouth 
would  have  been  futile.  Two  years  ago  the  author  treated  another 
child  of  this  man  (his  wife,  by  the  way,  has  had  four  miscarriages), 
for  gastralgia,  nausea,  eructations,  and  vomiting,  by  mercurial  inunc- 
tions and  a saturated  solution  of  iodid  of  potassium.  The  child  took 
as  much  as  forty  drops  of  the  saturated  solution  of  KI  three  times  a 
day,  with  evidences  of  distinct  improvement,  the  symptoms  subsiding 
entirely  at  the  end  of  three  weeks.  In  both  of  these  children  the  vomit 
during  the  attacks  contained  no  free  HCl,but  enormous  quantities 
of  mucus,  and  curdled  milk  but  weakly.  Both  HC1  and  ferment 
secretion  were  restored  by  the  treatment.  Tullio  (loc.  cit)  reports 
improvement  and  cure  of  severe  chronic  gastritis  by  iodid  of  mer- 
cury given  internally.  The  patient  became  worse  when  the  mercury 
was  discontinued.  Non-syphilitics  were  made  dyspeptic  by  taking 


HISTOLOGY  OF  SYPHILITIC  GASTRITIS. 


599 


iodid  of  mercury.  The  following  conclusions  appear  to  us  to  be 
logical.  When  digestive  disturbances  resembling  those  of  gastritis 
occur  in  a syphilitic,  and  other  etiological  factors  can  be  excluded, 
the  diagnosis  of  syphilitic  gastritis  is  correct  if  the  phenomena  dis- 
appear under  antisyphilitic  treatment.  The  diagnosis,  then,  depends 
upon  the  evidence  of  undeniable  syphilis  as  a cause,  and  the  disap- 
pearance of  gastric  symptoms  under  antisyphilitic  treatment.  Pro- 
fessor S.  Flexner  (pathologist  to  the  Johns  Hopkins  Hospital)  pre- 
sented us  with  the  stomach  of  a syphilitic  negro  who  had  gummata 
in  the  following  places:  (i)  Frontal  bone,  extending  into  the  men- 
inges and  frontal  cerebral  convolutions ; (2)  one  in  the  liver  ; (3)  one 
in  the  spleen ; (4)  three  in  mesenteric  glands ; (5)  one  in  the  testes 
and  epididymis.  The  author  was  present  at  the  autopsy,  which  was 
made  by  Dr.  Flexner.  After  hardening  in  formol,  the  sections  were 
stained  in  orange-G.  and  hematoxylin.  All  the  sections,  no  matter 
from  what  portion  of  the  stomach  they  were  taken,  showed  an 
intense  diffuse  gastritis.  At  first  we  failed  to  find  characteristic 
evidence  of  lues.  The  surface  of  the  mucosa  was  covered  with 
finely  granular  elevations,  quite  evident  to  the  naked  eye.  The 
surface  cylindrical  epithelium  was  lost  entirely.  There  was  a very 
characteristic  endarteritis  and  thickening  of  the  vessel  walls,  pro- 
ducing occlusion  of  the  lumen  (endarteritis  obliterans).  Through- 
out the  mucosa  and  submucosa  were  countless  miliary  nodules, 
about  the  size  of  a pin’s  head,  composed  of  apparently  densely 
packed  collections  of  small  round  cells.  Some  of  these  nodules 
exhibited  themselves  in  the  submucosa,  but  in  that  situation  they 
were  rare.  The  majority  of  them  rested  upon  the  muscularis 
mucosae,  and  thence  extended  upward  into  the  glandular  layer, 
pushing  apart,  compressing,  and  distorting  what  was  left  of  the 
gland  ducts.  Some  of  the  small  round-cell  infiltrations  resem- 
bled normal  lymph-glands  of  the  stomach.  The  majority  of  them 
were,  however,  larger  than  the  gastric  lymph-glands,  extending 
from  the  submucosa  to  the  surface  of  the  mucous  membrane.  (See 
illustration,  plate  IX.)  One  of  our  artists  (Mr.  Louis  Schmidt)  has 
given  a graphic  illustration  of  the  condition  present.  In  many 
places  collections  of  round  cells  had  forced  asunder  the  fibers  of 
the  muscularis  mucosae,  splitting  apart  this  layer,  which  usually 
runs  along  in  one  stratum.  In  some  places  the  muscularis  mucosae 
was  seemingly  torn  apart  and  forced  either  downward  into  the 
submucosa,  or  upward  into  the  mucosa,  in  large  bundles,  by 
infiltrating  masses  of  round  cells  and  also  by  proliferation  of 


600  STOMACH  DISEASES  CAUSED  BY  INFECTIOUS  GRANULOMATA. 

the  muscle-fibers.  The  longitudinal  layer  of  muscle-fibers  was 
similarly  split  up  by  enormous  collections  of  round-cell  infil- 
tration. The  fibers  of  the  muscularis  mucosae  normally  as- 
cend into  the  glandular  layer  and  surround  the  gland  tubules. 
We  have,  however,  never  seen  these  muscle-fibers  ascending  in 
such  masses  as  in  these  specimens.  In  places  the  entire  glandular 
layer  was  replaced  by  a mass  of  small  round  cells.  The  left  side 
of  the  illustration  represents  one  of  the  miliary  nodules,  showing 
a gradual  breaking  down  or  softening  at  the  side.  Although  at 
first  inclined  to  consider  this  whole  process  due  to  indirect  syphilis, 
caused  by  passive  congestion  due  to  the  luetic  hepatitis  (a  large 
gumma  being  present  in  the  liver),  the  finding  of  nodules  as  large 
as  a pin’s  head  (which  showed  signs  of  softening)  suggests  that 
we  may  possibly  be  dealing  with  minute  miliary  gummata.  Chiari 
( loc . cit.)  reported  243  autopsies  of  undoubted  syphilitics  : 145  were 
hereditary  and  98  acquired  syphilis.  His  conclusions  are  the  fol- 
lowing : (1)  Pathological  changes  caused  by  syphilis  really  occur  in 
the  stomach  ; (2)  they  may  be  direct  syphilitic  changes,  or  owe  their 
origin  indirectly  to  syphilis ; (3)  the  direct  syphilis  of  the  stom- 
ach is  a great  rarity,  and  is  either  a gummatous  process  or  a simple 
inflammatory  infiltration;  the  latter  occurs  only  in  the  hereditary 
form ; (4)  the  indirect  syphilitic  affections  of  the  stomach  are  due 
to  circulatory  disturbances  caused  by  syphilis  of  the  other  organs, 
especially  of  the  liver,  or  else  they  are  due  to  gastric  hemorrhages 
occurring  interstitially  as  phenomena  of  a syphilitic  hemorrhagic 
diathesis ; (5)  gummatous  processes  in  the  stomach  are  character- 
ized by  presence  of  gummatous  tissues ; they  are  first  developed  in 
the  submucosa,  and  enter  the  other  layers  from  there  ; (6)  syphilitic 
gastric  ulcers  may  be  caused  by  disintegration  and  autodigestion. 
The  cicatrices  in  the  stomach  demonstrated  by  Cornil  {loc.  cit.) 
and  Weichselbaum  (loc.  cit.)  could  be  attributed  to  syphilis  only  if 
gummatous  tissue  or  other  non-ulcerating  gummata  were  present. 

Only  in  three  cases  could  Chiari  designate  the  changes  as  direct 
syphilis — one  gumma  in  a case  of  hereditary  syphilis,  one  gumma 
in  a case  of  acquired  syphilis,  and  one  in  diffuse  inflammatory 
infiltration  of  the  mucosa  and  submucosa  in  hereditary  syphilis. 
His  percentage  of  gastric  syphilis  was  1.2  per  cent,  of  the  total 
material  of  243  sections:  1.3  per  cent,  in  hereditary  syphilis,  and 
1.2  per  cent,  of  acquired  syphilis. 

Syphilitic  Ulcers  of  the  Stomach. — In  a study  of  the  sub- 
joined literature  authentic  cases  of  syphilitic  gastric  ulcers  are  not 


GASTRIC  ULCER  RESULTING  FROM  SYPHILIS. 


601 


so  scarce  as  one  might  presume.  Galliard  ( loc . cit.)  and  Cruveilhier 
( loc . cit.)  were  disposed  to  believe  in  a causative  relation  between 
simple  gastric  ulcer  and  syphilis.  Among  one  hundred  cases 
of  gastric  ulcer,  Engel  could  trace  a syphilitic  history  in  ten  per 
cent.  T.  Lang  (loc.  cit.)  stated  that  twenty  per  cent,  of  gastric  ulcers 
occur  in  syphilis.  Ewald  expresses  himself  with  doubt  on  this 
subject:  “ It  must  remain  questionable,”  he  says,  “ in  two  diseases 
as  common  as  those  under  discussion,  whether  we  are  dealing 
with  cause  and  effect,  or  with  accidental  coincidents.”  Frerichs, 
Drozda,  Murchison,  and  Chvostek  found  scars  in  the  stomach, 
coincidently  with  general  syphilis.  Gastric  ulcers  may  occur  in 
syphilitics  from  necrosis  of  the  mucosa,  due  to  specific  endarteritis, 
or  to  disintegration  and  breaking  down  of  a gumma.  In  1838 
Andral  (loc.  cit.)  concluded  that  a gastric  ulcer  in  his  clinic  was 
due  to  syphilis  because  it  was  cured  by  mercurial  treatment. 
Rosanow  (loc.  cit.)  described  a case  in  a soldier  who  had  suffered 
from  gastric  ulcer  for  eight  years  and  had  been  treated  by  him  for 
two  months  by  typical  ulcer  treatment.  The  cardialgia,  however, 
continued,  and  was  associated  with  pains  in  the  lower  extremities. 
The  patient  showed  no  signs  of  lues.  He  was  cured  in  forty-seven 
days  by  treatment  by  inunctions  and  iodid  of  potassium.  It  is 
necessary  to  distinguish  between  typical  simple  round  ulcers 
occurring  in  syphilitics,  and  gummatous  ulcerations,  with  gastritis. 
According  to  Wagner  (loc.  cit.)  and  Klebs  (loc.  cit.),  all  ulcers  found 
in  the  stomachs  of  syphilitics  have  arisen  from  gummata,  but 
Galliard  (loc.  cit.),  Lang  (loc.  cit.),  and  Mauriac  (loc.  cit.)  differ  from 
this  opinion,  and  hold  that  the  syphilitic  gastric  ulcers  do  not 
necessarily  arise  from  gummata. 

T.  Lang’s  (loc.  citi)  statistics  indicate  that  twenty  per  cent,  of 
gastric  ulcers  occur  in  luetic  subjects,  and  Neumann  (loc.  cit.) 
asserts  that  syphilis  is  more  often  the  cause  of  gastric  ulcer  than 
has  been  hitherto  believed ; furthermore,  that  gastric  ulcers 
occurring  in  syphilis  do  not  develop  from  gummata,  but  have 
the  same  manifold  etiology  as  the  non-specific  ulcer.  They 
may  develop  from  erosions,  which  are  very  frequent  in  syphili- 
tics ; from  endarteritis ; from  diminution  in  the  amount  of  hemo- 
globin; and  from  reduction  of  the  alkalinity  of  the  blood,  increase 
and  disintegration  of  the  leukocytes.  These  states  are  character- 
istic of  lues,  and  are  accepted  as  etiological  factors  of  round 
ulcers  also.  To  these  might  be  added  hyperacidity  and  bacterial  in- 
fection causing  necrosis.  In  a case  of  Fauvel’s  (loc.  cit.)  the  stomach 
showed  chronic  gastritis  and  several  ulcers.  In  a case  of  Capozzi’s 


602  stomach  diseases  caused  by  infectious  granulomata. 

(loc.  cit .)  numerous  ulcerations  of  the  mucosa  extended  from  the 
cardia  along  the  greater  curvature  to  the  pylorus.  In  a case  of 
Oser’s  the  patient  was  affected  with  a syphilitic  papulous  eruption 
and  psoriasis  palmaris,  the  gastric  mucosa  was  injected  and  per- 
meated by  numerous  hemorrhagic  erosions. 

The  symptoms,  course,  and  termination  of  syphilitic  gastric  ulcers 
are  not  different  from  the  non-syphilitic.  In  a case  of  Rosanow’s 
(loc.  cit.)  the  gastralgia  occurred  only  at  night,  and  from  this  the 
author  diagnosticated  the  probable  syphilitic  nature  of  the  ulcer. 
Bartumeus  (loc.  cit.)  speaks  of  nightly  vomiting  occurring  with 
syphilitic  ulcer. 

Diagnosis. — When  other  etiological  factors — such  as  tuberculo- 
sis, alcoholism,  chlorosis,  and  the  manifold  causes  which  have  been 
enumerated  in  the  article  on  ulcer — can  be  excluded,  and  undoubted 
syphilis  can  be  established,  the  diagnosis  of  the  syphilitic  origin  of 
gastric  ulcer  might  be  made,  although  not  with  certainty.  The 
diagnoses  of  Andral  (loc.  cit),  Hayem  (loc.  cit),  and  Mark  (loc.  cit) 
were  based  upon  the  curative  effect  of  antisyphilitic  treatment. 

Prognosis. — Wagner  (loc.  cit),  Lanceraux,  and  others,  report  cures 
of  syphilitic  ulcers  by  iodid^of  potassium.  The  conditions  after  the 
reported  cures  were  similar  to  those  existing  after  the  cures  of  non- 
specific ulcers.  Stenosis  of  the  pylorus  and  chronic  gastritis  fol- 
lowing syphilitic  ulcers  have  been  observed  by  Cornil,  Capozzi, 
Wagner,  Fauvel,  and  Klebs.  The  direct  cause  of  death  in  autopsies 
of  cases  of  syphilitic  gastric  ulcers  hitherto  reported  was  plainly 
attributable  to  pathological  states  in  other  organs,  such  as  tuber- 
culosis, amyloid  and  fatty  degeneration  of  various  viscera,  dropsies, 
and  edema.  Some  of  the  cases  reported  as  syphilitic  are  doubtful. 
This  is  my  opinion  of  the  case  reported  by  Zavadski  and  Luxen- 
bourg  (loc.  cit),  in  which  no  characteristic  syphilitic  lesions  are 
described,  for  the  endarteritis  and  the  small  round-cell  infiltration 
may  occur  in  chronic  gastritis  of  a non-luetic  character.  The 
patient,  a medical  student,  had  denied  luetic  infection. 

Syphilitic  Neoplasms  of  the  Stomach. — The  percentage  of 
gastric  gummata  occurring  in  syphilis  has  already  been  stated  in 
the  results  given  from  243  autopsies  on  syphilitics  performed  by 
Chiari  (loc.  cit). 

Gastric  gummata  have  been  described  by  Galliard  (loc.  cit), 
Cornil  (loc.  cit),  Birch-Hirschfeld  (loc..  cit),  Chiari  (loc.  cit),  Wagner 
(loc.  cit),  Klebs  (loc.  cit),  and  Lanceraux  (loc.  cit).  Cornil’s  case, 
which  may  be  regarded  as  typical,  was  that  of  a woman  who  had 
gummata  both  in  the  liver  and  stomach.  That  in  the  stomach 


SYPHILITIC  NEOPLASMS. 


603 


was  located  on  the  lesser  curvature,  and  had  the  appearance  of  a 
flattened  reddish  tumor,  two  to  five  centimeters  in  diameter.  The 
gastric  gummata  reported  by  Chiari  (loc.  cit .)  were  sharply  circum- 
scribed elevated  swellings.  They  occur  together  with  gastric  or 
intestinal  ulcers  or  cicatrices,  and  develop  in  the  submucous  layer 
as  dense,  compact,  felt-like  masses,  formed  of  fasciculi  of  con- 
nective tissue  infiltrated  with  small  round  cells.  From  the  sub- 
mucosa they  advance  into  the  serosa  and  mucosa.  The  mucosa 
is  thickened,  smooth,  and  glistening,  and  of  a pale  yellow  color. 
The  muscularis  and  the  serosa  are  also  thickened.  The  condition 
of  the  gummata  will  vary  with  the  stage  in  which  they  are  found. 
In  one  case  Cornil  found  three  gummata — respectively  two,  three, 
and  five  centimeters  in  diameter — in  the  neighborhood  of  the 
pylorus.  The  mucosa  over  these  gummata  was  thinned  out  and 
adherent.  Lanceraux  (loc.  cit)  found  an  ulceration  thirty  centi- 
meters in  diameter  in  close  proximity  to  the  pylorus  on  the  lesser 
curvature.  The  case  was  that  of  a man  sixty-six  years  old,  with 
many  manifestations  of  syphilis.  The  ulceration  had  destroyed 
the  gastric  wall — thinned  it  down  to  a very  delicate  lamella.  The 
nodule  was  in  a state  of  fatty  disintegration,  and  apparently  had 
prevented  a perforation  by  its  own  structure.  Birch-Hirschfeld’s 
case  occurred  in  a new-born  infant,  with  skin  syphilis  and  a gumma 
in  the  liver  and  lungs.  In  the  pylorus  was  a slightly  elevated 
thick  area,  as  large  as  the  palm  of  the  hand.  It  was  of  a whitish 
color  and  of  tolerably  firm  consistence,  formed  of  granulation 
tissues  infiltrated  with  masses  of  small  round  cells.  Weichselbaum 
(loc.  cit.)  described  two  ulcers  and  one  cicatrix  at  a spot  where  the 
transition  of  the  fundus  into  the  pyloric  part  occurs.  One  of  the 
ulcers  had  a triangular  shape  and  was  twelve  millimeters  long. 
This  occurred  in  a man  twenty-five  years  old,  with  syphilitic  mani- 
festations of  the  cranium,  nose,  throat,  larynx,  and  liver.  Another 
case  of  Chiari’s,  a child  three  weeks  old,  with  pemphigus  syphiliti- 
cus, swelling  of  the  inguinal  glands,  and  fissures  in  the  lips,  tongue, 
and  penis,  showed  in  the  lungs  numerous  nodules  as  large  as  peas, 
some  as  large  as  hazelnuts.  There  was  an  induration  in  the  hilus 
of  the  liver,  and  a similar  callosity  on  the  common  bile-duct,  and  also 
on  the  cystic  duct.  The  wall  of  the  gall-bladder  neck  was  strongly 
infiltrated.  The  gastric  mucosa  showed  five  plate-like  gummata. 
The  gastric  gummata  generally  soften,  break  down,  and  ulcerate  ; 
this  has  been  the  cause  of  assigning  all  syphilitic  ulcers  to  the 
breaking  down  of  gummata.  The  ulcer  which  arises  from  a 


604  stomach  diseases  caused  by  infectious  granulomata. 

gumma  is  a loss  of  substance  that  is  smaller  in  the  true  mucosa 
than  in  the  submucosa.  The  simple  perforating  gastric  ulcer  is  a 
loss  of  substance  that  is  greatest  in  the  true  mucosa,  becomes 
smaller  in  tjie  submucosa,  and  still  smaller  in  the  muscularis. 

This  gives  the  simple  gastric  ulcer  the  characteristic  terraced 
appearance,  which  is  never  seen  with  a gummatous  gastric  ulcer. 
The  edge  of  the  simple  gastric  ulcer  is  not  undermined,  but  has 
the  appearance  as  if  cut  out  with  a punch.  The  edge  of  the 
gummatous  gastric  ulcer,  however,  is  irregular,  angular,  rolled  up, 
and  often  undermined.  The  surroundings,  the  walls,  and  the  floor 
of  the  simple  gastric  ulcer  exhibit  no  pus  and  no  necrotic  tissue 
elements ; perhaps  some  slight  hemorrhagic  infiltration  is  observa- 
ble, if  a previous  hemorrhage  has  occurred.  The  gummatous  gas- 
tric ulcer  is  covered  by  a yellow,  tough,  gelatinous  deposit.  In  the 
surroundings  one  frequently  finds  gummata.  Old  and  extensive 
simple  ulcers  may  closely  resemble  gummatous  ulcers  on  account 
of  the  fibrous  thickening  of  the  edges.  The  occurrence  of  gum- 
mata in  other  parts  of  the  digestive  tract  or  organs  may  then 
decide  the  nature  of  the  gastric  neoplasm.  Gummata  of  the  stom- 
ach, according  to  Neumann,  are  manifestations  of  late  lues.  The 
cases  of  Birch-Hirschfeld  (Joe.  cit.)  and  Chiari  (loc.  cit .),  however, 
were  inherited  syphilis. 

Diagnosis. — These  lesions  do  not  give  symptoms  sufficiently 
characteristic  to  make  their  clinical  recognition  possible.  In 
pronounced  syphilitics,  with  palpable  hepatic  gummata  and  steno- 
tic symptoms  in  the  stomach,  antisyphilitic  treatment  may  possibly 
give  some  clue  regarding  the  nature  of  the  gastric  neoplasm. 

Hemorrhage  from  the  Stomach  as  a Result  of  Syphilis. — 
This  is  an  extremely  rare  occurrence.  Hayem  reports  a case  of 
grave  hematemesis  which  baffled  the  usual  treatment,  but  ceased 
after  the  administration  of  iodid  of  potash.  Gastric  hemorrhage 
may  occur  as  a result  of  intense  passive  congestion,  caused  by 
obstruction  of  the  portal  circulation.  Hiller  (loc.  cit.)  reports  a case 
of  a man  thirty-nine  years  old,  who  admitted  having  acquired 
lues  in  1868.  In  the  night  from  the  3d  to  the  4th  of  December, 
1 88 1 , he  vomited  large  quantities  of  blood,  and  passed  blood  by  the 
stool.  On  the  5th  of  December  the  vomiting  of  bright  red  blood 
was  repeated ; he  also  had  three  passages  that  were  black  with 
partially  digested  blood.  The  gums  and  uvula  were  covered  with 
numerous  radiating  scars;  the  pharynx  showed  two  recent  scars. 
In  the  nasal  partition  there  was  an  irregular,  deepened  ulcer  with 


LITERATURE  ON  SYPHILIS  OF  THE  STOMACH.  605 

callous  edges.  For  several  months  there  had  been  a purulent 
offensive  discharge  from  the  nose.  There  was  decided  enlarge- 
ment of  the  spleen  and  liver.  Several  uneven  prominences  were 
palpable  on  the  surface  of  the  liver.  The  diagnosis  of  syphilis  of 
the  liver  was  made,  with  passive  congestion  in  the  spleen  and 
stomach.  The  patient  recovered  under  antisyphilitic  treatment. 
It  is  impossible  to  decide  in  these  cases  whether  the  hemorrhage 
comes  from  an  ulcer,  from  hemorrhagic  erosions,  or  from  disease 
of  the  blood-vessels. 


LITERATURE 

ON  SYPHILIS  OF  THE  STOMACH. 

1.  Andral,  “Clinique  med.,”  tome  iv,  121. 

2.  Bartumeus,  “ Gastralgia  Intermittente  Sifilitica  Accompananda  de  Vomi- 
tos  Vespertinos  y Otros  Accidents  Especificos  Dolorosos,”  “ Revista  de  Cien- 
cias  Med.,”  Barcelona,  1878,  348. 

3.  Berthold’s  “ Statistischer  Beitrag  zur  Kenntniss  des  chronischen  Magen- 
geschwiirs,”  “ Aus  den  Sections-protokollen  des  patholog.  Institutes  zu  Berlin,” 
i868-’82.  Berlin,  1883;  Dissertation. 

4.  Bittner,  “ Centralbl.  f.  allgem.  Pathologie,”  Bd.  v,  1894,  S.  175;  also 
“ Prag.  med.  Wochenschr.,”  1893,  No.  48. 

5.  Birch-Hirschfeld,  “ Lehrbuch  der  patholog.  Anatomie,”  1885,  II,  531. 

6.  Capozzi,  11,  Morgagni,  1867,  ix,  2,  89;  Schmidt’s  “ Jahrbiicher,” 
cxxxv,  41. 

7.  Chiari,  “ Prag.  med.  Wochenschr.,”  1885,  No.  47. 

8.  Chiari,  “International.  Beitrag  z.  Wissenschaft : Medicin,”  Rudolf  Vir- 
chow, gewidmet,  1891,  Bd.  11. 

9.  Cornil,  “ Lec^ons  sur  la  Syphilis,’’  1879,  4°6  ; and  “ Manuel  de  l’Histolog. 
Patholog.,”  1882,  11,  296. 

10.  Dieulafoy,  “ Syphilis  de  l’estomac,”  Acad,  de  med.,  17.  Mai,  1898. 

11.  Dubuc,  “Un  cas  de  syphilis  de  l’estomac,”  “Soc.  de  med.  de  Paris,” 
28.  Juin,  1898. 

12.  Fauvel,  “ Bullet,  de  la  Societe  d’Anatom.,”  1858. 

13.  Flexner,  S.,  “Gastric  Syphilis,  with  the  Report  of  a Case  of  Perforating 
Syphilitic  Ulcer  of  the  Stomach,”  “Am.  Jour,  of  the  Med.  Sciences,”  Oct., 
1898. 

14.  Fournier,  “ Notes  sur  Certains  Cas  Curieux  de  Boulimie  et  de  Polydipsie 
d’Origine  Syphillitique,”  “ Gaz.  hebdomadaire  de  Med.  et  de  Chirurg.,”  Paris, 
1871,  Nos.  1 and  2 ; “ Gaz.  des  Hopitaux,”  Paris,  1871,  Nos.  109,  no,  112. 

15.  Galliard,  “ Syphilis  Gastrique  et  Ulcere  Simple  del’Estomac,”  “ Archiv. 
Generates  de  Medecine,”  1886,  pp.  65-83. 

16.  Hayem,  G.,  Hayem  et  Tissier,  “ De  la  Syphilis  de  l’lntestin,”  “ Revue 
de  Med.,”  Paris,  1889,  231. 

17.  Hiller,  “ Monatshefte  f.  prakt.  Dermatologie,”  1882,  1,  97  ff. 

18.  Von  Jaksch,  Cit.  nach  Bamberger,  “ Krankheiten  des  chylopoetischen 
Systems,”  “ Handb.  d.  spec.  Pathologie  u.  Therapie,”  von  Virchow,  VI,  1 
Abth.,  280. 


6o  6 


BENIGN  TUMORS  OF  THE  STOMACH. 


19.  Jullien,  L.,  “ Traite  Pratique  des  Malad.  Vener.,”  1879,  p.  615. 

20.  Klebs,  “ Pathologische  Anatomie,”  1869,1,  262,  263. 

21.  Lanceraux,  “ Traite  Historique  et  Pratique  de  la  Syphilis,”  Paris,  1873, 
249. 

22.  Lanceraux,  “ Traite  de  la  Syphilis,”  1874,  248. 

23.  Lang,  T.,  “ Zur  Lehre  von  der  Eingeweidesyphilis.”  Sonderdruck  der 
“ Wiener  med.  Presse,”  1885,  No.  11. 

24.  Lang,  T.,  “Eingeweidesyphilis,”  “Wien.  med.  Presse,”  85,  No.  11. 

25.  Mauriac,  “ Syph.  tert.,”  p.  723. 

26.  Neumann,  in  “ Nothnagel’s  specielle  Patholog.  u.  Therapie,”  Bd.  xxm, 
Syphilis,  S.  351. 

27.  Nolte,  “ Ueber  die  Haufigkeit  des  Magengeschwiirs  in  Miinchen,” 
Munchen,  1883  ; Dissertation. 

28.  Orth,  “ Lehrbuch  d.  speciellen  pathol.  Anatomie,”  Berlin,  1887,  1,  S. 
709,  744. 

29.  Oser’s  “ Vierteljahresschrift  fur  Dermatologie  und  Syphilis,”  1871, 
No.  27. 

30.  Rosanow,  V.,  “ Magengeschwiir  syphilitischen  Ursprungs,”  “ La  Sem- 
aine  Medicale,”  1890,  No.  43. 

31.  Tullio,  “ Contributo  alio  Studio  delle  Lesioni  Funzionale  Gastriche,  per 
Sifilide  edei  coro  Magri  curative,”  “ Polyclinica,”  xv,  Giugni,  1894. 

32.  Virchow,  “ Handb.  der  spec.  Pathol,  und  Ther.,”  xi,  1,  S.  71,  78. 

33.  Wagner,  “ Das  Syphilom,”  “ Archiv  der  Heilkunde,”  1863,  Bd.  IV, 
225  und  226,  369. 

34.  Weichselbaum,  “ Bericht  d.  Rudolfspitals  in  Wien,”  1883,  S.  383. 

35.  Zavadski  and  Luxembourg,  “ Gaz.  Lekaroka,”  1893,  vol.  xm,  p.  1233, 
et  seq. 

36.  “ Jahresbericht  der  k.  k.  Krankenanstalt  Rudolf-Stiftung,”  1883,  383. 

37.  Flexner,  Simon,  “Gastric  Syphilis;  A Case  of  Perforating  Syphilitic 
Ulcer  of  the  Stomach,”  “Am.  Jour.  Med.  Sciences,”  October,  1898. 


CHAPTER  VI. 

BENIGN  TUMORS  OF  THE  STOMACH. 

Myomata. — Fibromata. — Lipomata. — Polypi. — Myxomata. — Papillo- 
mata.— Lymphadenomata. — Pedunculate  Tumors.  — Foreign 
Bodies. — Gastroliths. — Hypertrophic  Stenosis 
of  the  Pylorus. 

The  stomach  may  be  the  seat  of  a great  diversity  of  tumors. 
A neoplasm  that  can  be  determined  by  palpation,  however,  is,  as  a 
rule,  a carcinoma.  Benign  tumors  are  very  rare,  and  their  clinical 
history  does  not  present  any  great  interest.  But  occasionally  they 
may  become  the  cause  of  errors  in  diagnosis.  This  reason  obliges 


POLYPI — MUCOUS  POLYPI.  607 

me  to  say  a few  words  about  them,  as  well  as  of  other  foreign  bodies 
and  gastroliths  which  are  liable  to  occur  in  the  stomach. 

Myomata,  lipomata,  papillomata,  and  lymphadenomata  have  been 
found  in  the  stomach. 

In  acute  toxic  gastritis  caused  by  the  ingestion  of  corrosive 
sublimate,  calcareous  masses  may  develop  in  the  depths  of  the 
mucous  membrane.  In  comparing  simple  chronic  gastritis  with 
gastric  tuberculosis  we  have  shown  that  in  the  former  the  glands 
were  capable  of  undergoing  a cystic  degeneration  more  or  less  pro- 
nounced. Aneurysms  of  vessels  in  the  walls  of  the  stomach  have 
also  been  described. 

Polypi. — Papillomata  arising  from  the  mucous  membrane  some- 
times form  very  well-developed  villosities  in  the  pyloric  region. 
In  their  interior  one  finds  a very  fine  fibrillous  network,  formed 
by  the  prolongations  of  branched  cells ; their  surface  is  covered 
with  cylindrical  epithelium. 

Polypi  may  develop  from  myomata,  lipomata,  fibromata,  and 
papillomata.  They  vary  in  size  from  that  of  a pea  to  that  of  a wal- 
nut. They  may  be  pedunculated  or  attached  by  broad  bases.  The 
term  polypus  is  only  descriptive,  and  not  so  important,  anatomic- 
ally, as  the  terms  for  other  gastric  neoplasms.  In  the  structure  of 
polypi  at  times  the  connective  tissue,  at  others,  the  glandular  ele- 
ment, predominates.  They  might,  therefore,  be  classed  logically 
among  the  fibromata  and  adenomata.  They  may  present  smooth, 
warty,  or  villous  surfaces,  the  latter  resembling  the  surface  of  a 
raspberry  or  at  times  of  cauliflower. 

Villous  growths  presenting  warty  surfaces  and  a papillomatous 
structure  are  classed  among  the  fibromata.  They  are  covered  by  a 
single  layer  of  cylindrical  cells. 

Mucous  Polypi. — Cornil  (“  Gaz.  des  Hopitaux,”  1864,  No.  20) 
has  brought  to  light  two  cases  of  mucous  polypi  which  had  not 
manifested  any  symptoms  during  life.  In  one  of  these  cases  the 
red,  mammillated,  in  places  slate-colored,  stomach,  presented 
eight  vegetations,  from  the  size  of  a grain  of  wheat  to  that  of  a 
bean,  which  had  their  seat  in  the  vicinity  of  the  pylorus.  These 
vegetations  were  soft,  rosy,  and  injected  with  blood;  their  surface 
was  irregularly  mammillated,  and  they  were  formed  exclusively  at 
the  expense  of  the  mucous  membrane.  In  the  other  case  there 
existed  only  one  pedunculated  polypus,  rounded  like  a cauliflower, 
and  as  large  as  a hazelnut.  This  tumor,  formed  at  the  expense  of 
the  mucous  membrane  and  of  the  submucosa,  was  very  vascular  at 
40 


6o8 


BENIGN  TUMORS  OF  THE  STOMACH. 


its  center.  Lambl  (“  Beobachtungen  aus  dem  Franz  Joseph  Kinder- 
spital,”  Prag,  i860,  p.  376)  has  described  a tumor  as  large  as  a 
pigeon’s  egg,  extending  three  centimeters  along  the  fundus  of  the 
stomach,  and  covered  by  the  mucous  membrane,  which  had  become 
thin ; no  sign  had  revealed  its  existence  during  life.  Debove 
found  a mucous  polypus  by  means  of  the  tube,  in  a patient  suffer- 
ing from  nervous  dyspepsia. 

Rokitansky  attributed  the  formation  of  these  tumors  to  chronic 
gastritis;  they  would  thus  develop  around  the  glands  of  the  papillae 
in  unusual  numbers  and  sizes.  Wilson  Fox  also  admits  the  part 
played  by  inflammation  in  the  genesis  of  these  polypi.  Canus 
Govignon  (“  Polypes  de  l’Estomac,”  “These,”  Paris,  1883)  attrib- 
utes a certain  influence  to  alcoholism.  These  polypi,  whatever 
may  be  their  structure,  are  somewhat  rare.  The  first  case  was 
pointed  out  by  Cruveilhier  (“  Atlas  de  l’Anatomie,”  xxx  livraison, 
Fig.  2,  p.  2) ; the  stomach,  the  drawing  of  which  he  gives,  con- 
tained ten  pedunculate  excrescences,  one  of  which  obliterated  the 
pylorus.  Andral  (“  Clinique  Medicale,”  tome  11)  in  one  case  dis- 
covered laminated  structures  analogous  to  the  gastric  mucosa  of 
ruminants.  Ripault  (1833),  Mercier  (1887),  Castilhes  (1843),  Barth 
(1845),  Richard  (1846),  Leudet  (1847),  Barth  (1849), have  reported  a 
certain  number  of  cases  of  the  same  character.  Ebstein  (“  Arch.  p. 
Anat.  u.  Physiol.,”  1864)  has  collected  all  these  observations,  and 
has  added  14  cases  which  he  had  himself  obtained  from  600 
autopsies.  Of  the  24  cases  thus  collected,  1 5 occurred  in  men 
and  8 in  women ; in  1 case  the  sex  of  the  patient  is  not  men- 
tioned. The  frequency  of  these  tumors  increases  after  forty  years  ; 
in  half  the  cases  they  are  isolated ; in  1 case  there  were  50  of 
them,  and  in  2 cases  there  was  a number  varying  from  150  to  200. 
Their  form  is  variable — they  are  rounded,  club-shaped,  cylindrical, 
ramified;  their  color  depends  on  their  vascularization  ; frequently 
they  are  pigmented.  The  mucous  membrane  which  covers  them 
is  sometimes  entirely  smooth,  sometimes  villous,  or  thickened. 
They  are  usually  located  at  the  pylorus,  and  their  size  is  in  inverse 
ratio  to  their  number. 

Lipoma  (Murray,  “ Fatty  Tumor  in  Wall  of  the  Stomach,” 
“Pathol.  Tr.,”  vol.  xi,  1890). — The  lipoma  is  also  very  rare. 
Starting  from  the  submucosa,  it  sometimes  makes  a projection 
toward  the  gastric  cavity,  pushing  back  the  mucous  membrane 
which  continues  to  cover  it,  but  grows  thinner  in  proportion  as 
the  tumor  increases  ; sometimes  it  pushes  aside  the  muscular  fibers 


MYOMA — LYMFHA  DENOMA. 


609 


and  succeeds  in  making  a hernia  under  the  serosa.  A large  tumor 
of  this  kind  might  cause  digestive  troubles  by  the  dragging  of  its 
weight  on  the  wall  of  the  stomach,  but  the  rareness  of  these  cases 
interferes  with  an  exact  knowledge  and  description  of  their  symp- 
toms. Orth  has  observed  lipomata  growing  from  the  serosa  in  a 
pendulous  manner  (/.  c.t  S.  717). 

Myoma. — The  myoma  develops  in  the  interior  of  the  muscular 
layer,  gradually  projects  under  the  mucous  membrane,  and  occa- 
sionally ends  by  forming  polypi — sometimes  isolated,  sometimes 
in  numbers.  These  tumors  do  not  differ  in  a histological  point  of 
view  from  those  which  may  be  found,  for  example,  in  the  uterus, 
but  their  size  rarely  exceeds  that  of  a pea  or  a cherry.  Their 
development  is  not  accompanied  by  any  symptoms,  and  they  are 
rarely  discovered  at  the  autopsy.  (Myoma,  see  Virchow-Onkol, 
hi,  126.) 

Symptoms. — The  symptomatology  of  these  tumors  is  variable. 
Sometimes  they  become  ulcerated,  and  Rondeau  (“  Presse  med. 
Beige.,”  No.  18,  1881)  has  pointed  out  a case  where  their  presence 
was  revealed  by  serious  hemorrhages;  naturally,  the  observer  was 
not  able  to  diagnose  the  cause  of  this  hematemesis.  At  other 
times,  as  in  the  case  of  Cruveilhier’s  patient,  the  tumor  may 
obstruct  the  pylorus  and  cause  a dilation  of  the  organ.  Bernabes 
(“  Rivista  Clinica  di  Bologna,”  Juillet  et  Auot,  1882)  had,  in  this 
way,  the  opportunity  of  observing  a woman  seventy  years  old  who, 
for  a long  time,  had  vomited  a few  hours  after  meals,  and  experi- 
enced sharp  epigastric  pains,  in  the  absence  of  characteristic  symp- 
toms. At  the  autopsy  there  was  found  a polypus  of  six  or  eight 
centimeters,  implanted  on  the  anterior  surface  of  the  stomach,  five 
centimeters  from  the  pylorus.  Five  other  smaller  polypi  were 
scattered  on  the  pyloric  antrum  and  along  the  greater  curvature 
(Bruman,  “ Th.  de  Paris,”  1883;  Brissaud,  “ Arch.  Gen.  de  Med.,” 
1885  \ Marfan,  “ Th.  de  Paris,”  1887  ; Menetrier,  “ Arch,  de  Phys.,” 
15.  Fevrier,  1888). 

Lymphadenoma. — The  stomach  may  also  be  the  seat  of  lym- 
phoid tumors.  These  likewise  constitute  a pathological  rarity. 
Pitt  (“  Pathol.  Trans.,”  vol.  xi,  1890)  has  reported  one  case,  and 
states  that  he  has  been  unable  to  find  more  than  seventeen  in  the 
literature  on  the  subject.  The  patient  had  succumbed  to  phenom- 
ena which  were  all  attributed  to  a tumor  of  the  lungs,  and  to  an 
empyema  of  the  left  pleura.  Soft  nodules  were  scattered  over  the 
stomach  and  intestines,  which  had  perforated  the  mucous  membrane, 


6io 


BENIGN  TUMORS  OF  THE  STOMACH. 


or  had  made  greater  or  lesser  projections  at  its  surface ; histologi- 
cally, all  the  characteristics  of  lymphadenoma  were  exhibited.  The 
spleen,  the  mesenteric,  and  the  bronchial  ganglia  were  invaded; 
the  liver  and  the  kidneys  were  not  affected,  however.  The  neo- 
plasm develops  in  the  mucosa  and  submucosa,  and  forms  tumors 
projecting  into  the  cavity.  On  the  other  hand,  at  times  the 
serosa  is  first  attacked.  The  muscular  stratum  then  becomes 
more  or  less  affected  by  distention,  and  a dilation  of  the  organ 
becomes  evident.  In  other  cases  the  tumors  which  project  into 
the  gastric  cavity  become  ulcerated,  and  the  patient  succumbs 
to  a hematemesis,  as  in  Reimer’s  observation  (“  Deut.  Arch.  f.  klin. 
Med.,”  Bd.  xxxm,  S.  632,  1879).  To  these  phenomena  are  always 
added  a diarrhea  of  varying  seriousness;  but  when  the  tumors 
remain  limited  to  the  stomach,  health  may  be  little  affected  by  it. 
Anatomically,  one  finds  around  the  base  of  the  tumor  a hardening 
of  the  mucous  membrane;  the  glands  affected  are  in  fatty  degen- 
eration, while  at  their  periphery  there  exists  a characteristic  reticu- 
lated tissue.  The  degenerated  glands  finally  disappear,  and  there 
remains  nothing  more  than  the  reticulated  tissue  of  the  tumor. 

Pedunculated  adenomata,  attaining  the  size  of  an  apple,  have 
been  observed,  which  were  composed  exclusively  of  tortuous,  irreg- 
ularly dilated  gland  tubules.  Tumors  may  occur  in  the  stomach 
as  well  as  in  the  intestines,  which  anatomically  and  clinically  must 
be  considered  cancers,  and,  having  a pronounced  glandular  structure 
are  designated  as  destructive  or  malignant  adenomata  or  adenocar- 
cinomata.  The  case  reported  by  Pitt  (/.  cl)  is  suggestive  of  this 
type.  They  have  been  considered  under  the  malignant  tumors. 

Cysts. — Retention  cysts  of  the  gastric  glands  occur  in  “ gastritis 
polyposa”  and  polypoid  hypertrophy.  Ruysch  (“Adversaria  Ana,” 
tome  in,  p.  1,  Dec.,  1732)  described  a gastric  dermoid  cyst  contain- 
ing hair.  Engel- Reimers  (“  Deut.  Arch.  f.  klin.  Med.,”  xxm,  p.  632, 
1879)  describe  a multilocular  lymphangioma  occurring  in  the  outer 
gastric  wall  beneath  a chronic  ulcer  of  the  lesser  curvature.  This 
cyst  contained  a milky  liquid,  produced  by  stasis  of  lymph  in  con- 
sequence of  occlusion  through  inflammatory  processes  in  the 
vicinity  of  the  ulcer.  Albers  (“  Erlauterungen,”  iv,  p.  1 51)  men- 
tions a cyst  2j{  inches  long  found  on  the  lesser  gastric  curvature 
in  a child. 

Foreign  Bodies. — Foreign  bodies  are,  in  certain  cases,  capable 
of  simulating  a tumor,  both  by  the  subjective  symptoms  which  they 
cause,  and  by  the  deception  to  which  they  give  rise  on  palpation. 


FOREIGN  BODIES  IN  THE  STOMACH.  6 1 I 

A patient  of  Baillarger's  (“  Union  Med.,”  No.  48,  1874)  had  kept  in 
his  gastric  cavity  for  six  years  a zinc  fork  ; an  epileptic,  cited  by 
Foville  (“  Gaz.  hebd.  de  Med.  et  de  Chir.,”  No.  18,  1874),  had  swal- 
lowed 28  dominoes;  an  ecclesiastical  patient  thus  preserved  his 
rosary  in  his  stomach  for  a time.  Labbe  (“  De  l’Acad.  des  Sci- 
ences,” 21  Avril,  1866)  extracted  a fork  by  gastrotomy.  A sailor 
(“  Med.  Chir.  Transact.,”  vol.  xii,  p.  72),  cited  by  Ewald,  in  imita- 
tion of  a juggler,  swallowed  35  small  knives,  and  succumbed  only 
a long  time  afterward  to  digestive  troubles.  There  were  found  at 
the  autopsy  32  blades,  more  or  less  corroded:  30  in  the  stomach 
and  2 in  the  intestines.  It  is  unlikely,  however,  that  such  objects 
as  these  could  produce  the  signs  of  tumors. 

Schonborn  (“  Berl.  klin.  Wochenschr.,”  Nr.  17,  1883,  und  “Arch, 
f.  klin.  Chirurgie,”  Bd.  xxix,  S.  609,  1883)  has  reported  an  observa- 
tion in  which  a gastrolith  (movable  tumor)  was  discovered  in  a girl 
fifteen  years  old,  occupying  the  left  half  of  the  abdomen;  it  was 
easily  pushed  back  under  the  left  edge  of  the  ribs,  and  very  painful, 
both  spontaneously  and  on  palpation.  The  patient  grew  thin, 
would  not  tolerate  any  food,  and  her  state  became  so  serious  that 
it  was  decided  to  perform  a laparotomy,  after  having  hesitated  for  a 
long  time  between  the  diagnosis  of  a movable  kidney  and  that  of 
movable  spleen. 

The  opening  being  made,  the  stomach  was  found  distended ; it 
was  cut  into,  and  a mass  of  281  gm.  was  found,  formed  by  a net- 
work of  short  hairs,  and  molded  to  the  form  of  the  gastric  cavity. 
The  patient  then  confessed  that  four  years  before  she  had  swallowed 
the  hair  in  order  to  “ make  her  voice  clear.”  After  this  case, 
Schonborn  made  a careful  collection  of  the  known  cases,  and  found 
seven  of  them,  the  oldest  of  which  dates  back  to  1777.  These 
cases  include  six  women  and  one  boy ; none  were  insane.  All 
these  subjects  had  died;  some  from  peritonitis  through  perfora- 
tion, others  from  uncontrollable  vomiting.  One  case  ended  in 
hematemesis,  and  Russel  (“  Med.  Times  and  Gazette,”  June  16, 
1869),  who  published  it,  reports  that  the  tumor  weighed  four 
pounds  seven  ounces,  was  twelve  inches  long,  five  inches  broad, 
and  four  inches  thick.  Never  before  had  there  been  digestive 
troubles,  and  it  had  been  supposed  that  it  was  a tumor  of  the 
spleen.  In  the  observation  of  Inmann  (“  Med.  Times  and  Gazette,” 
July  3,  1869)  the  mass  of  hair  was  equally  large.  Best  (“  Brit. 
Med.  Jour.,”  Dec.  11,  1869)  reported  a case  of  a woman  thirty 
years  old  who,  for  sixteen  years,  had  complained  of  pains  after 


6 12 


BENIGN  TUMORS  OF  THE  STOMACH. 


meals,  and  had  frequent  vomitings,  occasionally  streaked  with 
blood.  For  six  years  the  pain  had  been  almost  intolerable,  and 
hindered  the  patient  from  giving  herself  to  any  occupation.  At  the 
epigastrium  a movable  tumor  was  discovered,  not  sensitive  to  pres- 
sure, smooth,  hard,  extending  from  the  right  hypochondriac  region 
to  the  left  of  the  umbilicus,  the  prolonged  palpation  of  which  caused 
emesis.  Peritonitis  from  perforation  ended  the  case.  The  stomach 
and  the  esophagus  were  filled  with  a quantity  of  hairs,  some  of 
which  were  from  ten  to  twelve  inches  long,  and  which  altogether 
weighed  thirty  ounces.  The  patient  had  acquired  the  habit  of 
swallowing  her  hair  fifteen  years  before.  Since  Schonborn’s  notice, 
Kooyker  (“  Zeitschrift  f.  klin.  Med.,”  xiv,  S.  203,  1888,  also 
“ Weekbl.  v.  d.  Nederl.  Tydsch.  v.  Geneerk.,”  December,  1887)  has 
reported  the  case  of  an  individual  of  fifty-two  years  old  who,  after 
having  presented  phenomena  of  cachexia,  with  hematemesis,  suc- 
cumbed at  the  end  of  three  years  of  sickness.  During  life  a tumor 
the  size  of  a small  apple  had  been  felt  at  the  epigastrium ; and  dis- 
placement of  the  spleen,  a floating  kidney,  a cancer  of  the  stomach, 
and  a cancer  of  the  colon  were  suspected,  one  after  the  other.  On 
opening  the  stomach  at  the  autopsy  a renal-shaped  foreign  body 
was  found,  18  by  8 cm.,  weighing  885  gm. ; two  other  masses  were 
also  discovered,  the  size  of  a hen’s  egg.  On  examination  with 
the  microscope,  these  bodies  showed  some  grains  of  starchy  mat- 
ter and  some  vegetable  cells,  some  of  which  contained  chlorophyl, 
but  no  trace  of  animal  substances.  This  case  is  analogous  to  that 
of  Capelle’s  (“Jour,  de  Med.  de  Bruxelles,”  Fevr.,  1861),  who 
treated  a woman  forty-three  years  old  for  a tumor  of  the  stomach, 
who  had  been  ill  for  a long  time.  The  symptoms  were  emesis, 
intense  gastric  pains,  and  constipation.  The  tongue  was  coated, 
palpitations  frequent,  the  pulse  small  and  wreak.  Under  the  xyphoid 
cartilage  was  found  a hard,  immovable  tumor  as  large  as  a pigeon’s 
egg,  which  disappeared  when  vomitings,  more  violent  than  others, 
had  caused  the  expulsion  of  a foreign  body  of  nine  cubic  centime- 
ters, half  softened,  and  formed  exclusively  of  vegetable  debris. 
The  patient  recovered.  Lastly,  Bollinger  (“  Munchener  med. 
Wochenschr.,”  Nr.  22,  1891)  published  the  case  of  a girl  sixteen 
years  old  in  whom  there  existed  a hairy  tumor  which  caused  death 
by  inanition.  A malignant  tumor  had  been  suspected,  and  there 
was  found  in  the  stomach  and  in  the  dilated  duodenum  a tumor 
55  cm.  long  by  11  cm.  broad,  and  28  cm.  in  circumference,  formed 
by  500  gm.  of  hairs,  which  measured  about  10  cm. 


HYPERTROPHIC  STENOSIS  OF  THE  PYLORUS.  6 1 3 

The  presence  of  foreign  bodies  in  the  stomach  may  give  rise  to 
the  following  signs  and  symptoms : The  organ  dilates,  becomes 
displaced  (Russel) ; the  mucous  membrane  atrophies  ; the  pylorus 
may  become  expanded  through  muscular  efforts  to  pass  out  the 
foreign  body,  which  will  act  as  a ball  valve  when  expulsion  is 
impossible;  the  peptic  secretions  disappear;  the  erosions  allow 
the  escape  of  blood  in  more  or  less  abundance,  and  the  patients 
usually  succumb  to  a cachexia,  since  in  the  end  alimentation 
becomes  impossible. 

Therapeutic  measures  are  useless  in  these  cases.  An  explora- 
tory laparotomy  is  the  only  rational  procedure. 

Erlach  removed  a myoma  from  the  stomach  weighing  5400  gm. 
(“  Centralbl.  f.  allge.  Patholog.,”  Bd.  vi,  1895,  S.  240).  In  the 
same  journal  (vol.  vi,  S.  717)  Hansemann  is  reported  as  having 
found  four  peculiar  tumors  in  the  stomach  : (1)  A myoma  with 
cystic  degeneration ; (2)  a sarcoma  with  hyaline  degeneration  and 
containing  large  calcareous  bodies  ; (3)  a tumor  of  myxomatous 
nature  ; (4)  a tumor  composed  of  finely  fibered  connective  tissue, 
inclosing  hollow  spaces  which  contained  cells  in  a state  of  fatty 
degeneration,  simulating  the  cortical  substance  of  the  adrenal 
bodies.  Professor  Julius  Schreiber  reported  a case  of  phyto- 
bezoar composed  of  the  fibrous  roots  of  a plant  (“  Schwarzwurzel  ”), 
which  is  a popular  remedy  for  all  sorts  of  ailments  in  Germany. 
The  patient  was  a female  peasant  forty-five  years  old.  The  tumor 
very  much  resembled  a floating  spleen  or  malignant  neoplasm. 
The  diagnosis  was  correctly  made  and  the  woman  successfully 
operated  upon  by  von  Eiselberg  (“  Mittheil.  a.  d.  Grenzgebieten  d. 
Medicin  u.  d.  Chirurg.,”  Bd.  1,  1896,  S.  729). 

In  the  “Jour,  of  the  American  Medical  Assoc.,”  March  5,  1898, 
A.  H.  Meisenbach  ably  reviews  the  literature  on  gastrotomy  for 
removal  of  foreign  bodies  in  the  stomach. 


HYPERTROPHIC  STENOSIS  OF  THE  PYLORUS. 

Sienosing  gastritis , hypertrophic  stenosis  of  the  pylorus , is  a thicken- 
ing of  the  tissue  about  the  pyloric  region,  caused  by  certain  forms 
of  chronic  gastritis.  The  consequences  of  this  obstruction  and 
constriction  may  be  and  generally  are  as  serious  as  if  the  pylorus 
was  stenosed  by  malignant  neoplasm  ; except  that  in  the  former 
case  the  obstruction  may  be  radically  removed  by  operation,  which 


6 14  HYPERTROPHIC  STENOSIS  OF  THE  PYLORUS. 

is  doubtful  in  cases  of  carcinoma  or  sarcoma.  The  condition  was 
known  to  Cruveilhier  and  Andrae.  In  England  the  disease  has 
been  described  by  Brinton,  Bennett,  Habershon,  Handheld  Jones, 
and  Hughes;  and  in  this  country  by  Einhorn,  W.  H.  Welch,  and 
the  author. 

In  the  literature  of  the  subject  thus  far  presented  one  can  dis- 
tinguish three  similar  types  of  this  affection  : In  the  first  place, 

(i)  gastric  cirrhosis,  the  “ linitis  plastica  ” of  Brinton.  In  this  dis- 
ease the  normal  tissue  of  the  gastric  walls  is  replaced  by  prolifer- 
ated fibrillar  connective  tissue,  which  causes  a marked  reduction 
in  the  size  of  the  organ.  (2)  The  sclerosing  gastritis  of  the  French 
authors,  first  described  by  Hanot  and  Gombault  in  1882,  and  later 
by  Dubujadoux  and  von  Kahlden.  This  disease  ( gastrile  chronique 
avec  sclerose  sous  muqueuse  hypertrophique')  is  characterized  by 
changes  in  the  other  viscera,  particularly  in  the  liver,  pancreas, 
kidneys,  and  especially  in  the  omentum.  (3)  Congenital  hyper- 
trophic pyloric  stenosis.  Two  cases  belonging  to  this  class  were 
reported  to  the  Association  of  American  Physicians  in  May,  1898, 
by  Adler  and  Meltzer.  This  third  type  has  no  direct  bearing  upon 
the  etiology  of  the  benign  stenosis  of  adults.  We  are  concerned 
here  only  with  types  (1)  and  (2).  The  symptomatology  of  the 
sclerosing  gastritis  of  Hanot  and  Gombault  and  of  the  gastric 
cirrhosis  of  Brinton  is  quite  obscure,  and  it  is  probable  that  it  is 
hardly  ever  diagnosed  with  certainty.  In  1893  Tilger  gave  a his- 
torical review  of  our  knowledge  of  stenosing  pyloric  hypertrophy 
(“  Virchow’s  Archiv,”  Bd.  cxxxn,  S.  290). 

A very  exact  and  scientific  presentation  of  the  subject  from 
the  clinical  as  well  as  from  the  pathological  standpoint  has  been 
given  by  Lebert  (/.  cl),  who  gives  an  account  of  six  personal 
observations  with  the  results  of  the  autopsies.  Einhorn  reported 
four  cases  in  January,  1895  (“  N.  Y.  Medical  Record”),  which 
recovered  after  operation ; and  six  other  cases  in  which  either 
surgical  interference  was  refused  or  the  patient  temporarily  im- 
proved by  other  methods,  but  the  diagnosis  of  benign  stenosis 
appeared  to  him  quite  certain.  Personally,  I have  observed  a 
benign  hypertrophy  of  the  pylorus  in  four  patients.  The  fol- 
lowing is  a typical  case : A white  laborer  had  suffered  from 
motor  insufficiency,  absence  of  HC1  and  ferments,  and  presence 
of  lactic  acid  for  three  years.  I was  on  three  occasions 
able  to  demonstrate  a stenosis  at  the  pylorus  by  my  method  of 
duodenal  intubation.  Operation  was  strongly  advised,  but  as  it 


TYPICAL  CLINICAL  HISTORY. 


615 


was  repeatedly  refused,  an  attempt  was  made  to  dilate  the  pylorus 
by  means  of  larger  and  larger  sounds  introduced  according  to  my 
system.  The  patient  was  unable  to  remain  under  hospital  treat- 
ment continuously,  and  while  the  pyloric  dilation  by  means  of 
sounds  rendered  the  pylorus  sufficiently  permeable,  it  inevitably 
contracted  again  within  eight  to  ten  weeks  after  cessation  of  treat- 
ment. The  patient  finally  succumbed  to  his  disease,  and  at  the 
autopsy  I found  that  the  wall  of  the  pylorus  measured  in  the  fresh 
state  2.3  cm.  in  thickness.  All  of  the  layers  of  the  pyloric  structure 
were  thickened,  but  the  true  muscularis  and  the  muscularis  mucosae 
showed  the  greatest  increase.  Next  in  thickness  was  the  sub- 
mucosa, while  the  peritoneal  layer  was  only  slightly  thickened. 
The  true  mucosa  had  disappeared  entirely  from  the  pyloric  region. 
In  cutting  a piece  one  millimeter  in  thickness  into  serial  sections, 
I could  not  discover  even  remnants  of  gastric  glands.  In  Lebert’s 
case  there  was  still  some  glandular  layer  left,  which  was  being 
pressed  upon  by  connective-tissue  proliferation.  The  greatest 
amount  of  work  in  the  expulsive  efforts  of  the  stomach  falls  to  the 
pylorus  and  the  antrum  pylori  immediately  preceding  it.  This 
region  is  naturally  prone  to  muscular  hypertrophy.  The  special 
incentive  cause  in  these  cases  is  a proliferating  gastritis  resulting 
in  a hyperplastic  inflammation,  expressing  itself  most  intensely  in 
the  pyloric  antrum  and  sphincter,  because  all  of  the  layers  of  the 
stomach  except  the  glandular  layer  are  most  abundantly  devel- 
oped in  this  neighborhood. 

Boas  very  aptly  calls  the  catarrhal  inflammation  resulting  in  this 
condition  a stenosing  gastritis,  to  which  designation  no  objection 
can  be  found  because  hypertrophy  of  the  pylorus  may  occur 
under  a variety  of  circumstances — for  instance,  corrosive  agents 
may  traumatically  injure  the  pylorus,  and  the  hypertrophic  process 
may  also  arise  from  an  ulcer.  Pathologically,  it  is  a chronic 
hypertrophic  gastritis.  Hirsch  (/.  c.)  has  reported  a case  of 
pyloric  stenosis  caused  by  a benign  tumor  that  had  originated 
from  a peptic  ulcer.  Another  fact  justifying  the  nomenclature  of 
Boas  is  that  the  symptomatology  of  chronic  gastritis  generally 
precedes  the  phenomena  of  this  kind  of  stenosis  for  a long  time. 
Boas  reports  three  cases  (“Archiv  f.  Verdauungskrankheiten,”  Bd. 
iv,  S.  47),  but  he  is  evidently  mistaken  when  he  asserts  that  neither 
Einhorn  nor  the  author  consider  benign  pyloric  stenosis  in  our 
works,  or  that  his  three  cases  are  the  first  of  their  kind  that  have 
ever  been  cured  (/.  c.,  p.  49). 


6i6 


HYPERTROPHIC  STENOSIS  OF  THE  PYLORUS. 


Before  proceeding  to  a consideration  of  the  diagnostic  value  of 
the  prominent  symptoms,  a clinical  history  of  a second  case  from 
our  clinic  will  be  in  order. 

Mr.  W.  L.,  age  thirty-eight,  sick  since  February,  1892.  Presents  himself  for 
treatment  June,  1892.  His  suffering  began  with  pressure,  fullness,  and  disten- 
tion in  the  stomach.  Bowels  were  at  that  time  regular,  and  appetite  was  good. 
After  the  first  six  months  of  his  suffering  he  had  an  interval  of  four  months  in 
which  he  was  comparatively  well,  when  a relapse  of  the  symptoms  of  gastritis 
occurred,  ascribed  to  the  ingestion  of  crabs.  In  January  of  1893  he  consulted 
the  author  again,  and  was  then  suffering  much  from  pain  in  the  stomach  after 
meals,  and  occasional  attacks  of  vomiting  following  immediately  after  meals. 
An  examination  of  the  peristalsis  of  the  stomach  showed  that  at  this  time  it  was 
in  a fairly  good  condition — no  remnant  of  the  meal  of  the  previous  evening 
could  be  found  before  breakfast  the  following  morning.  The  contents  of  the 
stomach  before  breakfast  consisted  of  from  20  to  50  c.c.  of  liquid  containing 
much  mucus,  and  showing  presence  of  free  HC1,  but  no  food  remnants. 
Results  of  chemical  analysis  (Salzer  double  test-meal) : Presence  of  traces  of 
meat,  egg,  bread  from  the  larger  meal  taken  five  hours  before;  no  sarcinas,  no 
Oppler-Boas  bacilli;  total  acidity,  40;  free  HC1,  24;  combined  HC1,  12.  For 
the  pain  and  vomiting  the  patient  was  put  on  a milk  diet,  and  small  doses  of 
codein.  This  was  followed  by  prompt  improvement,  the  patient  returning  to 
work.  Six  months  later  (July,  1893)  the  patient  returned  suffering  from  a 
repetition  of  the  symptoms,  which  had  returned  intensified.  The  main  suffer- 
ing was  due  to  vomiting  and  pain.  He  was  taught  to  use  the  stomach-tube 
himself,  because  now  there  were  very  evident  signs  of  stagnation,  as  decom- 
posed remnants  of  previous  meals  were  found  every  morning  before  breakfast. 
These  remnants  were  the  more  abundant  the  more  solid  food  the  patient  had 
taken,  but  if  the  diet  had  existed  exclusively  of  milk  and  egg-albumen,  or  very 
finely  scraped  beef,  no  food  remnants  were  found  in  the  stomach  the  following 
morning.  By  my  gastrograph  it  was  found  that  the  rate  of  peristalsis  was  now 
unmistakably  impeded,  though  there  was  no  evident  dilation. 

The  results  of  the  analysis  of  the  gastric  contents  were  now  as  follows  : Free 
HC1,  6;  combined  HC1,  4;  lactic  acid,  a trace  ; total  acidity,  18  ; biuret  reac- 
tion positive,  erythrodextrin,  o.  The  patient  was  allowed  to  take  only  a 
liquid  diet.  Nevertheless,  120  c.c.  of  offensive  stomach-contents  could  be 
drawn  away  every  morning  before  breakfast,  which  contained  no  free,  but 
only  combined,  HC1,  and  lactic  acid.  Microscopically,  large  numbers  of 
bacteria  in  threads  were  found,  yeast  in  moderate  amounts,  no  sarcinae,  but 
many  cylindrical  and  cuboidal  epithelial  cells.  The  urine  contained  no 
sugar  nor  albumin  ; the  amount  in  twenty-four  hours  was  about  one  liter. 
Indican  was  present,  but  not  in  excess.  Once  daily  the  patient  suffers  from 
severe,  cramp-like  pains  in  the  region  of  the  stomach,  but  these  attacks  were 
not  associated  with  vomiting.  After  the  patient  had  mastered  the  technic 
of  lavage  he  improved  very  much,  and  gained  eighteen  pounds  in  weight  in 
eight  months.  In  October,  1895,  he  returned  again  for  medical  treatment 
because  he  began  to  have  vomiting  attacks  again,  although  he  had  been  ex- 
ceedingly careful  in  his  diet.  He  now  had  very  aggravated  motor  insuffi- 
ciency, so  that  we  once  more  attempted  to  dilate  his  pylorus  by  intubation. 


EXAMINATION  OF  THE  ABDOMEN. 


617 

The  lavage  and  liquid  diet  were  continued.  There  were  evidences  of  very 
severe  chronic  gastritis,  as  shown  in  a fragment  of  mucosa  brought  out  during 
lavage  by  the  patient.  As  HC1  was  absent  on  repeated  examination,  both  in 
the  free  and  combined  form,  the  ferments  were  very  much  reduced.  Rennin 
zymogen,  active  in  dilution  1 : 30;  discs  of  serum  albumin  placed  in  the 
filtrates,  acidified  with  HC1,  required  four  hours  for  digestion.  Lactic  acid  present 
to  such  an  amount  as  to  give  very  distinct  reaction  with  Uffelmann’s  test. 

Examination  of  the  Abdo7nen. — The  stomach  was  so  distended  that  its  con- 
tours were  very  distinctly  visible  without  artificial  distention.  No  tumor  could 
be  palpated.  Liver  normal  on  percussion  and  palpation.  Spleen  and  kidneys 
normal.  Distention  of  the  colon  with  C02  showed  it  in  normal  position. 

By  electrodiafhany  the  stomach  was  found  to  be  not  enlarged,  though  the 
lower  curvature  was  distended  to  within  one  inch  of  the  navel.  By  the  use  of 
liquid  diet  and  daily  lavage,  together  with  intubation  of  the  pylorus,  the  patient 
improved  once  more.  As  the  diagnosis  of  the  hypertrophic  stenosis  of  the 
pylorus  was  now  clear,  the  patient  was  once  more  urgently  advised  to  undergo 
an  operation.  This  he  refused  emphatically.  After  he  left  my  supervision  I 
did  not  see  him  again  until  June,  1896.  He  was  so  much  emaciated  that 
I failed  to  recognize  him.  He  appeared  like  a patient  in  the  last  stages  of  pul- 
monary tuberculosis.  The  stomach  was  not  very  much  dilated,  but  filled  with 
putrescent  material,  and  had  descended  lower  than  at  the  last  examination. 
Notwithstanding  artificial  feeding  with  enemata,  the  patient  died  within  ten 
days  after  this  visit. 

At  the  autopsy  I found  the  pylorus  very  much  thickened — its  walls  in  one 
place  measuring  three  centimeters  in  thickness.  The  muscular  layer  showed 
the  greatest  increase  in  thickness.  The  mucous  layer  was  lost  entirely  over 
this  region.  The  thickening  extended  throughout  the  entire  pyloric  region  of 
the  stomach.  The  atrophy  of  the  glandular  layer  extended  all  over  the  surface 
of  the  stomach.  In  the  middle  portion  of  the  stomach,  on  the  greater  curva- 
ture, there  was  a small  polypus  about  the  size  of  a lentil.  The  passage  through 
the  pylorus  was  tortuous,  so  that  not  even  a straight  needle  two  millimeters  in 
thickness  could  be  made  to  pass.  There  were  no  histological  evidences  of  car- 
cinoma. In  plate  X the  histological  features  of  chronic  hyperplastic  gastritis 
with  pyloric  stenosis  are  successfully  reproduced.  The  enormous  hyperplasia 
of  the  muscularis  and  the  connective  tissue,  and  the  hypertrophy  of  the  pylorus 
are  especially  clear. 

Age. — Pyloric  hypertrophy  in  the  sequence  of  hypertrophic  gas- 
tritis is  a disease  occurring  at  a comparatively  young  age : thus 
the  cases  of  Einhorn  (/.  c.),  in  which  the  ages  are  stated,  show 
the  following.  Some  of  these  cases  were  not  due  to  stenosing 
gastritis  but  to  other  causes,  probably  cicatrices  : 


Einhorn’s  Cases.  Number  of  Cases.  Ages. 

Males, 4 28,  34,  40,  48  years. 

Females, 3 38,  43,  58  “ 

Boas’  Cases.  Number  of  Cases.  Age. 

Males, 2 32,  47  years. 

Females, 1 43  “ 


6i8 


HYPERTROPHIC  STENOSIS  OF  THE  PYLORUS. 


Hemmeter’s  Cases.  Number  of  Cases.  Age. 

Males, 2 23,  38  years. 

Females, 2 28,  36  “ 


Tilger  (/.  c.)  reported  23  cases,  as  follows : 

4 cases  at  the  age  of  from  20  to  30  years. 

7 “ “ “ “ 30  to  40  “ 

6 “ “ “ ‘ ‘ 40  to  50  “ 

2 “ “ “ “ 50  to  60  “ 

2 “ f‘  “ “ 60  to  70  “ 

2 cases  over  70  years. 

If  it  were  known  how  long  these  cases  had  been  suffering  before 
they  came  to  the  physician,  a more  uniform  age  could  be  arrived 
at.  Thus,  one  of  Einhorn’s  cases  suffered  from  digestive  troubles 
for  twenty  years,  another  for  eight,  another  for  eighteen,  another 
for  fourteen.  One  of  Boas’  cases  had  suffered  for  nineteen  years, 
a second  six,  and  a third  two  and  a half  years.  In  my  own  cases 
the  one  that  came  to  me  at  the  age  of  thirty-eight  had  been  suffer- 
ing for  four  years  ; and  the  female  patient  who  consulted  me  at  the 
age  of  thirty-six  had  suffered  for  three  years.  Deducting  the  time 
of  the  suffering  already  experienced  from  the  age  of  the  patient 
when  presented  for  diagnosis,  it  is  evident  that  a comparatively 
early  period  of  life  will  be  found  to  have  been  the  stage  at  which 
these  total  35  cases  were  first  affected.  From  these  figures  another 
important  moment  in  the  diagnosis  is  evident — viz.,  the  chronicity 
of  the  process. 

Symptomatology. — When  the  cases  first  present  themselves, 
the  first  symptoms  have  existed  for  a long  time.  The  anamnesis 
resembles  the  beginning  of  chronic  gastritis.  The  complaints  are 
fullness,  pressure,  distention,  pain,  eructation,  and,  occasionally, 
pyrosis.  As  the  stenosing  gastritis  progresses,  motor  insufficiency 
of  the  first  degree  develops  ; and  then  the  principal  symptoms  are 
vomiting  and  pain.  Gradually  the  classical  signs  of  dilation  of 
the  stomach  may  develop  ; but  not  in  all  cases  where  we  have 
these  symptoms  is  the  stomach  dilated.  Owing  to  the  obstruc- 
tion there  are  loss  of  weight,  constipation,  and  reduction  in  the 
amount  of  urine.  The  appetite  remains  good,  or  it  is,  at  least, 
good  in  the  majority  of  cases  for  a long  time. 

Size  of  the  Stomach . — In  the  three  cases  we  observed  the  size  of 
the  stomach  was  not  markedly  increased,  and  in  the  second  male, 
aged  twenty-three  years,  the  stomach  at  the  autopsy  held  only  one 
ounce.  This  stomach  in  its  actual  size  is  represented  in  plate 


PLATE  X, 


Hypertrophic  Stenosis  of  the  Pylorus  from  Chronic  (Stenosing)  Gastritis.  Section  through  Thickened  Pylorus  and  Normal  Duodenum. 
The  designations  Fig.  I and  Fig.  2 denote  the  locations  from  which  the  histological  drawings  in  the  chapter  on  Chronic  Gastritis  were  made. 


SYMPTOMATOLOGY  OF  STKNOSING  GASTRITIS.  619 

XI;  in  another  case  there  was  an  undoubted  gastroptosis.  In 
only  one  of  the  cases,  which  Einhorn  describes  in  detail,  was  the 
stomach  dilated.  In  the  other  three  it  appears  that  this  condition 
was  not  especially  investigated.  Boas  describes  dilation  in  but 
one  of  his  three  cases.  Hematemesis  has  not  been  observed  in 
connection  with  this  disease  by  Boas,  Lebert,  Einhorn,  or  the 
author.  If  the  hyperplasia  has  involved  only  the  pylorus,  a dila- 
tion is  likely  to  result  ; but  if  it  has  extended  uniformly 
throughout  the  organ  (linitis  plastica),  a cirrhotic  contraction 
ensues. 

Tumor. — Einhorn  found  a palpable  tumor  in  only  one  of  his 
cases,  and,  similarly,  Boas  reports  the  existence  of  tumor  in  one 
out  of  his  three  cases.  In  the  case  described  in  this  account,  al- 
though the  pyloric  mass  was  as  large  as  a hen’s  egg  at  the  autopsy, 
it  had  not  been  detected  before  death  because  the  pylorus  was  in 
the  normal  position — under  the  right  lobe  of  the  liver. 

Condition  of  the  Gastric  Secretions. — The  state  of  the  secretion  of 
the  gastric  juice  will  vary  according  to  the  duration  of  the  disease 
and  the  period  at  which  the  patient  presents  himself.  It  is  rational 
to  presume  that  if  the  stenosis  is  brought  on  by  a chronic  gastri- 
tis, the  longer  the  disease  has  existed  the  more  atrophic  will  the 
mucosa  have  become  and  the  less  gastric  juice  will  be  secreted. 
Nevertheless,  Einhorn  found  free  HC1  in  one  of  his  cases  that  had 
suffered  for  eight  years  prior  to  consulting  him.  In  all,  Einhorn 
gives  an  account  of  ten  cases  (“  New  York  Medical  Record,”  Jan- 
uary, 1895),  but  only  four  of  them  are  described  in  detail;  not  all 
of  these  cases,  it  seems,  were  due  to  hyperplastic  gastritis.  They 
all  showed  retention  of  food,  considerable  quantities  of  gastric 
juice,  presence  of  free  HC1,  absence  of  lactic  acid,  a high  total 
acidity,  and  a long  duration  of  sickness.  Only  in  one  of  these 
cases  did  he  find  absence  of  free  HC1  and  presence  of  lactic  acid. 
In  the  three  cases  reported  by  Boas  free  HC1  was  regularly  absent, 
and  in  two  cases,  in  addition  to  absence  of  free  HC1,  the  ferments 
were  very  much  reduced.  All  three  had  an  unmistakable  lactic 
acid  reaction.  In  my  cases  free  HC1  was  present  at  the  begin- 
ning, but  as  the  disease  progressed,  it  gradually  became  less  and 
less,  and  finally  both  free  and  combined  HC1  was  absent;  then 
the  reaction  for  lactic  acid  became  positive. 

Boas  considers  the  absence  of  free  HC1  and  ferments  an  impor- 
tant factor  in  the  diagnosis  of  hypertrophic  stenosis  caused  by  gas- 
tritis. This  was  the  condition  in  two  of  my  cases.  It  is  evident 


620 


HYPERTROPHIC  STENOSIS  OF  THE  PYLORUS. 


from  the  autopsy  report  of  one  of  my  cases  that  it  was  undoubt- 
edly due  to  stenosing  gastritis;  free  HC1  was  absent,  but  the  fer- 
ments active  at  a time  when  the  diagnosis  of  hypertrophic  pyloric 
stenosis  could  be  made  beyond  a doubt. 

Diagnosis. — At  the  time  when  the  patient  first  presents  himself, 
the  differential  diagnosis  between  benign  stenosing  gastritis  and 
carcinoma  presents  difficulties;  but  if  we  can  clearly  ascertain  a 
history  of  many  years  of  suffering,  with  alternating  improvements 
and  aggravations  of  the  symptoms,  and  the  increase  and  decrease 
of  body  weight,  the  improvement  on  carefully  selected  liquid  diet 
and  aggravation  on  a solid  diet,  we  should  be  justified  in  suspect- 
ing a slowly  developing  benign  process.  Rosenheim  (/.  c.)  has 
reported  a case  of  benign  stenosis*  in  which  the  presence  of  a 
tumor  was  recognized,  and  the  same  gastric  chemistry  as  in  car- 
cinoma, with  the  same  pernicious  tendency.  A differential  diag- 
nosis between  such  a case  as  this  and  carcinoma  seems  impossible. 

It  may  become  necessary  to  distinguish  between  stenosis  caused 
by  gastritis  and  that  caused  by  cicatricial  contraction  of  the 
pylorus  resulting  from  a gastric  ulcer,  and  also  from  the  dilation 
and  food  retention  from  primary  and  atonic  gastrectasia.  In  the 
stenosis  resulting  from  gastritis  there  will  have  been  no  preceding 
gastric  nor  intestinal  hemorrhages,  which  will  in  most  cases  have 
occurred  in  case  there  is  a cicatrix  from  an  ulcer.  If  the  stenosis 
is  due  to  gastritis,  free  HC1  will  eventually  be  absent.  The  fact 
that  Einhorn  found  free  HC1  in  so  many  of  his  cases  makes  it 
probable  that  the  constriction  of  the  pylorus  was  not  due  to  sten- 
osing  gastritis,  but  to  some  other  cause — cicatrices,  for  instance. 
A histological  examination  of  the  pyloric  tissue  does  not  seem 
to  have  been  made  in  his  cases.  From  primary  atonic  dilation 
stenosing  gastritis  can  be  differentiated  by  the  absence  of  the 
symptoms  of  gastritis  in  the  former.  Visible  spasmodic  peristalsis 
indicates  stenosing  gastritis. 

The  previous  history  of  the  case  with  its  peculiar  variations  will 
be  extremely  important.  Marked  and  lasting  improvements,  with 
increment  of  weight,  do  not  occur  in  carcinoma.  The  periods  of 
improvements  in  this  latter  disease,  if  they  occur  at  all,  do  not 

’ * A similar  case  originally  reported  by  Dr.  W.  S.  Thayer  is  often  quoted  in  text-books 
as  having'shown  the  same  gastric  chemistry  as  carcinoma  and  yet  proved  to  be  a benign 
tumor.  Dr.  Thayer  has  informed  me  privately  that  the  detection  of  lactic  acid  in  this 
case  was  due  to  an  error  in  the  preparation  of  the  patient’s  stomach  before  the  test-meal 
was  drawn  for  analysis. 


CARDIAC 


PLATE  XI. 


4> 


PROGNOSIS  OF  STENOSING  GASTRITIS. 


621 


exceed  one  month.  In  benign  hypertrophic  stenosis  the  symp- 
toms of  stagnation  are  more  amenable  to  treatment  than  in  car- 
cinoma. The  disturbances  of  the  motor  function  in  the  latter  dis- 
ease increase  progressively,  and  the  quantity  of  food  remnants 
retained  and  found  in  the  stomach  before  breakfast  becomes  more 
and  more  from  week  to  week,  no  matter  upon  what  diet  the  patient 
is  placed.  In  hypertrophic  stenosis  the  symptoms  of  stagnation 
may  disappear  for  years  under  the  aid  of  a liquid  diet  and  lavage. 
Only  in  the  very  last  stages  of  the  disease  does  the  stagnation  be- 
come absolute.  Whenever  there  are  glandular  swellings,  coffee- 
ground  vomiting,  ascites,  or  evidences  of  metastases,  presence  of 
Oppler-Boas  bacilli  in  the  stomach-contents,  the  case  will  have  to 
be  considered  carcinoma.  The  tendency  is  toward  early  diagnosis 
and  early  operation  in  both  conditions.  From  this  standpoint,  a 
possible  error  in  differentiating  the  two  conditions  will  not  be  a 
serious  one. 

The  presence  or  absence  of  tumor  in  the  region  of  the  pylorus 
is  of  no  diagnostic  value  in  the  differentiation  in  benign  stenosis 
and  carcinoma.  If  a tumor  is  present,  it  may  as  readily  be  a benign 
hypertrophy  as  a cancer;  and  if  it  is  absent,  it  does  not  exclude 
the  diagnosis  of  either  of  these  conditions.  It  is  of  greatest 
importance  in  such  cases,  when  the  diagnosis  lies  between  these 
two  conditions,  to  take  the  weight  of  the  patient  frequently  and 
analyze  the  gastric  contents  repeatedly.  In  a case  which  we  had 
examined  since  June,  1892,  and  who  died  in  June,  1896,  free  HC1 
was  present  ten  months  before  the  fatal  termination;  but  after  that, 
an  examination  made  eight  months  before  the  end,  showed  no  free 
HC1  and  excess  of  lactic  acid. 

Prognosis. — The  disease  is  fatal  unless  an  operation  is  under- 
taken in  time.  The  remarkable  variations  in  improvement  and 
aggravation  are  apt  to  mislead  the  clinician  into  a favorable  prog- 
nosis. In  order  to  form  an  approximate  idea  of  the  gravity  of  the 
case,  it  is  necessary  to  test  the  motor  function.  We  give  preference 
to  Hemmeter’s  method  by  means  of  the  intragastric  rubber  bag, 
and  a small  water  manometer;  because  after  trying  the  other 
methods  for  testing  the  motility  we  have  found  that  they  failed  to 
give  accurate  results.  There  are  three  means  by  which  we  may 
gage  the  state  of  the  motor  functions  clinically:  (1)  The  amount 
of  stagnating  stomach-contents  gained  by  the  expression  method, 
without  addition  of  water,  from  the  fasting  stomach ; (2)  repeated 
consecutive  weighings  of  the  body ; (3)  repeated  and  consecutive 


622 


HYPERTROPHIC  STENOSIS  OF  THE  PYLORUS. 


measurements  of  the  urine  passed  in  twenty-four  hours.  During 
the  beginning  stages  of  the  process,  and  as  the  stenosis  is  not  very 
much  advanced,  it  will  be  possible  to  introduce  the  amount  of 
calories  necessary  to  maintain  the  nitrogen  balance  by  giving  a 
liquid  diet,  consisting  of  milk,  soft-boiled  eggs,  and  predigested 
foods.  When  the  gastritis  has  advanced,  there  is  no  secretion  of  HC1 
and  ferments,  and  therefore  there  can  be  no  gastric  digestion  of  the 
food  whatever,  and  it  is  offered  to  the  pylorus  in  a much  coarser 
state  than  if  the  secretions  were  normal. 

Treatment. — This  may  be  palliative  or  curative.  The  palliative 
treatment  consists  in  avoiding  everything  that  might  increase  the 
gastritis.  Alcohol,  tobacco,  irritating  condiments,  and  spices  must 
be  excluded.  The  diet  had  best  consist  of  milk  and  soft-boiled  or 
raw  eggs ; the  latter  only  as  long  as  free  HC1  is  present  in  the 
stomach.  After  the  gastric  stagnation  has  advanced,  and  offensive 
residues  are  found  in  the  stomach  every  morning,  lavage  is  the 
treatment  indicated.  It  is  best  carried  out  with  water  acidulated 
with  dilute  HC1,  or  with  water  containing  one  teaspoonful  of  table 
salt  to  the  quart.  Rectal  alimentation  is  indicated  in  advanced 
emaciation  from  absolute  pyloric  stenosis,  whenever  immediate 
operation  is  not  feasible. 

Medicinal  Treatment. — This,  in  our  experience,  is  of  little  or  no 
utility,  though  according  to  the  chemical  nature  of  the  case  HC1, 
pancreatin,  and  papain  may  be  employed. 

Duodenal  Intubation. — A method  by  which  a tube  can  be  passed 
through  the  stomach  and  pylorus  into  the  duodenum  is  original 
with  the  author,  and  was  first  employed  at  his  clinic  (“Arch.  f. 
Verdauungskr.,”  Bd.  n,  S.  85).  I have  carried  out  this  method 
in  a case  of  hypertrophic  stenosis,  but  it  was  followed  by  partial 
success  only.  Although  I succeeded  in  dilating  the  stricture 
of  the  pylorus  for  a time,  the  disease  that  caused  it  could  not  be 
cured  thereby,  and  sooner  or  later^the  stenosis  resumed  its  former 
degree.  The  only  method  to  cure  the  patient  is  by  operation. 

Operation. — Every  influence  should  be  brought  to  bear  upon  the 
patient  to  obtain  the  consent  for  an  early  operation.  If  the  steno- 
sis is  absolute,  and  food  no  longer  passes  the  pylorus,  the  opera- 
tion should  not  be  postponed  a single  day.  The  types  of  operation 
that  are  available  are  gastro-enterostomy  and  the  pyloroplastic 
operation  of  von  Heineke-Mikulicz.  The  so-called  pyloroplastic 
operation  or  digital  divulsion  of  Loreta  does  not  compare  favorably 
in  its  results  to  the  operative  methods  just  mentioned. 


LITERATURE  ON  HYPERTROPHIC  STENOSIS  OF  PYLORUS.  623 


Postoperative  Treatment. — After  the  stenosis  lias  been  cured,  the 
still-existing  gastritis  will  require  further  dietetic,  mechanical,  and 
medicinal  treatment,  according  to  the  principles  laid  down  in  the 
section  on  Chronic  Gastritis. 


LITERATURE  ON  THE  HYPERTROPHIC  STENOSIS  OF  THE 
PYLORUS. 

1.  Boas,  I.,  “ Ueber  hypertrophische  Pylorusstenose,”  etc.,  “ Archiv  f.  Ver- 
dauungskrankh.,”  Bd.  IV,  S.  41. 

2.  Codivilla,  “ Gazeta  degli  ospitali  die  Milano,”  1888. 

3.  Dubujadoux,  “Sur  une  variete  de  cirrhose  encore  inedite  accompagnant 
la  gastrite  chronique  avec  sclerose  sous  muqueuse  hypertrophique,”  “ Gaz. 
hebd.,”  1883. 

4.  Einhorn,  “ New  York  Med.  Jour.,”  January,  1895  ; see  also  “ Diseases  of 
the  Stomach,”  by  same  author. 

5.  Finkelstein,  H.,  “ Ueber  angeborene  Pylorusstenose,”  “ Jahrb.  f.  Kinder- 
heilkunde,”  Bd.  xliii,  S.  1,  1896. 

6.  Gran,  Chr.,  “ Bemerkungen  iiber  die  Magenfunktionen  u.  die  anatom- 
ischen  Veranderungen  bei  angeborener  Pylorusstenose,”  ibid. 

7.  Hammerschlag,  “Boas’  Archiv  f.  Verdauungskrankh.,”  Bd.  11,  S.  19. 

8.  Hanot  et  Gombault,  “Archives  de  Physiologie  normale  et  Pathologique,” 
Bd.  ix,  p.  412,  1882. 

9.  Hemmeter,  John  C.,  and  Wm.  R.  Stokes,  “ Hypertrophic  Gastritis  and 
Pyloric  Stenosis  ” ; Memorial  Vol.  in  honor  of  25th  Anniversary  of  Doctorate 
of  Prof.  Wm.  H.  Welch,  Johns  Hopkins  University  (Feb.,  1900). 

10.  Hirsch,  “ Freie  Vereinigung  der  Chirurgen,”  22.  Juni,  1896. 

11.  Von  Kahlden,  “ Centralbl.  f.  klin.  Med.,”  1887. 

12.  Lebert,  “ Die  Krankheiten  des  Magens,”  Tubingen,  1878,  S 525. 

13.  Nauwerck,  “Deutsches  Arch.  f.  klin.  Med.,”  1878,  Bd.xxi,  S.  574. 

14.  Rosenheim,  “ Berl.  klin.  Wochenschrift,”  1894,  No.  39. 

15.  Schoch,  Inaug. -Dissert.,  Zurich,  1857. 

16.  Thayer,  W.  S.,  “Johns  Hopkins  Hospital  Report,”  1893,  No.  31. 

17.  Tilger,  “Ueber  die  stenosierende  Pylorushypertrophie,”  “Virchow’s 
Arch.,”  Bd.  cxxxit,  H.  2,  S.  290. 


624 


MOTOR  INSUFFICIENCY. 


CHAPTER  VII. 

MOTOR  INSUFFICIENCY. 

Gastric  Atony  or  Myasthenia.  — Gastrectasis  ( Dilation  oy  the 
Stomach). — Obstruction  of  the  Orifices. 

There  is  no  uniformity  in  the  classification  of  the  various  forms 
and  degrees  of  abnormal  enlargement  of  the  stomach. 

The  defective  function  in  these  cases  is  not  commensurate  with 
the  size  and  capacity,  but  with  the  tonicity  of  the  peristalsis.  A 
very  large  stomach  (megalogastria)  may  have  a perfect  motor 
function,  and  a very  small  stomach  may  have  a defective  motility. 

Boas  recognizes  a mechanical  insufficiency  of  the  first  degree , 
which  is  a myasthenia  or  atony  of  the  gastric  muscularis  in  which 
the  ingesta  remain  in  the  stomach  too  long,  but  finally  are 
completely  moved  out  into  the  intestines.  There  is  no  absolute 
retention  of  food,  but  simply  a delay  in  the  expulsion.  Boas  calls 
the  fully  developed  dilation  mechanical  insufficiency  of  the  second 
degree. 

Riegel  differentiates : 

1.  Simple  atony , or  insufficiency  of  the  stomach. 

2.  Atonic  or  typical  ectasia , or  dilation. 

3.  Secondary  ectasia , or  pyloric  stenosis  with  ectasia  [dilation). 

Naunyn  speaks  simply  of  motor  insufficiency,  and  Rosenbach 

of  mechanical  gastric  insufficiency.  Schreiber  (Boas,  “ Archiv  f. 
Verdauungskrankheiten,”  Bd.  11,  S.  423),  in  attempting  to  select  a 
designation  which  should  signify  the  most  constantly  present  con- 
dition of  all  these  morbid  states  of  motility,  and  one  which  should 
unite  them  all  around  itself,  reached  and  suggested  the  term  stasis 
stomach  (“  Stauungsmagen  ”),with  permanent  digestion  or  “perma- 
nently digesting  stomach.”  Besides  being  a cumbersome  circumlo- 
cution, the  term  does  not  even  include  all  conditions  of  this  type,  for 
in  Boas’  mechanical  insufficiency  of  the  first  degree  and  in  Riegel’s 
simple  atony — conditions  which  we  are  convinced  really  do  exist 
— there  is  certainly  no  permanent  digestion. 

Permanent  digestion  goes  on  in  fully  developed  dilations  with 
impaired  peristalsis  as  long  as  hydrochloric  acid  and  ferments  are 


CLASSIFICATION  OF  MOTOR  INSUFFICIENCY.  625 

secreted.  But  as  there  undoubtedly  are  long-standing  dilations 
with  achylia  gastrica,  or  loss  of  secretion  (Einhorn),  there  can  be 
no  digestion  in  them.  The  fact  that  the  food  is  overretained 
in  them  does  not  imply  that  it  is  digested;  only  in  dilations  that 
show  hydrochloric  acid  and  ferments  can  we  speak  of  permanent 
digestion.  The  efforts  of  Schreiber  to  establish  Reichmann’s 
chronic  secretion  as  a complication  of  dilation  with  retained 
food  products  and  permanent  secretion  caused  by  stimulation  of 
the  retained  food,  are  very  convincing.  We  shall  speak  of  the 
pathogenesis  of  gastrosuccorrhea,  or  Reichmann’s  disease,  under 
the  Nervous  Affections  of  the  Stomach.  It  is  impossible,  however, 
to  invent  a term  which  shall  comprise  the  important  features  of  all 
types  of  motor  and  mechanical  insufficiency,  and  probably  as  clear 
a classification  as  any  is  one  based  on  Riegel  and  Boas,  as  follows : 

1.  Simple  gastric  atony  or  motor  insufficiency  or  myasthenia 
without  dilation. 

2.  Atonic  dilation  (motor  insufficiency  due  to  relaxation  of  the 
gastric  walls)  without  pyloric  stenosis. 

3.  Secondary  dilation  (motor  insufficiency  due  to  pyloric 
stenosis). 

The  one  common  sign  is  not  the  retention  of  food  nor  per- 
manent digestion,  but  the  impaired  motility. 

Etiology. — Two  kinds  of  cases  may  occur : either  the  atony  of 
the  gastric  wall  is  not  due  to  a mechanical  obstacle, — in  this  case 
nothing  will  oppose  the  free  course  of  the  contents,  and  they  will 
only  linger  in  the  stomach  because  the  latter  is  really  incapable  of 
ejecting  them  from  its  cavity  in  proper  time, — or  the  atony  will  be 
due  to  a pyloric  stenosis  ; the  muscular  tonicity  will  have  been 
overcome  by  an  impassable  obstacle,  the  fibers  exhaust  themselves 
in  contending  with  an  excessive  resistance,  and  the  dilation  may 
then  be  considered  as  following  on  existence  of  the  obstacle.  In 
the  first  case  the  etiology  is  variable,  and  arises,  finally,  from  a 
defect  in  the  nutrition  of  the  muscular  layer  or  in  the  innervation  ; 
in  the  other  case  it  is  purely  mechanical. 


DILATION  CAUSED  BY  A MECHANICAL  OBSTACLE. 

Intrinsic  causes  of  opposition  to  the  passage  of  stomach-contents 
into  the  intestines,  and  of  such  a resistance  to  the  contractions  of 
the  stomach  that  it  dilates,  are,  first  of  all,  the  constrictions  of  the 
pylorus.  These  are  generally  the  result  of  anatomical  alterations 


626 


MOTOR  INSUFFICIENCY. 


— viz.,  cancer,  cicatrices,  circular  ulcer,  or  muscular  hypertrophy 
of  the  pyloric  sphincter. 

Nauwerk  (/.  c.)  was  one  of  the  first  to  draw  attention  to  hy- 
perplasia and  hypertrophy  of  the  pyloric  sphincter  as  a cause  of 
dilatation  (which  has  been  considered  in  a special  chapter).  A 
spasm  of  the  pylorus,  which  can  be  compared  to  a spasm  of  the 
sphincter  of  the  anus,  can  constitute  an  obstruction  equally  well. 
This  spasm,  which  has  been  admitted  by  authors  for  a long  time, — 
for  reasons  a little  theoretical  perhaps, — has  been  demonstrated 
since  gastric  surgery  has  permitted  a more  direct  exploration. 
Martin  (/.  c .)  has  reported  a case  in  which  a pylorus  large  enough 
to  admit  the  passage  of  two  fingers  brought  on  a considerable 
dilation  by  its  spasmodic  constriction,  consequent  upon  a circular 
ulcer  accompanied  by  considerable  hyperacidity.  Landerer  (/.  c.) 
is  said  to  have  proved  the  existence  of  a congenital  pyloric 
constriction  analogous  to  the  congenital  mitral  constriction  de- 
scribed by  some  authors.  He  collected  ten  such  observations,  and 
claimed  that  this  orifice,  though  large  enough  during  infancy,  might 
undergo  an  arrest  of  development  and  remain  very  small,  while  the 
stomach  grows  larger  with  age ; a serious  dilation  would  result 
from  these  diverging  effects.  (See  Congenital  Stenosis  of  Pylorus.) 

However,  the  obstacle  does  not  necessarily  have  its  seat  in  the 
tissue  of  the  pylorus  itself.  In  the  chapter  on  Benign  Tumors  we 
have  described  the  possibility  of  a polypus  growing  from  the 
mucosa  some  distance  from  the  pylorus  and  by  means  of  a long 
pedicle  capable  of  bringing  about  a dilation  by  becoming  fixed, 
more  or  less,  in  the  intestinal  orifice,  and  thus  causing  its  occlu- 
sion, acting  like  a ball-valve.  Deiters  (/.  c.)  has  collected*  a 
large  number  of  observations,  in  which  congenital  malformations, 
abnormal  foldings,  diverticula,  and  atresia  had  provoked  dilations 
by  constricting  the  intestine  in  the  immediate  vicinity  of  the  pylorus. 
An  anatomical  lesion  of  the  duodenum — the  cicatrix  of  an  ulcer, 
for  example — would  produce  the  same  effects  by  diminishing  the 
caliber  of  the  passage. 

The  causes  of  extrinsic  origin  which  have  been  observed  to 
effect  compression  of  the  pylorus  or  duodenum  are  very  numerous. 
Among  these  are  peritoneal  adhesions,  circumscribed  or  not,  the 
results  of  former  inflammations.  Fibrous  bands  issuing  from  a 
gastric  cicatrix  may  so  distort  the  normal  location  of  the  pylorus 


From  the  Anatomical  Pathological  Institute  of  Greifswald. 


ETIOLOGY  OF  DILATIONS.  627 

(although  not  situated  in  the  pylorus  itself)  as  to  compel  the  duo- 
denum to  describe  an  abnormal  course. 

Inflammations  originating  in  the  liver  and  the  pancreas  may 
be  the  starting-point  of  similar  anatomical  modifications.  The 
head  of  the  pancreas,  so  intimately  connected  with  the  duodenum, 
may  become  cystic  or  cancerous,  and  cause  a duodenal  stenosis 
by  compression,  with  following  dilation  of  the  stomach.  A con- 
genital displacement  of  the  duodenum  would  bring  about  the  same 
disorders  (Cechini).  Biliary  concretions,  by  dilating  the  diverticu- 
lum of  Vater,  or  by  compressing  the  intestinal  wall,  may  pro- 
duce a compression  of  the  duodenum  sufficient  to  bring  about 
gastric  dilation  ; Grundzach  has  recently  reported  a case  of  this 
kind.  Landau  (/.  c.),  Bartels  (/.  c.),  Warnek  (/.  c.),  Mueller  (/.  c.), 
Litten  (/.  c.)}  and  other  authors  have  studied  the  relations  of 
dislocation  of  the  right  kidney  to  gastric  dilation.  Similar 
studies  have  been  made  in  an  interesting  work  by  Bruhl,  and 
Mathieu  has  also  recently  reported  new  cases  (Societe  Medicale 
d’Hopitaux).  Patients  presenting  this  coincidence  of  movable 
kidney  and  dilation  of  the  stomach  are  usually  young  girls  or 
women  of  the  working  class,  who  are  in  the  habit  of  fixing  their 
skirts  above  their  hips,  or  lacing  tightly,  causing  an  external  con- 
striction, which  is  shown  by  the  presence  of  a permanent  furrow. 
We  append  two  illustrations  showing  the  effect  of  tight  lacing  in 
producing  distortions  and  dislocation  of  the  stomach. 

Figure  39  illustrates  the  female  skeleton  and  the  funnel  shape 
given  to  the  lower  thorax  by  lacing — the  stomach  being  pressed 
down  into  approximately  the  position  indicated  by  the  dotted  out- 
line, the  antrum  pylori  coming  immediately  beneath  the  umbilicus. 
The  stomach  is  not  pressed  upon  directly,  but  is  displaced  by  the 
pressure  of  the  liver.  This  vertical  position  can  also  be  brought 
about  by  the  weight  and  dragging  of  neoplasms. 

A second  malformation  of  the  gastric  cavity  is  the  looped  or 
tzvisted  stomach , caused  by  lacing  and  probably  by  cicatricial  con- 
tractions along  the  lesser  curvature.  The  loop  form  is  brought  about 
by  closer  and  closer  approximation  of  cardia  and  pylorus  (Plate 
XII).  Dilation  is  easily  developed  from  the  vertical  position, be- 
cause overretained  ingesta  dilate  at  first  the  antrum  and  later  the 
entire  gastric  cavity.  The  vertical  part  of  the  duodenum,  it  must  be 
remembered,  is  firmly  adherent  to  the  spinal  column  and  can  not 
descend ; if,  therefore,  the  antrum  or  the  pylorus  lies  lower, — as, 
for  instance,  in  the  loop  form  and  vertical  position, — the  evacuation 


628 


MOTOR  INSUFFICIENCY. 


is  much  more  difficult  than  in  the  normal  stomach  position,  because 
the  ingesta  must  be  lifted  up  to  the  pylorus.  Only  in  the  recumbent 
position  and  when  the  patient  lies  on  the  left  side  can  the  organ  be 
evacuated.  The  musculature  of  such  distorted  and  dislocated  stom- 
achs is  called  upon  to  make  excessive  and  superfluous  expulsive 
efforts,  whereby  it  readily  becomes  exhausted.  The  time  of  gastric 


Fig.  39. — Diagrammatic  Illustration  of  the  Mechanism  Effecting  Vertical  Position 
of  the  Stomach. 

Compression  of  thorax  by  lacing,  producing  a funnel  shape,  forcing  liver  down  upon  the 
stomach.  Antrum  of  pylorus  (A)  descends  below  umbilicus  (U). 


digestion  consequently  becomes  prolonged,  and  the  gastric  wall  is 
overdistended  and  a motor  insufficiency  is  gradually  established. 
Kussmaul  first  called  attention  to  kinking  of  the  duodenum,  occur- 
ring at  the  juncture  of  the  movable  horizontal  and  the  fixed  vertical 
portion  of  duodenum,  and  caused  by  the  dragging  of  dilated  or  dis- 
torted stomachs.  This  constitutes  an  additional  mechanical  obstruc- 
tion, and  has  been  observed  by  the  author  during  a laparotomy — the 


PLATE  XII. 


Malformation  and  Distortion  of  the  Stomach  Caused  by  Lacing  or  Tight 
Clothing,  Belts,  Etc. 

Figures  I,  2,  3,  and  4 illustrate  the  origin  of  the  loop  form  of  the  stomach  by  approxi- 
mation of  the  cardia  (C)  and  the  pylorus  (P).  Figures  5,  6,  and  7 illustrate  the 
vertical  position  and  descent  of  the  pylorus  (see  text). 


LIBRARY 

OF  THE 

UNIVERSITY  ef  ILLINOIS. 


DUODENAL  ABNORMALITIES  AND  DILATION.  629 

horizontal  part  of  duodenum  was  kinked  off  and  the  first  part  fol- 
lowing the  pylorus  was  dilated.  H.  W.  Bettman  has  presented  some 
instructive  diagrammatic  representations  of  the  descent  of  the 
stomach  and  the  formation  of  subpyloric  (antral)  pouch  (“  Phila- 
delphia Monthly  Medical  Journal,”  vol.  i,  p.  144). 

Men  who  wear  a belt  or  strap  may  produce  the  same  results. 
Lud.  Knapp  (“  Wanderniere  bei  Frauen,”  Berlin,  1896)  associates 
the  frequency  of  floating  kidney  with  abnormalities  in  the  pelvic 
organs  in  women,  causing  constant  dragging  on  the  kidneys  by 
means  of  the  ureters.  The  right  kidney  may  become  displaced 
forward  and  inward,  pressing  upon  the  fixed,  descending  portion  of 
the  duodenum,  which  is  situated  between  the  hilum  of  the  kidney 
and  the  vertebral  column.  Such  partial  obliteration  of  the  intes- 
tine would  bring  about  a slower  and  more  difficult  evacuation  of 
the  contents  of  the  stomach  ; but  this  is  conceivable  only  if  the  dis- 
located kidney  has  become  fixed  in  its  abnormal  position.  We 
shall  treat  the  effects  of  floating  kidney  more  fully  in  the  chapter 
on  Enteroptosis. 

Ewald  (/.  c .)  and  Pertick  (/.  c.)  have  gathered  together  a cer- 
tain number  of  cases  in  which  a hernia  of  the  floating  portion  of 
the  duodenum,  or  of  the  first  part  of  the  jejunum  through  a 
laceration  in  the  mesentery,  or  a diverticulum  of  these  portions  of 
the  intestine,  has  brought  about  an  impediment  to  the  normal 
course  of  the  ingesta,  and  caused,  in  the  end,  a gastric  dilation. 


ATONIC  DILATION. 

Gastric  atony  is  a condition  of  reduced  or  lost  tonicity  of  the 
musculature.  It  is  a state  of  sub-  or  hypotonicity,  also  very  aptly 
designated  as  gastric  myasthenia.  (See  special  chapter  on  this 
subject.) 

Dilations  resulting  from  this  state  that  seem  to  be  primary 
may  be  acute  or  chronic.  The  first  kind,  which  are  very  rare, 
have  for  their  cause  either  a traumatism  or  a surgical  intervention 
(laparotomy),  or  else  a serious  infectious  disease;  Hilton  Fagge 
(/.  c.),  Bartels  (/.  c.)f  Montaya  (/.  c.)}  and  Lepoil  (/.  c.)  have  cited 
examples  in  which  typhoid  fever  seems  to  have  played  the  part 
of  the  chief  cause.  In  this  case  the  dilation  seems  to  be  due  to 
the  loss  of  tonicity  of  the  musculature  of  the  stomach  and  of 
the  abdomen.  In  other  cases  the  origin  of  the  evil  is  an  excess 


630 


MOTOR  INSUFFICIENCY. 


of  food,  an  error  committed  so  frequently  by  convalescents  after 
they  have  been  confined  to  one  diet  for  a long  time. 

Chronic  forms  of  atonic  dilations  are  dependent  upon  a great 
number  of  factors.  Those  addicted  to  excessive  indulgence  in  food 
suffer  first  with  distention  of  the  stomach;  then,  later,  with  dila- 
tion. This  phenomenon  is  comparatively  frequent  with  persons 
into  whose  ordinary  diet  a large  quantity  of  liquids  enters;  with 
excessive  beer-drinkers,  for  instance,  the  beer  acting  not  only 
mechanically  by  its  volume,  but  also  through  the  irritating  and 
poisonous  substances  with  which  it  may  be  adulterated.  Debove 
(/.  c.)  has  called  attention  to  the  drawbacks  of  prescribing  milk 
in  considerable  quantities,  and  has  cited,  among  others,  a case  of 
circular  ulcer  cured  by  the  daily  allowance  of  eight  liters  of  milk; 
but  an  enormous  dilation  of  the  stomach  resulted.  In  the 
chapter  on  Acute  Gastritis  we  have  pointed  out  that  overfeeding 
produces  a certain  amount  of  gastritis.  The  dilation  is  produced 
under  this  double  influence  of  the  inflammation  and  of  the  disten- 
tion; without  the  addition  of  the  first  of  these  causes,  megalo- 
gastria  alone  would  occur. 

Simple  chronic  gastritis  may  result  in  a considerable  atrophy  of 
the  muscular  fibers  of  the  stomach,  which  may  lead  to  dilation  of 
the  stomach.  The  same  may  be  said  of  hyperchylia,  provided  that 
it  is  one  of  the  forms  where  a hyperacid  secretion  causes  a pro- 
longed stasis  of  the  amylaceous  substances;  such  cases  have  been 
collected  by  Mathieu  and  Remond,  under  the  name  of  dyspepsia 
with  organic  hyperacidity  and  stasis.  In  other  cases  muscular  atony 
is  the  result  of  a prolonged  retention  in  the  stomach  of  undigested 
food,  with  fermentation  thereof,  when  hydrochloric  acid  is  absent. 
Drawn  out  by  a weight  more  or  less  considerable,  and  distended 
by  the  gases  that  are  developed  in  the  putrefying  mass,  the  mus- 
cular fibers  gradually  become  diseased  and  lose  their  elasticity. 
The  dilation  found  in  consumptives,  in  chlorosis,  etc.,  is  due  solely 
to  chronic  gastritis,  which  is  caused  by  asthenia  and  the  alterations 
in  the  blood,  the  results  of  these  diseases.  In  diabetes  both  the 
chronic  gastritis  and  superabundance  of  food  cooperate  in  the  alter- 
ation of  the  walls,  and  may  finally  lead  to  amyloid  and  colloid 
degenerations  of  the  muscular  fibers. 

Atony  of  purely  nervous  origin,  concerning  which  the  French 
writers  Germain-See  (/.  c.)  and  Mathieu  (/.  c.)  have  published 
numerous  researches,  is  held  by  them  to  be  a consequence  of 
“ crises,”  by  which  term  they  mean  successive  and  alternating 


NATURE  AND  CONCEPT  OF  DILATION.  63  I 

intervention  of  spasm  and  of  atony  of  the  gastro-intestinal  tract. 
These  crises  are  produced  by  an  occasional  and  general  cause, 
such  as  sad  emotions,  mental  shock,  neurasthenia,  etc. 

The  atonic  form  of  dilation  was  first  recognized,  toward  the  end 
of  the  last  century,  by  John  Peter  Frank  (/.  c.),  who  separates  it 
distinctly  from  the  forms  caused  by  stenosis.  The  atony  due  to 
neurasthenia  can  be  brought  about  by  lesion  of  the  central  or 
peripheral  nervous  system,  and  the  dilation  will  then  depend  on 
a deep-seated  alteration  either  of  the  central  organs  or  of  the 
peripheral  nerves.  Bouveret,  Dujardin-Beaumetz,  and  Glenard 
have  represented  general  ptosis  of  the  abdominal  organs  as  the 
expression  of  a particular  diathesis,  a condition  of  relaxation  of  the 
tissues  with  unstriated  muscular  fibers ; and  have  suggested  that 
there  is  a dilation  depending  upon  this  general  state.  The  dila- 
tions resulting  from  nephroptosis  are  included  in  this  class  by 
Glenard,  Debove,  and  Remond.  (See  Enteroptosis.) 

Pathological  Anatomy. — Having  already  considered  the  patho- 
logical histology  of  the  various  causes  of  dilation, — viz.,  neoplasms, 
benign  and  malignant  cicatrices,  chronic  interstitial  gastritis,  etc., 
— the  pathological  anatomy  of  the  dilation  per  se  is  simple.  At 
the  autopsy  of  a subject  dead  from  cancer  of  the  pylorus,  for 
instance,  one  finds  the  abdomen  filled  by  a voluminous  sac,  which 
comes  down  more  or  less  near  the  pubes.  This  sac,  which  repre- 
sents the  stomach,  having  lost  all  its  normal  relations,  and  exces- 
sively dilated,  may  contain  enormous  quantities  of  liquid,  and  the 
ancient  authors,  who  knew  only  the  extreme  cases,  have  cited  ex- 
traordinary examples  of  this.  (The  history  of  the  subject  is  given 
by  Penzoldt,  “ Die  Magenerweiterung,”  Erlangen,  1875.)  Plem- 
pius  (/.  c.)  is  said  to  have  seen  a stomach  that  held  nine  pints  of 
liquid;  Stengel  mentions  a stomach  containing  12  “measures”; 
Schurig,  a stomach  containing  48  liters;  Henricus  ab  Herr  found  a 
stomach  that  filled  the  whole  of  the  abdomen.  Portal  (quoted  by 
Ewald  and  Pick)  states  that  the  stomach  of  the  Duke  of  Chausnes, 
one  of  the  greatest  gourmands  of  his  time,  had  a capacity  of 
liters.  The  largest  stomach  observed  by  the  author  had  a 
capacity  of  4 liters,  measured  by  his  method. 

All  the  layers  of  the  walls  of  the  gastric  sac  have  become  thin  ; 
and  microscopically  one  finds  atrophy  of  the  mucosa ; at  the  same 
time  the  muscularis  is  now  composed  only  of  isolated  bunches  of 
muscular  fibers,  separated  by  the  connective  tissue.  When  the 
dilation  is  caused  by  an  obstruction  at  the  pylorus,  hypertrophy  of 


632 


MOTOR  INSUFFICIENCY. 


the  muscular  wall  is,  as  a rule,  produced  first;  then  interstitial 
sclerosis  comes  on,  little  by  little,  submerging  the  true  elements, 
and  the  final  atony  of  the  wall  is  due  to  the  disappearance  of  the 
contractile  fibers.  An  apparent  hypertrophy,  through  exagger- 
ated proliferation  of  the  connective  tissue,  sometimes  masks  the 
actual  atrophy  of  muscle-fibers  in  these  cases  which  occasionally 
can  not  be  distinguished  from  scirrhus,  even  microscopically. 
The  muscular  hypertrophy  continues  very  long  in  the  pyloric 
region,  where  it  also  attains  its  maximum  point.  The  increased 
resistance  and  thickening  of  the  walls  sometimes  results  from 
ulcer,  and  may  simulate  a tumor. 

A dilated  stomach  may  present  variable  forms  due  to  the  action 
of  the  special  cause.  If  a cicatricial  or  scirrhous  constriction 
causes  the  cardia  and  the  pylorus  to  approach  each  other,  the 
stomach  will  be  pyriform  ; but  if  the  same  lesion  has  plowed  a trans- 
verse furrow,  more  or  less  deep,  on  the  wall,  a dilation  in  the 
shape  of  an  hour-glass  will  be  produced  ; but  the  symptoms  do  not 
differ  from  those  caused  by  occlusion  of  the  pylorus. 

Symptomatology. — The  tongue  is,  in  most  cases,  coated  by 
necrobiotic  epithelium,  mucus,  and  retained  food  debris,  the  breath 
frequently  being  very  offensive ; there  is  generally  a stomatitis, 
glossitis,  or  gingivitis  present. 

State  of  the  Appetite. — The  appetite  is  normal  at  the  beginning  ; 
but  when  the  disease  has  developed,  it  may  be  lost,  or  may  become 
considerably  decreased : some  patients,  for  instance,  will  not  need 
more  than  one  meal  a day.  In  other  cases,  since  the  stomach 
merely  plays  the  part  of  a reservoir  with  no  outlet,  and  the  foods 
are  no  longer  evacuated  from  the  stomach  into  the  intestine,  diges- 
tion and  absorption  can  not  occur.  In  rare  instances  the  patients 
may  be  tormented  with  hunger,  and  they  are  in  a condition  anal- 
ogous, so  far  as  effects  are  concerned,  to  that  of  persons  affected 
with  an  impassable  stenosis  of  the  esophagus.  They  try  to  satisfy 
their  appetites,  and,  yielding  to  the  solicitation  of  hunger,  actu- 
ally present  bulimic  phenomena.  In  reality  it  is  not  hard  to 
understand  this  difference,  which  depends  practically  on  the 
nature  of  the  obstruction  to  the  course  of  the  foods;  anorexia  is 
observed  chiefly  in  cancerous  patients  and  in  those  seized  with 
chronic  gastritis,  while  a cicatrix  of  a circular  ulcer  may  have 
obliterated  the  pylorus  without  bringing  about  serious  loss  of 
appetite. 

Pyrosis. — The  regurgitation  of  a certain  quantity  of  very  acid  or 


SYMPTOMATOLOGY  OF  MOTOR  INSUFFICIENCY.  633 

alkaline  ingesta  often  accompanies  the  eructations  that  pass  through 
the  cardia,  causing  intense  pyrosis. 

Eructations  and  Gaseous  Discharges. — In  motor  insufficiency  of 
the  first  degree  the  gastric  heaviness  and  the  distention  give  way 
little  by  little,  and  if  the  patient  takes  his  meals  at  regular  intervals, 
his  stomach  at  last  empties  itself  and  his  p^tins  disappear.  But 
in  motor  insufficiency  of  the  second  degree  generally  the  distress 
ceases  only  when  more  or  less  copious  emesis  has  relieved  the 
gastric  cavity  of  the  foods  that  have  burdened  it,  sometimes  for 
more  than  twenty-four  hours. 

To  this  feeling  of  fullness  are  added  disgusting  gaseous  dis- 
charges, often  very  fetid.  The  alimentary  contents,  in  fact,  are 
liable  to  set  free  many  different  gases  in  considerable  quantity. 
(See  chapter  on  the  Gases  of  the  Stomach.)  The  principal  gases 
are  carbonic  acid,  hydrogen,  oxygen,  nitrogen,  hydrogen-sulphid, 
and  carbonic  dioxid.  Whenever  there  is  stasis,  presence  of  gases 
may  be  verified  by  directly  extracting  them  from  the  stomach 
by  the  tube  or  by  allowing  the  drawn  gastric  contents  to  stand  in  a 
closed  vessel.  This  gaseous  development  is  due  to  bacteria  which 
may  resist  the  antiseptic  action  of  the  hydrochloric  acid,  even  when 
present  in  excess;  some  of  these  organisms  have  been  isolated  and 
cultivated.  These  fermentations,  which  are  very  frequent,  are 
modified  by  salicylic  acid  or  saccharin.  Boric  acid,  carbolic  acid, 
creasote,  and  chlorin  water  have  no  decided  effect,  in  my  experi- 
ence, except  in  doses  that  are  incompatible  with  their  thera- 
peutic uses.  The  great  quantity  of  liquid  contained  in  the  stomach 
facilitates  the  development  of  anaerobic  germs,  giving  rise  to  com- 
plex and  toxic  products  of  fermentation. 

Pain. — The  pain  of  dilation  is  not  marked ; the  uncomfortable 
sensations  are  those  of  pressure,  fullness,  and  distention.  Naturally, 
if  cancer  or  ulcer  is  coexistent  with  dilation,  pain  will  be  a prom- 
inent symptom. 

Vomiting. — In  motor  insufficiency  of  the  second  degree  the  at- 
tacks of  emesis  are  quite  characteristic.  They  are  not  so  frequent 
as  they  are  at  certain  stages  of  the  development  of  cancer  or  of 
ulcer,  and  are  generally  separated  from  each  other  by  variable  but 
comparatively  long  periods,  and  they  rarely  occur  at  the  time  of 
the  maximum  of  digestion.  For  one  or  two  days  a patient  suffers, 
after  each  meal,  from  a sensation  of  growing  uneasiness,  and  from 
a feeling  of  weight  in  the  epigastrium,  more  and  more  painful; 
then,  suddenly,  often  toward  the  middle  of  the  night,  he  is  seized 
42 


634 


MOTOR  INSUFFICIENCY. 


with  very  abundant  vomitings,  after  which  he  can  enjoy  a little 
rest. 

The  vomited  material  is  sometimes  composed  of  several  liters 
of  a mixture  of  solid  food,  drinks,  and  mucus.  The  quantity  of 
vomited  matter  is  a first-rate  symptom  of  dilation,  and  allows  it 
to  be  distinguished,  for  instance,  from  simple  displacements  of  the 
stomach.  Chronic  gastritis,  cancer,  etc.,  may  also  give  rise  to 
slight  hemorrhages,  and  in  this  case  the  very  much  modified 
blood  remains  a long  while  in  the  stomach ; the  same  phenomenon 
can  be  recognized  in  dilation. 

Boas  has  pointed  out  that  the  persistent  presence  of  bile  and  of 
pancreatic  fluid — of  which  the  characteristics  have  been  given — is 
an  indication  of  stenosis  of  the  duodenum,  and  is  a valuable 
symptom  of  dilation  resulting  from  the  compression  of  this  part 
of  the  intestine  by  a dilated  gall-bladder  or  hepatic  neoplasm,  for 
instance.  The  vomited  matter  will  have  a more  offensive  odor  the 
longer  it  has  remained  in  the  stomach.  Later  on  in  the  disease, 
when  the  walls  are  distended,  the  vomiting  comes  on  at  greater 
intervals,  the  odor  of  substances  vomited  becomes  more  revolting, 
and  then  the  emesis  is  rarely  sufficient  to  evacuate  the  stomach  ; 
the  feeling  of  relief  which  at  first  followed  is  no  longer  experi- 
enced. Sometimes  the  vomitings  cease  after  they  have  been  very 
frequent — a grave  sign  of  exhaustion. 

Symptoms  of  autointoxication  from  dilation  have  been  described 
by  Al.  Pick  (“  Wien.  klin.  Wochenschr.,”  1892,  No.  46),  Boas  (/.  c. 
p.  73),  and  J.  Friedenwald  (“  Med.  News,”  Dec.  23,  1893).  A most 
exhaustive  account  of  the  autointoxication  with  motor  insufficiency 
will  be  found  in  the  works  of  Albu  (l.c.)  and  Bouveret  (/.£.). 

In  dilation  through  an  organic  cause  the  disturbance  of  the 
general  state  will  vary  with  this  cause.  Thus,  it  is  observed  that 
in  cancerous  patients  the  dilation  is  accompanied  by  the  most 
evident  cachexia.  In  ulcer,  Reichmann’s  disease,  and  chronic  gas- 
tritis, dilation  will  be  coincident  with  an  emaciation  more  or  less 
marked,  but  no  cachexia. 

In  the  case  of  children,  Comby  and  Moncorro  have  attributed 
to  dilation  caused  by  overfeeding  a role  in  the  etiology  of  rachitis. 
The  latter  author  also  considers  it  to  be  the  cause  of  certain  con- 
vulsions, of  insomnia,  of  ringworms,  of  urticaria,  and  of  bronchitis. 

Constipatioji. — Constipation  is  frequent  and  obstinate  ; and  not 
only  are  the  stools  rare,  but  the  quantity  of  substances  evacuated 
is  also  much  less  than  in  the  normal  state.  This  is  a very  valuable 


STATE  OF  URINE,  BOWELS,  ETC. 


635 


indication,  for  it  shows  the  approximate  amount  of  food  that  passes 
into  the  intestines.  From  four  to  six  ounces  of  solid  feces  are 
normally  discharged  in  twenty-four  hours.  In  atonic  dilation  this 
amount  is  reduced  to  2 y2  ounces,  and  in  extreme  cases  to  1 y2 
ounces,  in  twenty-four  hours,  on  the  average.  The  amount  of  water 
in  the  feces  is  normally  75  per  cent. ; this  is  reduced  to  from  30  to 
40  per  cent,  in  dilation.  The  prognosis  is  influenced  by  the  degree 
to  which  food  may  be  made  to  take  its  normal  course  (Kussmaul). 
Persistent  constipation  or  absence  of  stools  indicates  an  incurable 
stenosis  of  the  pylorus.  Putrefactive  diarrhea  may  alternate  with 
constipation. 

Gastrorrhexis  (Rupture  of  the  Stomach). — Newmann  (/.  c.),  Buist 
(/.  c.)t  Lautschner  (/.  c.),  and  Hoffmann  have  reported  rupture  of  the 
stomach  and  sudden  extravasation  of  its  contents  into  the  peritoneal 
cavity.  Rupture  may  occur  after  a very  sudden,  acute  dilation,  or 
in  the  last  stage  of  one  of  long  standing.  The  tear  generally  occurs 
near  an  old  cicatrix.  A case  reported  by  Chiari  (/.  c.)  had  a cica- 
trix near  the  lesser  curvature,  through  which  the  tear  occurred 
after  overindulgence  in  food.  In  a case  observed  by  Hoffmann 
(/.  c.),  in  which  a rupture  of  the  lesser  curvature  had  taken  place, 
no  other  cause  but  food  engorgement  was  assigned. 

State  of  the  Urine. — The  quantity  passed  in  twenty-four  hours 
may  be  reduced  to  500  c.c.  Boas  makes  use  of  the  daily  quantity 
for  an  approximate  estimate  of  the  degree  of  dilation. 

First  degree.  Quantity  of  urine  in  twenty-four  hours,  1500  to  1000  gm. 

Second  “ “ “ “ “ 1000  to  500  “ 

Third  “ “ “ “ “ 500  gm.  and  less. 

The  urine  is  generally  alkaline ; the  chlorids  are  diminished. 


The  urine  is  frequently  modified  in  quantity  and  in  quality.  The 
patients  are  in  a state  of  chronic  inanition,  and  the  urea  is  therefore 
necessarily  diminished.  The  stomach  absorbs  little  liquid,  as  the 
constant  thirst  by  which  these  patients  are  tormented  testifies  ; thus 
the  dilation  brings  about  a deficient  urinary  secretion.  Lastly, 
when  the  dilation  accompanies  an  excessive  secretion  of  hydro- 
chloric acid,  and  the  latter  is  thrown  out,  either  by  frequent  vomit- 
ings or  by  frequent  lavage,  the  urine  becomes  alkaline. 

Nervous  Phenomena. — Erb  found  increased  galvanic  and  faradic 
irritability  of  all  accessible  motor  nerves,  with  the  exception  of  the 
facial.  The  increase  of  the  galvanic  irritability  of  the  nerves  is  a 
more  constant  symptom  than  the  increase  of  faradic  irritability. 


636 


MOTOR  INSUFFICIENCY. 


Von  Frankl-Hochwart  found  the  latter  to  be  normal  at  times. 
Trousseau  found  that  tetany  could  be  caused  by  compression  of 
the  main  nerve-trunks  or  compressing  the  principal  blood-vessels  of 
the  limbs,  so  that  the  arterial  and  venous  circulation  was  impeded. 
When  this  compression  was  kept  up  for  two  or  three  minutes,  the 
tetany  began,  but  would  cease  when  the  pressure  was  relieved. 
Chvostek  discovered  an  increase  of  mechanical  irritability  of  the 
nerves  in  the  extremities,  and  also  of  the  facial  nerve  in  particular. 
This  irritability  became  evident  on  tapping  the  nerves  lightly  with 
a percussion  hammer  or  with  the  finger,  which  brought  on  rapid 
instantaneous  twitchings  in  the  muscles  supplied  by  those  nerves. 
On  passing  the  finger  over  the  face  from  the  temporal  regions  down 
to  the  chin,  distinct  twitchings  occurred  in  the  muscles  supplied  by 
the  facial  nerve,  because  this  stroke  of  the  finger  exerted  an  irrita- 
tion on  ail  branches  of  that  nerve  (Fr.  Schultze). 

General  State  of  Health. — -The  general  state  of  health  is  more 
deeply  influenced  by  the  cause  of  the  dilation  than  by  the  dila- 
tion itself.  Neurasthenia  often  causes  an  atony  of  the  muscle- 
fibers  of  the  stomach,  the  consequences  of  which  can  not  but  have 
a marked  influence  on  the  nutrition  of  the  patient,  encouraging 
and  keeping  up  the  neurasthenia.  Diabetes,  chlorosis,  and  great 
pyrexia,  which  may  have  caused  the  atony,  provoke  general  dis- 
orders also,  and  it  is  difficult  to  distinguish  from  among  the  result- 
ing disturbances  that  which  belongs  properly  to  gastric  atony. 

Cardiopulmonary  Symptoms. — These  have  been  considered  in  the 
chapter  on  the  Influence  of  Gastric  Diseases  on  Other  Organs, 
in  which  I have  dwelt  on  the  effects  of  distention  of  the  gastric 
cavity  by  gases  hindering  considerably  the  functions  of  the  dia- 
phragm and  disturbing  the  action  of  the  respiratory  and-circulatory 
apparatus.  Dyspneic  phenomena,  or  modifications  in  the  sound 
of  the  heart  and  in  the  rhythm  of  the  pulse,  are  frequently  met 
with. 

Mattheides  (/.  cl)  has  gathered  together  a number  of  cases  in 
which  he  observed  a sensation  analogous  to  that  of  globus  hyster- 
icus in  patients  afflicted  with  dilation.  He  called  attention  to  the 
fact  that  this  sensation  was  aggravated  when  the  stomach  had 
sunk ; on  the  other  hand,  it  diminished  when  it  had  risen  ; from 
this  he  concluded  that  the  displacement  of  the  stomach  so  often 
accompanying  the  dilatation  of  this  organ  was  the  cause  of  this 
sensation  of  globus,  through  dragging  on  the  esophagus.  Schmidt 
(/.  cl)  is  said  to  have  verified,  by  a laparotomy,  the  existence  of 


RESULT  OF  PERCUSSION  AND  PALPATION. 


637 


these  anatomical  disorders  in  a patient  who  had  previously  com- 
plained of  the  sensation  of  globus.  The  connection  between  the 
two  is  not  at  all  satisfactorily  proved,  or  even  significant. 

Percussion,  Palpation,  and  Auscultatory  Percussion  of  the 
Stomach. — Osier  (/.  c.)  emphasizes  the  fact  that  the  diagnosis  is 
often  possible  by  inspection.  Percussion  and  palpation  allow  us 
to  ascertain  the  limits  of  the  lower  edge  of  the  greater  curvature, 
and,  to  a certain  extent,  to  appreciate  the  degree  of  the  ectasia. 
The  percussion  should  be  performed  with  the  patient  standing 
up,  and  again  when  lying  on  his  back.  The  measured  ingestion 
of  a certain  quantity  of  water  will  allow  one  to  estimate  the 
atony  of  the  wall,  and  will  at  the  same  time  furnish  exact  data  on 
the  displacement  of  the  lower  edge  of  the  organ.  The  stomach 
may  be  distended  by  C02,  and  the  colon  by  water,  thus  facili- 
tating the  differentiation  between  the  two.  Other  authors  have 
proposed  to  perform  the  operation  inversely,  and  to  percuss  the 
stomach  made  heavy  by  a certain  quantity  of  water,  while  the 
colon  is  distended  by  gas  (Ewald).  Auscultatory  percussion — 
i.  e.,  percussing  over  the  abdomen  while  a phonendoscope  is  simul- 
taneously moved  over  it  and  in  constant  connection  with  the  ears — 
is  of  service  in  delineating  the  outlines  of  the  stomach  (A.  L. 
Benedict).  These  precautions  would  make  mistakes  very  diffi- 
cult ; they  are  available  to  general  practitioners,  which  can  not  be 
said  of  the  Rontgen  rays  and  the  electrodiaphane.  Osier  holds 
that  when  the  distended  stomach  is  outlined  on  the  abdominal 
wall,  one  can  usually  follow  its  delineations  with  the  eye,  and,  of 
course,  much  better  by  percussion.  In  the  “ Philadelphia  Medical 
Times”  for  May,  1891,  Pepper  reports  a case  of  dilation  caused 
by  scirrhus  of  the  pylorus  in  which  there  was  a visible  peristalsis. 

The  gaseous  distention  has  also  the  advantage  that  it  allows  the 
distinction  to  be  made  between  true  dilation  and  a simple  dis- 
placement of  the  organ. 

By  palpation  the  splashing  sound  can  be  investigated.  This  is 
easy  to  preceive  when  the  stomach,  the  pylorus  of  which  is  con- 
stricted, is  full  of  those  liquid  masses  already  mentioned  in  con- 
nection with  the  vomiting.  But  when  the  dilation  is  not  very 
marked,  the  splashing  becomes  less  clear,  and  Debove  has  recently 
shown  that  the  intestines,  when  half  distended  by  gases,  are  cap- 
able, under  the  influence  of  movements  communicated  by  the 
fingers,  of  producing  a sound  so  like  that  of  the  gastric  splashing 
as  to  make  the  distinction  very  difficult.  Chomel  (/.  c.)  had  already 


638  MOTOR  INSUFFICIENCY. 

drawn  attention  to  this  source  of  mistakes,  and  to  that  which  de- 
pends on  the  presence  of  liquid  and  gas  in  the  large  intestine  : 
“ The  splashing  in  the  stomach,”  he  says,  “ might  be  con- 
founded with  a similar  sound  of  which  the  large  intestine  is  some- 
times the  seat,  which  can  be  produced  by  the  lateral  movement  of 
the  body,  but  still  more  easily  by  the  pressure  of  the  hand  on  the 
regions  occupied  by  the  colon.”  It  is  met  with  especially  in  subjects 
who  have  recently  received  an  injection,  and  in  those  who  have  been 
seized  with  serous  diarrhea.  The  knowledge  of  these  conditions 
and  of  the  particular  source  of  the  gastric  splashing  sound  is 

sufficient  to  distinguish  it  from  in- 
testinal splashing.  Jaworski  (/.  c .) 
has  reported  four  cases  of  very 
audible  splashing  sound  even  when, 
on  introducing  the  probe  into  the 
stomach,  he  had  been  unable  to 
withdraw  any  liquid  whatever.  The 
author  has  observed  this  fact  in  a 
number  of  cases.  It  is  not,  there- 
fore, an  unmistakable  sign. 

For  determining  the  location  of 
the  greater  curvature,  Thiebaut 
(/.  c.),  of  Nancy,  has  devised  an  in- 
strument that  consists  of  a probe 
through  which  slides  a thread  with 
a leaden  weight.  The  probe  is  long 
enough  to  reach  the  cardia,  and  the 
quantity  of  thread  taken  by  the 
leaden  weight  before  it  arrives  at 
the  bottom  of  the  stomach  allows 
one  to  measure  the  vertical  dimen- 
sion of  the  gastric  cavity.  This  method  impresses  me  as  falla- 
cious. 

The  methods  of  procedure  based  on  the  employment  of  salol, 
oil,  iodid  of  potassium,  etc.,  designed  to  determine  the  state  of 
the  motor  functions  and  of  the  absorption  of  the  mucous  mem- 
brane, have  been  described.  In  dilation  they  give  information  of 
varying  value,  but  inferior  to  that  furnished  by  exploration  with 
the  sound.  Dr.  Harry  Adler  and  myself  have  been  able  to  map 
out  the  greater  curvature  with  ease  by  means  of  a metallic  spiral 
sound  inclosed  in  a stomach-tube  (Kuhn,  Turck,  Wegele).  The 


{Eichhorst. ) 

Outline  obtained  by  percussion. 


RESULTS  OF  TEST-MEAL  ANALYSIS. 


639 


sound  is  readily  palpable.  I have  already  stated  the  signs  by 
which  one  can  recognize  atony  of  a muscular  wall : either  pres- 
ence of  debris  of  food  in  the  morning  before  breakfast,  or  the 
prolonged  retention  of  a test-meal  in  the  gastric  cavity.  The 
Hemmeter  gastrograph  is  a graphic  method  of  obtaining  motor 
records  from  the  human  stomach,  and  the  results  obtained  there- 
with are  generally  reliable.  (Plates  in  and  iv,  between  pp.  72  and 
73-) 

Test-meals. — The  gastric  cavity  should  be  washed  out  on  the 
evening  of  the  day  before  a test-meal  is  given.  The  substances 
extracted  by  this  preliminary  lavage  are  sometimes  very  abundant, 
and  have  the  same  composition  as  those  vomited.  They  gener- 
ally become  separated  into  three  layers  when  allowed  to  stand  : 
an  upper  one,  frothy  and  turbid;  a middle  one,  liquid  ; and  a lower 
one,  composed  of  alimentary  detritus  of  all  kinds,  or  simply  of 
amylaceous  substances  (hyperacidity).  Organic  ferments  and  sar- 
cinse  will  be  discovered,  and  all  the  series  of  products  that  can, 
normally  or  abnormally,  be  contained  in  the  stomach.  If  the 
motor  insufficiency  is  caused  by  malignant  neoplasm,  the  Oppler- 
Boas  bacillus  will,  as  a rule,  be  found  in  this  material.  In  the 
morning  before  breakfast  the  gastric  cavity,  which  has  been  cleansed 
the  evening  before,  may  again  contain  the  normal  products  of  se- 
cretion, or  material  which  is  rich  in  organic  acids.  The  digestion 
of  the  test-meal  will  generally  be  slow,  and,  especially  in  cases  of 
cancer,  it  will  be  impossible  to  detect  free  hydrochloric  acid.  In 
other  patients  a normal  or  exaggerated  state  of  secretion  of  hydro- 
chloric acid  will  be  found.  When  the  normal  HC1  is  absent,  the 
filtered  gastric  contents  will  show  excess  of  lactic  and  butyric 
acids.  If  the  motor  insufficiency  is  due  to  alcoholism,  acetic  acid 
will  be  a prominent  constituent. 

Diagnosis. — Dilation  or  motor  insufficiency  of  the  second 
degree  may  have  to  be  differentiated  from  atony,  or  myasthenia 
from  gastroptosis  and  physiologically  large  stomach,  or  megalo- 
gastria.  No  sign,  unless  it  is  the  presence  in  notable  quantity 
of  food  in  the  stomach  before  breakfast,  is  pathognomonic.  Bugge 
(/.  c.)  recommended  the  following  operation : After  determin- 

ing, by  percussion, — the  patient  standing  up, — the  lower  edge 
of  the  stomach,  he  drove  the  needle  of  a hypodermic  syringe 
above  the  discovered  limit.  If  the  liquid  extracted  was  acid,  he 
concluded  that  the  stomach  had  been  reached.  It  is  evident  that 
this  procedure  is  not  without  danger,  and  it  is  not  even  accurate. 


640 


MOTOR  INSUFFICIENCY. 


I prefer  the  simple  exploration  by  means  of  the  sound,  asso- 
ciated or  not  with  artificial  gaseous  distention  of  the  stomach ; 
these  are  the  most  available  and  practical  methods  for  the  gen- 
eral practitioner,  and,  in  fact,  suffice  to  distinguish  a dilated 
from  a displaced  stomach,  and  from  a naturally  large  stomach. 
But  if  they  do  not,  the  method  of  the  author  (p.  72)  will  leave  no 
room  for  doubt. 

Gastroptosis  (displacement  of  the  stomach)  will  be  fully  consid- 
ered in  a special  chapter  on  that  subject.  The  pylorus  may  be  dis- 
placed, and  may  be  freely  movable  below  the  epigastric  region, 
without  in  reality  causing  any  gastric  disturbance.  By  palpation 
and  percussion  the  greater  curvature  of  the  stomach  can  be  made 
out  below  the  umbilicus.  One  might  then  be  very  much  disposed 
to  suspect  a dilation  ; but  on  distention  with  C02  gas,  one  sees 
not  only  the  greater,  but  also  the  smaller,  curvature  outlined  under 
the  skin,  and  the  outline  of  the  whole  stomach  can  be  traced  on 
the  abdominal  wall,  and  the  limits  of  the  corresponding  resonant 
zone  can  be  ascertained  by  percussion. 

The  points  of  difference  between  a dilation  and  atony  are  the 
following:  In  the  morning,  before  food  has  been  ingested,  the 
dilated  stomach  contains  an  accumulation  of  putrefactive  products 
and  food  material,  showing  either  excess  of  lactic  and  fatty  acids 
or,  when  these  are  absent,  abnormal  amounts  of  HC1.  In  simple 
atony  the  stomach  is,  as  a rule,  entirely  empty  in  the  morning ; 
in  atonic  dilation  it  may  contain  trifling  amounts  of  food,  but 
not  in  a state  of  decomposition.  In  atony  the  bowel  evacuations 
are  less  likely  to  be  so  few  in  number  and  so  small  in  amount,  and 
the  total  quantity  of  urine  voided  in  twenty-four  hours  is  normal 
or  only  slightly  reduced.  dilation  the  amount  of  urine  is  sub- 
normal, and  it  is  concentrated  and  in  rare  cases  contains  diacetic 
acid  and  acetone. 

In  megalogastria  we  are  not  dealing  with  a diseased  stomach, 
and  hence  a differentiation  is  unnecessary.  Tetany  occurs  only 
with  dilation,  but  gastric  vertigo  is  frequent  in  atony.  The  differ- 
entiation between  a dislocated  and  a dilated  stomach  is  facilitated 
by  the  clinical  history.  In  a dislocated  stomach  the  motor  func- 
tion is  frequently  normal,  and  hence  we  find  that  emesis,  if  it 
occurs,  does  not  bring  out  such  very  large  amounts  as  in  dilation. 
Diuresis  and  thirst  are  normal  in  gastroptosis  ; in  dilation  thirst 
is  intense,  but  on  account  of  the  regurgitation  or  vomiting  of  fluids, 
diuresis  is  subnormal.  No  matter  where  a stomach  may  be  located 


PLATE  XIII. 


Transillumination  (electrodiaphany)  of  the  stomach.  The  organ  is  filled  with  600  c.c. 
of  water,  and  has  sunk  downward  to  the  left.  The  electric  lamp  has  just  reached 
the  fundus ; on  being  pushed  further,  the  intensest  part  of  the  transillumination 
would  appear  below  the  umbilicus. 


Gastrectasia. 


LIBRARY 

OF  THE 

UNIVERSITY  ef  ILLINOIS. 


DIFFERENTIAL  DIAGNOSIS. 


64I 


within  the  abdomen,  or  how  large  it  may  be,  it  does  not  become 
abnormal  until  the  motor  function  is  interfered  with.  A Leube 
or  Herschell  test-meal  or  the  Salzer  double  test-meal  will  instruct 
us  concerning  these  points. 

The  success  of  inspection,  palpation,  and  percussion  will  depend 
upon  the  thickness  and  resistance  of  the  external  abdominal  wall. 
When  there  is  very  little  or  no  emaciation,  it  is  by  no  means  easy 
to  palpate  through  the  abdominal  wall.  Then,  again,  much  gas 
escapes  into  the  intestine  when  the  stomach  is  distended  by  effer- 
vescent mixtures. 

But  by  means  of  the  author’s  stomach-shaped  intragastric 
rubber  bag,  or  by  Einhorn’s  electrodiaphane,  it  is  possible  to 
make  the  differential  diagnosis  without  much  difficulty.  By  the 
Hemmeter  apparatus,  which  was  originally  designed  to  obtain 
records  of  the  gastric  peristalsis,  it  is  also  possible  to  measure  the 
capacity  of  the  stomach  by  determining  the  amount  of  air  required 
to  distend  it  within  the  stomach.  (See  p.  75.)  This  will  at  once 
enable  one  to  diagnose  a dilated  stomach  from  one  that  has  pro- 
lapsed but  has  retained  its  normal  capacity.  Einhorn’s  diaphane 
is  a practical  method  for  demonstrating  these  two  conditions  to  the 
eye.  (See  special  article  on  Diaphany.)  The  Roentgen  rays  are 
also  available  for  the  same  purpose,  as  demonstrated  by  the  author. 
(Hemmeter,  “ Photography  of  the  Human  Stomach  by  the  Roent- 
gen Rays,”  “ Boston  Medical  and  Surgical  Journal,”  1896.)  Re- 
cently the  author  has  used  the  following  method  : The  dilated  stom- 
ach is  coated  internally  with  bismuth  subnitrate  by  means  of  the 
stomach  powder-blower ; thereafter  its  outline  can  be  distinctly 
recognized  through  the  fluoroscope.  The  greater  curvature  may 
be  outlined  by  photographing,  by  the  Roentgen  rays,  a metallic 
spiral  electrode  that  has  been  introduced  and  made  to  apply  itself 
along  the  greater  curvature,  according  to  suggestions  first  made  by 
Wegele.  For  private  practice  distention  and  the  Einhorn  electro- 
diaphane are  most  expedient,  as  they  permit  a diagnosis  to  be  made 
by  inspection.  Debove  and  Remond  (“  Maladies  de  l’Estomac,” 
p.  87)  state  that  the  execution  of  this  method  is  difficult,  and  im- 
poses much  suffering  upon  the  patient.  From  what  I have  seen 
almost  weekly  with  Einhorn’s  apparatus,  I differ  emphatically  from 
these  observers,  and  believe  a further  experience  with  the  apparatus 
will  effect  a change  in  their  opinion. 

Diagnosis  of  the  Cajise. — The  cause  is  more  difficult  to  detect 
than  the  dilatation  itself.  In  this  connection  I refer  to  what  has 


642 


MOTOR  INSUFFICIENCY. 


been  said  in  the  consideration  of  ulcer,  carcinoma,  benign  neo- 
plasms, etc.,  and  their  respective  diagnoses. 

The  anamnesis,  the  examination  of  the  substances  vomited,  and 
the  results  furnished  by  test-meals  will  provide  the  principal  data. 
The  clinical  history  differs,  in  fact,  considerably,  according  as  one 
finds  a dilation  of  cancerous  origin  or  one  caused  by  ulcer  or  gas- 
tritis. The  effects  of  the  ingestion  of  poisons  have  been  con- 
sidered under  Toxic  Gastritis.  The  corrosive  poisons  frequently 
produce  a cicatricial  contraction  of  the  pylorus.  The  significance  of 
HC1  in  the  gastric  contents  has  been  stated  in  the  chapter  on  Car- 
cinoma. If  the  bile  is  always  absent  in  the  substances  vomited,  or 
in  the  gastric  contents  either  before  or  after  eating,  one  will  be  led 
to  think  of  constriction  of  the  pylorus ; this  will  probably  be  of 
cancerous  origin  if  the  hydrochloric  acid  is  missing  at  the  same 
time. 

The  constant  presence  of  bile  and  of  pancreatic  juice  in  the 
stomach  would  be  a proof  that  the  dilation  is  a consequence  of  a 
stenosis  of  the  duodenum,  which  may  result  from  a movable  kid- 
ney, a fibrous  adhesion,  gall-stones,  pancreatic,  cystic,  or  hepatic 
neoplasm,  etc. 

The  author  has  devised  a method  by  which  a stenosis  of  the 
pylorus  and  of  the  duodenum  can  be  accurately  determined. 
(Hemmeter,  “ Intubation  des  Duodenum,”  “ Archiv  f.  Verdauungs- 
krankh.,”  Bd.  11,  S.  85.  See  also  part  first,  this  volume.) 

F.  Kuhn,  who  belongs  to  Riegel’s  school  (Giessen),  has  also  de- 
vised a method  for  sounding  the  pylorus,  which  is,  however,  a devel- 
opment of  a revolving  spiral  sound  first  invented  by  F.  B.  Turck,  of 
Chicago.  The  Turck-Kuhn  method  is  very  ingenious  and  simple  ; 
but  owing  to  the  necessity  of  revolving  of  the  spiral  sound  within 
the  stomach,  the  method  is  not  free  from  danger  in  cases  in  which 
we  should  suspect  open  ulcers  or  carcinoma,  since  the  intragastric 
revolutions  of  the  sound  may  bruise  or  tear  the  ulcer  or  neoplasm 
and  set  up  hemorrhage  or  lead  to  perforation. 

The  accuracy  of  these  results,  it  is  true,  is  not  absolute ; but  in 
practice,  in  associating  them  with  other  data  furnished  by  the  ele- 
ments of  the  diagnosis  of  each  gastric  affection,  a diagnosis  should, 
as  a rule,  be  attainable. 

Prognosis. — The  evolution  of  motor  insufficiency  varies  accord- 
ing to  the  cause ; when  it  is  a case  of  simple  atony  of  recent 
date,  a proper  treatment — of  which  I shall  speak  again  further  on 
— may  bring  amelioration  rapidly,  and  even  cure.  But  when  it  is  a 


PLATE  XIV. 


Adhesions,  Causing  Motor  Insufficiency  but  Retaining  Stomach  in  Normal 
Position. 

S.  Stomach.  L.  Liver.  B.  Gall-bladder.  C , C,  C.  Colon.  Adhesions  of  stomach 
to  liver  and  gall-bladder  (a3)  and  transverse  colon  (a4).  Adhesions  of  hepatic 
flexure  of  colon  to  abdominal  wall  (a1,  a1).  Adhesions  of  transverse  colon  to  de- 
scending colon  (a5,  a5)  and  of  descending  colon  to  abdominal  wall  (a6).  Adhesion 
of  hepatic  flexure  to  liver  (a2).  The  small  intestine  has  been  dissected  away,  only 
the  mesentery  remaining.  The  end  of  the  ilium  is  visible  in  the  lower  left-hand 
corner.  — ( From  Author1  s Clinic.') 


MALFORMATIONS  OF  THE  GASTRIC  CAVITY.  643 

case  of  dilation  with  atrophy  of  the  muscular  coat,  especially  when 
there  exists  an  impassable  obstacle  at  the  pylorus,  the  cure  is 
impossible,  except  sometimes  by  operation.  The  treatment  still 
relieves  the  painful  phenomena,  but  the  inanition  makes  progress 
from  day  to  day,  and  the  patient  succumbs  gradually,  unless  one 
of  the  complications  that  have  been  mentioned  appears  and  has- 
tens the  end. 

Malformations  of  the  Gastric  Cavity. — For  literature,  see  arti- 
cle by  H.  W.  Bettman,  “ The  Shape  and  Position  of  the  Stomach  ” 
(“  Philadelphia  Monthly  Medical  Journal,”  vol.  I,  p.  1 2 1),  contain- 
ing important  anatomical  contributions  to  this  subject.  As  dila- 
tion is,  in  reality,  a deformity  of  the  stomach,  a certain  number 
of  malformations  and  changes  of  form  may  be  appropriately  con- 
sidered in  this  connection. 

According  to  Debove  and  Remond,  atresia  of  the  gastric  cavity 
results  from  diminution  of  work  by  the  organ,  through  insufficiency 
of  alimentary  contributions.  Inanition  and  constriction  of  the 
esophagus  or  of  the  cardia  will  thus  have  been  the  first  cause  of 
this  atrophy.  In  other  cases  it  is  a cancerous  infiltration,  extend- 
ing over  the  whole  wall,  or  a chronic  gastritis  with  hypertrophy  of 
the  submucosa  and  of  the  connective  tissue  (linitis  plastica),  or  a 
fibrous,  deforming  peritonitis,  which  will  have  played  the  same  part. 
The  caliber  of  the  stomach  thus  narrowed  sometimes  does  not 
exceed  that  of  the  intestine.  This  condition  has  been  referred  to 
in  the  chapter  on  Hypertrophic  Gastritis.  When  the  upper  diges- 
tive paths  are  open,  attacks  of  emesis  occur,  appearing  as  soon  as 
the  quantity  of  food  exceeds  the  very  small  volume  of  the  stomach, 
the  small  caliber  becoming  still  more  evident  when  one  comes  to 
distending  it  with  carbonic  acid  or  to  expanding  it  with  the  intra- 
gastric  rubber  bag.  If  stenosis  of  the  esophagus  or  of  the  cardia 
exists,  the  passage  of  the  tube  becomes  impossible,  and  the  symp- 
toms of  these  constrictions  assume  enough  importance  to  obscure 
entirely  those  which  might  be  produced  by  the  state  of  the  stomach. 

The  Hour-glass  Stomach. — This  type  of  deformed  stomach  may  be  : 
(i)  Congenital ; (2)  due  to  extensive  cicatrization  of  a peptic  ulcer  ; 
(3)  due  to  cancer,  especially  to  scirrhus ; (4)  due  to  an  intense, 
spastic,  and  permanent  contraction  at  the  site  of  the  preantral 
sphincter ; (5)  due  to  peritoneal  adhesions  ; (6)  due  to  abdominal 
tumors;  (7)  due  to  twisting  of  the  stomach;  (8)  due  to  hernia  of 
stomach  through  the  mesocolon.  Stoker  (/.  cl)  has  published  one 
case  in  which  the  stomach  was  divided  into  two  parts  by  a con- 


644 


MOTOR  INSUFFICIENCY. 


genital  furrow,  and  had  never,  during  life,  presented  any  functional 
disturbance.  Iago  (/.  c)  has  related  the  story  of  a patient  who 
succumbed  when  forty-two  years  old,  after  having  suffered  for  ten 
months  from  uncontrollable  vomitings;  on  the  examination  of  the 
abdomen,  a soft  tumor  was  found  underneath  the  liver  which  had 
been  taken  for  a displaced  right  kidney;  no  tumor  existed  at  the 
pylorus;  emesis  took  place  without  pain,  and  was  not  preceded 
by  regurgitation ; there  was  no  cachexia.  At  the  autopsy  the 
stomach  presented  two  dilated  sacs,  which  communicated  by 
a closed  narrow  passage,  situated  about  the  middle  of  the  organ ; 
the  index-finger  could  not  pass  this  constriction.  The  cicatrices 
that  had  produced  this  deformity  had  been  caused  by  a former 
disease,  which  appeared  at  the  age  of  thirty  and  was  character- 
ized by  hematemesis  and  acute  pains.  A patient  fifty  years 
old,  observed  by  Luigi  Mazotti  (/.  c.)f  experienced  such  intense 
pains  after  meals  that  she  would  squirm  on  her  bed,  and  only 
found  relief  after  having  vomited  everything  that  she  had  just 
taken.  At  the  autopsy  the  stomach  was  found  divided  into  two 
parts — the  upper  one  vertical,  the  lower  one  directed  horizontally 
toward  the  right  side ; a narrow  passage  was  situated  between  the 
two  parts.  The  lower  portion  of  the  stomach  had  made  a com- 
plete circle,  and  the  contracted  point  was  exactly  the  center  around 
which  this  rotation  had  occurred.  The  upper  part  of  the  stomach 
was  distended  by  gases;  the  lower  part  was  empty  and  joined 
to  the  abdominal  wall  by  adhesions.  When  the  viscus  had  been 
replaced  in  its  normal  position,  it  was  found  that  neither  the  ori- 
fices nor  the  wall  presented  any  modification,  and  it  was  impossible 
to  discover  the  cause  of  this  displacement.  Two  cases  of  (i)  Bour- 
get,  (2)  one  of  Schmid  Monard,  (3)  one  of  Jaworski,  (4)  one  of 
Bouveret,  and  (5)  one  of  Watson  Cheyne  were  diagnosed  intra 
vitam.  The  most  practical  methods  for  such  diagnosis  are  disten- 
tion with  air  or  C02,  gastrodiaphany,  and  the  introduction  of  a 
sound,  or,  better,  of  the  spiral  sound  of  Kuhn  or  Wegele.  The 
cases  numbered  2,  4,  and  5 were  cured  by  operation  ; the  others 
improved  under  medical  treatment.  In  another  case,  Chiari  (/.  c.) 
suspected  a cancerous  constriction  of  the  pylorus  in  a patient  who, 
in  reality,  had  an  intussusception  of  the  stomach  into  the  duode- 
num. 

Further  particulars  concerning  similar  cases  can  be  found  in  the 
recent  memoirs  of  Bettman  (/.  c.),  Bauermeister  (/.  c.),  and  Saundby 
(/.  c.),  and  in  the  theses  of  Kern  (Inaug.-Dissert.,  Berlin,  1881), 


TREATMENT  OF  MOTOR  INSUFFICIENCY.  645 

Chiari  (“Wien.  med.  Wochenschr.,”  No.  42,  1890),  von  Hacker,  in 
his  monograph  (“  Magenoperationen,”  etc.,  published  by  Brau- 
muller,  Vienna),  gives  a number  of  illustrations  of  stomachs  divided 
into  three  parts  by  cicatrices  or  adhesions.  (See  Bibliography  at 
end  of  this  chapter.) 

Treatment  of  Motor  Insufficiency  of  the  First  Degree  ( Gas- 
tric Atony  or  Myasthenia). — Prophylaxis. — The  muscu laris  of  the 
digestive  organs  may  be  weak  by  inheritance.  Chlorosis,  anemia, 
tuberculosis  and  cholelithiasis,  exhausting  hemorrhages,  infectious 
diseases,  typhoid,  malaria,  diphtheria,  influenza,  may  bring  on  myas- 
thenia; and  frequent  and  rapidly  consecutive  childbirths  may,  by 
causing  increase  of  space  in  the  abdominal  cavity  and  loss  of  tone 
of  the  abdominal  muscles,  lead  up  to  gastric  atony.  Insufficient 
mastication,  hasty  eating  and  deglutition,  and  defective  teeth  pre- 
dispose to  atony.  The  treatment  in  all  cases  must  seek  the  cause 
and  adapt  itself  to  its  removal.  Anemia  must  be  treated  by  proper 
food,  iron,  extract  of  bone-marrow,  and,  in  proper  cases,  arsenic.  In 
women  with  gastroptosis  and  atony,  the  abdominal  muscles  must 
be  strengthened  and  supported  by  proper  bandages.  The  treat- 
ment proper  includes  diet,  hydropathic  and  electrical  procedures, 
massage,  and  medicines. 

Diet. — Patients  with  gastric  atony  may  pursue  one  of  two 
courses'  with  regard  to  diet : either  they  may  eat  frequently,  but 
very  little  at  a time,  or  they  may  limit  themselves  to  two  meals, — 
breakfast  and  dinner, — at  8 a.  m.  and  3 p.  m.  respectively,  and  permit 
the  stomach  to  rest  after  dinner  until  the  next  morning.  It  can  not 
be  determined  a priori  which  plan  will  give  the  best  results,  but  for 
most  cases  the  plan  that  secures  most  rest  to  the  overworked 
organ  is  the  most  efficacious.  Exclusive  rectal  feeding  for  three 
weeks  has  been  followed  by  very  good  results.  As  water  is  not 
absorbed  from  the  stomach,  the  quantity  of  liquids  must  not 
exceed  from  1 to  1^  quarts  in  twenty-four  hours,  including  all 
drinks,  coffee,  soups,  etc.  When  there  is  a craving  for  more  liquids 
than  this,  they  should  be  introduced  by  enema. 

My  experience  with  the  frequent  and  persistent  administration 
of  milk,  as  observed  in  milk-cure  sanatoriums  in  Germany,  is  dis- 
couraging. I believe  this  treatment  to  be  a useless  dietetic 
experiment  in  gastric  atony,  since  the  weight  of  the  milk,  used  in 
such  abundance,  inevitably  overdistends  the  organ. 

The  special  diet  must  be  selected  according  to  the  state  of  the 
gastric  secretions.  If  there  is  hyperacidity,  a generous  beef  and 
43 


646 


MOTOR  INSUFFICIENCY. 


mutton  diet,  with  limited  carbohydrates,  hard-  and  soft-boiled  eggs, 
ham,  tongue,  oysters,  duck,  and  deer  in  a finely  divided  form,  is 
recommended  ; of  vegetables,  carrots,  spinach,  soft-boiled  turnips, 
beans,  peas,  and  cauliflower,  all  finely  cut  up  or  as  purees,  are 
allowed.  Potato,  macaroni,  rice,  and  farina  gruel  are  permissible. 
If  the  hyperacidity  is  the  cause  of  the  atony,  I favor  restriction  of 
proteid  diet  and  a preponderance  of  amylaceous  food,  according  to 
principles  laid  down  elsewhere.  Strictness  should  be  observed 
concerning  the  use  of  alcohol,  and  when  a trial  proves  that  it 
injures  digestion,  I generally  forbid  claret,  Rhine  wine,  and  even 
beer.  But  when  a trial  with  light  wines  demonstrates  their  bene- 
ficial action,  about  two  ounces  of  wine  with  each  meal  may  be 
permitted.  Whenever  the  hydrochloric  acid  is  diminished,  the 
lighter  meat  varieties, — chicken,  pigeon,  birds, — fish,  and  boiled 
sweetbreads  or  calves’  brains,  should  be  allowed  only;  but  a larger 
amount  of  carbohydrates  may  be  conceded.  The  special  diet 
is  stated  more  explicitly  in  the  chapter  on  Dietetics. 

Constipation  is  a serious  and  a constant  accompaniment  of 
gastric  atony;  it  must,  therefore,  receive  our  undivided  atten- 
tion. Purgatives  should  be  used  only  as  a last  resort,  and  the  main 
reliance  should  be  placed  on  diet,  massage,  and  electricity.  A 
pint  of  cold  water,  preferably  Bedford  magnesia  spring- water,  in 
the  morning  on  an  empty  stomach,  black  (rye)  or  Graham  bread, 
abundance  of  vegetables, — turnips,  carrots,  asparagus,  tomatoes, 
rhubarb  plant,  beans,  peas,  lentils, — noodles,  macaroni,  barley, 
sweet  compotes,  plums,  figs,  apples,  currants,  cranberries,  cider, 
buttermilk,  kefyr,  sour  milk,  honey.  Figs,  plums,  and  senna 
leaves  stewed  under  constant  stirring  until  intimately  mixed,  with 
sugar  and  lemon-juice  added,  is  a useful  laxative.  When  sweeten- 
ing is  desired,  milk-sugar  should  be  preferred  to  cane-sugar.  The 
use  of  these  articles  very  rarely  fails  to  bring  about  regular  evacu- 
ations without  medicines  when  massage  and  electricity  are  used 
in  conjunction.  Whenever  drugs  are  positively  unavoidable,  I 
prefer  cascara  sagrada  or  aloes.  In  pronounced  atony  constipation 
can  not  be  treated  by  this  diet  alone,  because  it  increases  the 
weight  of  the  ingesta. 

The  hydropathic  treatment  consists  in  cold  morning  sponge 
baths,  cold  wet  packs,  and  Priessnitz  bandages  to  epigastrium.  In 
severe  neurasthenic  myasthenia  I am  in  the  habit  of  ordering  a 
daily  bath  containing  three  per  cent,  of  chlorid  of  sodium  and  two 
percent,  of  sodium  bicarbonate;  temperature  of  bath,  98°  F. ; the 


TREATMENT  OF  MOTOR  INSUFFICIENCY.  647 

patient  should  remain  in  twenty  minutes.  When  taken  in  the 
evening,  this  bath  favors  sleep. 

Electric  Treatment. — Intragastric  application  with  the  Einhorn 
electrode  within  the  stomach  is  most  effective  ; the  faradic  current 
is  applied  up  and  down  over  the  spinal  column  and  over  the  ab- 
dominal muscles.  The  constant  current  is  applied  in  the  same 
manner,  in  the  strength  of  20  milliamperes  and  for  about  ten  min- 
utes. Systematic  massage,  both  general  and  local,  over  the  stom- 
ach is  an  important  adjuvant. 

Medicinal. — This  form  of  treatment  should  be  as  limited  as  pos- 
sible. The  most  approved  tonic  for  the  motor  function  is  strychnin  : 

R . Strychnin,  sulphatis, 0.021  gm.  gr. 

Elixir  gentianse, 180.0  c.c.  ^vj.  M. 

SlG. — One  tablespoonful  three  times  daily. 

In  anemia  the  gentian  elixir  with  chlorid  of  iron  may  be  substi- 
tuted. 

When  the  hydrochloric  acid  is  deficient,  it  must  be  supplied  ; 
when  it  is  excessive,  it  must  be  neutralized  by  the  following  : 

R.  Magnes.  ust., 15.0  ^ss 

Bismuth  carbonate, 

Natron,  bicarbonat., aa  5-°  s;j  -f-  gr.  xv 

Strychnin,  sulphatis, o.i  gr.  iss.  M. 

SlG. — One-half  teaspoonful  one  hour  after  meals. 

Creasote  and  orexin  are  claimed  by  competent  authorities  (Pick 
and  Penzoldt)  to  be  able  to  excite  the  peristalsis  ; the  latter  may  be 
used  when  there  is  anacidity  or  subacidity.  Creasote,  in  my  ex- 
perience, does  not  increase  gastric  peristalsis. 

Lavage. — Asa  rule,  one  will  be  able  to  get  along  without  lavage 
in  the  first  stage  of  motor  insufficiency.  But  when  the  food  re- 
mained in  persistently  overtime,  I have  seen  improvement  of  mus- 
cular tonicity  follow  the  rapidly  alternating  cold  and  warm  intra- 
gastric douche.  This  exerts  a powerful  and  stimulating  effect  also 
on  the  secretion,  when  it  is  defective  ; when  the  latter  is  excessive, 
the  douching  should  be  carried  out  with  alkaline  water. 

Treatment  of  Motor  Insufficiency  of  the  Second  Degree 
( Fully  Developed  Dilation). — This  may  be  considered  under  three 
headings:  (1)  Dietetic,  (2)  medicinal,  (3)  surgical. 

The  diet  is  essentially  based  on  the  same  principles  as  in  simple 
myasthenia;  the  amount  of  liquid  permissible  must  not  exceed 
1500  c.c.  in  twenty-four  hours.  With  exaggerated  vomiting  and 


648 


MOTOR  INSUFFICIENCY. 


pains,  exclusive  feeding  by  the  rectum  for  fourteen  days  is  recom- 
mended. A specified  diet-list  for  both  simple  atony  and  pro- 
nounced dilation  will  be  found  on  pages  235  to  237.  It  is  impos- 
sible to  treat  the  latter  form  successfully  without  lavage ; this  is 
not  only  a palliative  measure  of  great  value,  but  in  cases  of  atonic 
dilatation  due  to  muscular  weakness,  and  not  dependent  upon 
mechanical  obstruction,  it  may  even  be  able  to  effect  a cure,  when 
combined  with  other  means  presently  to  be  described. 

The  first  washings  are  done  with  pure  warm  water,  but  the  last 
washings  are  done  with  solutions  adapted  to  the  chemical  and 
septic  states  prevalent  in  the  organ.  For  instance,  if  there  are  great 
excess  of  hydrochloric  acid  or  fermentation  by  sarcinae  and  yeast, 
sodium  biborate  or  bicarbonate  should  be  added,  as  these  salts  are 
not  only  antacid,  but,  with  regard  to  these  organisms,  are  also 
antiseptic.  If  there  is  butyric  or  lactic  acid  fermentation,  boric 
acid  (3  per  cent.),  salicylic  acid  (3  per  cent.),  or  creolin  or  lysol  (10 
to  15  drops  to  a quart)  should  be  used;  but  the  stagnation  can 
not  be  prevented  from  recurring  by  these  means  unless  the  motility 
is  improved  by  other  treatment. 

Electricity  is  indispensable : its  method  of  employment,  inter- 
nally and  externally,  has  been  described  in  a previous  chapter. 

Massage  undoubtedly  improves  the  gastric  musculature,  but 
should  be  used  only  on  days  when  the  stomach  has  been  washed 
out,  because  the  mechanical  compression  may  force  stagnating 
masses  into  the  intestines,  thus  spreading  the  putrefaction.  Ab- 
dominal bandages  properly  adapted  and  applied  have  proved  a val- 
uable palliative  measure.  Hy  dr  other apeutic  applications  are  indis- 
pensable, and  should  be  used  as  described  in  the  paragraph  devoted 
to  the  consideration  of  that  treatment. 

Medicinal  treatment  has  a twofold  object:  (1)  To  promote  the 
motor  function;  (2)  to  prevent,  as  far  as  possible,  gastric  fermenta- 
tion and  decomposition.  The  only  drug  in  which  I have  any 
faith  for  improving  gastric  peristalsis  Is  strychnin  sulphate;  it 
should  be  given  in  heavy  doses,  not  less  than  ^ of  a grain  for 
adults,  t.  i.  d. 

Boas  combines  strychnin  with  an  antifermentative  in  the  follow- 
ing manner : 

B=.  Strychnin,  sulphatis,  . 0.0022  gm.  gr.  Jg- 

Codein.  phosphoric., 0.03  “ gr.  | 

Bismuth,  salicylici  (basic), 0.5  “ gr.  viiss.  M. 

SiG. — One  powder  taken  after  each  meal. 


TREATMENT  OF  MOTOR  INSUFFICIENCY. 


649 


F.  Kuhn  has  proposed  salicylic  acid  (0.5  gm.  to  a dose),  salicy- 
late of  sodium  (15  to  50  grains),  or  saccharin  and  sodium  benzoate 
(of  each,  from  10  to  30  grains  to  a dose)  to  counteract  gastric  fer- 
mentation. Carbolic  acid  was  first  used  by  Naunyn  for  the  same 
purpose.  When  there  is  marked  lactic  or  butyric  acid  fermenta- 
tion, there  is  not  a better  agent  than  hydrochloric  acid  to  coun- 
teract it:  20  to  30  drops  of  the  dilute  form  in  2 ounces  of  water, 
through  a glass  tube,  or  in  a large  gelatin  capsule  of  extra  thick- 
ness (Aaron  capsules).  Among  other  remedies  that  are  recom- 
mended are  : Salol,  naphthol,  beta-naphthol,  beta-naphthol  bismuth, 
beta-naphthol  benzoate,  or  benzonaphthol,  hydrochloric  and  car- 
bolic acid.  Bouchard  is  very  enthusiastic  concerning  antifer- 
mentative  treatment  of  gastrectasia,  but  it  is  certain  that  this  treat- 
ment alone,  without  lavage  and  proper  diet,  is  fallacious. 

Dujardin-Beaumetz  employs  : 

B.  Bismuth,  salicyl., 

Magnes.  ustae, 

Sod.  bicarb.,  . . . . aa  10.0  gm.  gr.  cl.  M. 

SiG. — To  be  divided  into  30  powders ; one  powder  after  meals. 

Our  formula  for  gastric  fermentation,  particularly  when  asso- 
ciated with  putrid  diarrhea,  is  : 


Beta-naphthol  benzoatis,  . 

. 8 

3b 

Bismuth,  salicylatis,  . . . 

. 8 

3 b 

Magnesiae  ustae,  .... 

. 8 

3b 

Saccharin, 

- o-5 

gr.  viiss 

Menthol, 

gr.  xvj. 

SiG. — To  be  divided  either  into  12,  24,  or  36  powders,  to  suit  the  indications;  if 
there  is  much  fermentation,  it  should  be  divided  into  12  powders,  and  one  given  three 
times  daily.  Otherwise  it  should  be  divided  into  24  powders,  and  one  given  every  three 
hours. 

Ewald’s  formula  for  prevention  of  gastric  fermentation  is  the 
following : 

B • Resorcin,  resublim.,  . . 5.0  gr.  lxxv 

Bismuth,  salicyl., 

Pulv.  rad.  rhei, 

Natrii  sulphur.,  . . aa  10.0  gr.  cl,  about  3 iiss 

Sacch.  lact., 15.0  gr.  ccxxv,  about  £iij  + ^ ij-  M. 

SiG. — Make  a powder;  one-half  teaspoonful  twice  daily. 

When  HC1  secretion  is  lost,  dilute  HC1  should  be  administered, 
according  to  the  formula  given  on  page  475  ; if  HC1  is  not  well 
tolerated,  pancreatin  should  be  tried,  according  to  the  principles 
given  on  page  344. 


650 


MOTOR  INSUFFICIENCY. 


For  improving  the  appetite,  strychnin,  orexin,  HC1,  and  lavage 
are  the  most  approved  means  of  therapy. 

For  vomiting,  lavage  is  the  most  efficacious  treatment;  but  if  it 
fails,  resorcin  (2  grains  in  y2  of  an  ounce  of  chloroform  water),  ora 
hypodermic  injection  of  morphin  (jr  of  a grain),  and  atropin  sul- 
phate (‘2"o"0‘  of  a grain),  will  be  called  for.  Minute  doses  of  calomel 
(tV  a grain)  every  hour  act  as  gastric  sedatives  in  some  cases. 
As  a rule,  menthol  and  chloroform  do  not  disappoint  when  used 
for  the  relief  of  vomiting.  The  following  formula  is  practical: 

R . Menthol,  1.0  gr.  xvj 

Chloroform., 1. 5 gtt.  xxiv 

Elixir  simplic., q.  s.  60.0  f^ij.  M. 

SiG. — fgij  every  hour. 

Insomnia  must  sometimes  be  treated,  as  these  patients  impera- 
tively need  rest ; for  this  purpose  chloral,  1 5 grains  by  enema,  is 
most  advisable.  Correction  of  hyperacidity  will  often  induce  sleep. 
Sulphonal  and  chloral  combined,  eight  grains  of  each,  will  produce 
a more  lasting  sleep  than  if  either  is  used  alone.  Trional  is  recom- 
mended for  the  same  purpose  by  Boas. 

Surgical  Treatment. — The  operations  that  have  been  suggested 
for  the  relief  of  motor  insufficiency  vary  according  to  the  object 
to  be  accomplished.  Motor  insufficiency  from  simple  atonic  dila- 
tation may  be  relieved  by  reducing  the  size  of  the  stomach  by 
gastroplication  or  gastrorrhaphy  (Weir).* 

If  the  pylorus  is  stenosed  by  a simple  cicatrix  or  a hyperplastic 
sphincter,  Loreta’s  digital  divulsion  of  the  pylorus  is  an  operation 
that,  judging  from  the  statistics,  is  an  unsafe  and  unreliable  pro- 
cedure. The  pyloroplastic  operation  of  von  Heineke-Mikulicz, 
which  Boas  terms  the  ideal  surgery  for  the  relief  of  pyloric  stenosis 
of  a benign  nature,  produces  more  permanent  results. 

Gastro-enterostomy  and  resection  of  the  pylorus,  as  well  as 
gastrorrhaphy, — an  operation  originated  by  Dr.  Heinrich  Bircher, 
a Swiss  surgeon, — will  come  under  consideration.  The  indications 


* In  June,  1899,  Dr.  Randolph  Winslow  operated  on  a well-known  Baltimore  phy- 
sician who  had  an  enormous  gastrectasia  and  a kidney  that  could  be  moved  about  ad 
libitum  on  the  right  side.  The  doctor,  although  sixty-four  years  old,  submitted  to  opera- 
tion by  my  advice.  The  stomach  was  reduced  by  four  plaits  extending  from  cardia 
to  pyloric  antrum,  and,  at  the  same  time,  a nephrorrhaphy  executed.  He  made  a perfect 
recovery,  was  doing  well  on  December  16th,  1899,  and,  in  his  own  words,  was  “just 
beginning  to  enjoy  life.” 


DIETETIC  AND  SURGICAL  TREATMENT.  65  I 

for  these  operations  and  their  technic,  are  subjects  concerning 
which  the  reader  must  be  referred  to  the  chapter  on  Gastric  Sur- 
gery. The  larger  portion  of  dilatations  are  undoubtedly  due  to 
some  obstacle  to  the  exit  of  the  chyme  (ischochymia,  as  Einhorn 
calls  it),  and  it  is  rational  to  presume  that  purely  medical  means 
can  not  effect  a permanent  cure  of  these  conditions.  But  the 
obstructions  or  obstacles  to  the  chyme  are  not  all  found  in  the 
stomach  itself,  for  in  the  account  given  under  the  etiology,  dis- 
tended gall-bladder,  gall-stones  impacted  in  the  diverticulum  of 
Vater,  floating  kidney,  duodenal  cicatrices  and  neoplasm,  peritoneal 
adhesions,  etc.,  have  been  referred  to,  and  all  of  these  give  their 
separate  and  distinct  indications  for  operation. 


DIET  FOR  MOTOR  INSUFFICIENCY  OF  THE  FIRST  DEGREE 
— ATONY — MYASTHENIA. — {Boas.) 

Calories. 


8 A.  M. — 100  gm.  of  milk,  50  gm.  of  toast,  30  gm.  of  butter, 401.2 

10  A.  m. — 50  gm.  of  wheat  bread,  30  gm.  of  butter,  60  gm.  of  scraped  beef,  41 5.2 
12  m. — 150  gm.  of  boiled  beef,  50  gm.  of  potato  puree  or  macaroni,  . . 439.3 

3 p.  m. — 100  gm.  of  milk,  50  gm.  of  Zwieback, 401.2 

7 p.  m. — 100  gm.  of  cold  ham  or  beef,  150  gm.  of  wheat  bread,  30  gm. 

of  butter, 557-5 


Total,  2214.4 

About  three  ounces  of  good  port  wine  or  claret  may  be  allowed 
during  the  day. 


DIET  FOR  MOTOR  INSUFFICIENCY  OF  THE  SECOND  DEGREE 
—PYLORIC  STENOSIS— MYASTHENIC  DILATION. — {Hemmeter. ) 

Calories. 

8 A.  m. — 100  gm.  of  Mosquera’s  beef  chocolate  or  Somatose  chocolate, 
or  50  gm.  of  tea  with  50  gm.  of  milk  (sweetened  with  saccharin, 


no  sugar),  50  gm.  of  toast, 195.5 

10  A.  m. — 100  gm.  of  scraped  lean  beef, 437-0 

30  gm.  of  toast, 77.7 

10  gm.  of  butter 71.3 


Total,  586.0 

12  m. — 150  gm.  of  roast  beef, 320.7 

50  gm.  of  potato  puree, 63.7 


Total,  384.4 

In  place  of  the  potato  puree,  the  same  quantity  of  spinach,  car- 
rots, peas,  or  beans  may  be  allowed  as  above. 


652 


MOTOR  INSUFFICIENCY. 


Diet  for  Motor  Insufficiency  of  the  Second  Degree  .—{Continued.) 


Calories. 

2 p.  m. — 50  gm.  of  cream, 107.30 

4 p.  m. — 100  gm.  of  tea  or  coffee^with  milk  (no  sugar,  but  saccharin),  50 

gm.  of  toast, I95-50 

7 p.  m. — 100  gm.  of  broiled  fresh  fish  or  oysters, 7 1 .7 5 

50  gm.  of  wheat  bread, 129.00 

10  gm.  of  butter, 71.30 

100  gm.  of  cream, 214.00 

9 P.  m. — 50  gm.  of  cream, 162.30 


Total,  1885.15 

In  atony  and  dilation,  as  well  as  in  carcinoma,  experience  is  the 
best  guide  for  enlarging  and  varying  the  diet.  Every  new  article 
of  diet  must  at  first  be  tried  with  great  caution ; if  liquids  are  well 
tolerated,  they  may  be  increased,  and  soups  may  be  allowed  for 
the  noon  meal.  The  daily  lavage  should  at  times  be  undertaken 
at  hours  when  a test-meal  can  be  secured  thereby,  which  will 
incidentally  instruct  the  physician  concerning  the  digestibility 
of  new  foods  and,  what  is  more  important,  the  state  of  the  motor 
function. 


OBSTRUCTION  OF  THE  ORIFICES. 

Obstruction  of  the  cardia  and  of  the  pylorus  may  be  organic  or 
functional.  The  former  is,  as  a rule,  caused  by  the  consequences 
of  carcinoma,  peptic  ulcer,  phlegmonous  or  toxic  gastritis. 
The  functional  obstructions  are  due  to  cardiospasm  and  pyloro- 
spasm.  These  conditions  have  all  received  proper  consideration 
in  other  chapters.  There  are  other  very  rare  causes,  which  merit 
attention  more  from  a pathological  than  from  a clinical  standpoint. 

Obstruction  of  the  Cardia. 

In  considering  the  organic  causes  which  most  frequently  lead 
up  to  stenosis  of  the  cardia,  it  will  be  important  to  compare  the 
table  that  gives  the  situation  in  the  stomach  of  793  gastric  ulcers 
(p.  497)  with  the  table  on  page  545,  giving  the  situation  in  the 
stomach  of  1300  cases  of  carcinoma.  Thus  it  will  be  found  that 
the  pylorus  is  affected  in  gastric  ulcer  in  12  per  cent,  of  the  cases, 
and  the  cardia  in  6.3  per  cent,  of  the  cases,  making  the  total  per- 
centage of  involvement  of  the  orifices  by  gastric  ulcer  18.3  per 
cent.  In  carcinoma  the  pylorus  is  affected  in  60.8  per  cent.,  and 


OBSTRUCTION  OF  THE  ORIFICES. 


653 


the  cardia  in  8 per  cent.,  of  all  the  cases.  The  orifices  being, 
therefore,  involved  by  carcinoma  in  68.8  per  cent,  of  all  the  cases. 
The  greater  frequency  of  malignant  neoplasm  as  a cause  of  sten- 
osis of  the  orifices  is  evident  from  these  figures.  The  obstruction 
of  the  cardia  may  be  classified  under  the  following  types : 

1.  Congenital  Stenosis. — Like  congenital  stenosis  of  the  pylorus, 
this  is  a rare  disease,  and  may  be  partial  or  complete.  If  the  sten- 
osis is  absolute,  the  child  will  die  very  shortly  after  birth  from  in- 
anition. In  partial  congenital  stenosis  of  the  cardia  it  will  be 
impossible  for  solid  food  to  pass,  but  as  the  infant  lives  exclusively 
upon  milk,  the  condition  may  exist  fora  long  time  without  threat- 
ening life.  I have  seen  one  undoubted  case  of  congenital  stenosis 
of  the  cardia  in  a child  six  years  old  in  which,  after  careful  exami- 
nation of  the  esophagus  and  stomach,  the  symptoms  of  dysphagia 
could  not  be  explained  in  any  other  way.  This  child  has  been 
permanently  relieved  by  gradual  dilatation  of  the  cardiac  ring. 
Two  years  have  elapsed,  and  the  child  remains  well. 

2.  Stenosis  Due  to  Compression. — These  are  brought  about  by  the 
pressure  of  disease  or  dislocated  neighboring  organs — for  instance, 
aortic  aneurysm,  tuberculous  or  syphilitic  mediastinal  lymph- 
glands,  neoplasm  of  the  pleura  and  lungs,  diverticulum  of  the 
esophagus. 

3.  Obturation  stenosis , due  to  occlusion  of  the  lumen  by  the  most 
varied  kind  of  foreign  bodies — artificial  teeth,  coins,  ingesta,  masses 
of  the  thrush  fungus ; by  polypi  which,  arising  from  the  wall  of 
the  pharynx  or  esophagus,  may  extend  down  into  the  lumen  of  the 
cardia;  protrusion  of  a portion  of  the  mucosa  of  the  esophagus,  as 
in  phlegmonous  esophagitis  or  abscess  of  the  cardia  or  lower  end 
of  the  esophagus. 

4.  Stenosis  caused  by  cicatrices , resulting  from  gastric  ulcer, 
phlegmonous  or  toxic  gastritis,  corrosive  destruction  of  the  cardia 
by  acids  or  alkalies  or  other  caustic  materials,  and  in  the  healing 
of  syphilitic  neoplasms  and  ulcers. 

5.  Carcinomatous  Strictures. — These  compose  from  90  to  95  per 
cent,  of  stenoses  of  the  cardia. 

6.  Cardiospasm , causing  spastic  stenosis  and  cramp  of  the  muscu- 
lature. Stenosis  of  the  cardia  by  simple  hypertrophy  of  the  mus- 
cular layer  is  unknown.  This  condition  occurs  frequently  enough 
in  the  neighborhood  of  the  pylorus  to  merit  its  consideration  in  a 
special  chapter.  Stenosis  of  the  cardia  has  been  known  to  occur 
in  the  sequence  of  compression  of  the  lower  end  of  the  esophagus, 


654 


MOTOR  INSUFFICIENCY. 


caused  by  pericardial  exudates,  cardiac  hypertrophy,  curvature  of 
the  spine,  aneurysm  of  the  aorta.  When  the  lower  end  of  the 
esophagus  is  compressed  only  on  one  side  by  any  one  of  the  con- 
ditions enumerated,  this  tube  may  escape  to  one  side  and  thereby 
avoid  complete  occlusion ; but  when  it  is  compressed  from  several 
or  all  sides,  absolute  stricture  may  result.  When  the  cause  of  the 
trouble  is  in  the  immediate  neighborhood  of  the  foramen  rotundum, 
through  which  the  esophagus  perforates  the  diaphragm,  the  symp- 
toms may  be  identical  with  those  of  stenosis  of  the  cardia. 

Symptomatology. — This  has  been  given  under  the  heading  of 
Carcinoma  of  the  Cardia,  page  566.  Suffice  it  to  say  that  the  char- 
acteristic symptom  is  dysphagia.  When  the  stenosis  is  due  to  carci- 
noma, the  dysphagia  may  sometimes  become  temporarily  alleviated. 
This  is  due  to  exulceration  of  the  malignant  tumor.  At  first  only 
solid  food  becomes  arrested  in  the  lower  portion  of  the  esophagus, 
but  later  on  not  even  liquid  food  will  pass  the  constriction.  The 
patients  accurately  locate  the  obstruction  to  swallowing  at  the  level 
of  the  ensiform  cartilage.  In  the  beginning  of  the  stenosis  repeated 
swallowing  will  succeed  in  passing  on  the  morsels  of  food  through 
the  constriction.  Careful  chewing  and  thorough  insalivation  facili- 
tate the  act.  Sometimes  the  sufferers  seek  relief  by  drinking  water 
after  the  solid  food  or  by  stroking  downward  along  the  front  of  the 
throat  and  chest.  If  solid  food  clogs  up  the  upper  or  middle  third 
of  the  esophagus,  the  signs  of  dyspnea  become  very  intense.  In 
the  beginning  of  the  stenosis  practice  in  swallowing  seems  to  make 
the  act  easier.  After  each  pause,  when  nothing  has  been  swal- 
lowed for  a long  time,  the  act  becomes  more  difficult.  The  food 
is  regurgitated  after  varying  periods.  At  first  it  occurs  only  during 
ingestion  or  shortly  afterward,  but  later  on  a dilation  develops 
above  the  constriction,  and  the  food  is  retained  longer.  Then 
regurgitation  occurs  between  meals.  The  food  which  is  brought 
up  is  usually  covered  with  mucus  ; in  carcinoma,  with  blood  and 
mucus,  and  it  is  then  in  a state  of  putrefaction.  The  food  is  gen- 
erally neutral  or  slightly  alkaline.  Its  chemical  character  gives 
no  evidence  of  its  having  entered  the  stomach.  Blood  in  the 
regurgitated  food  may  come  from  carcinoma,  ulcer,  or  cardio- 
esophageal  veins  in  a state  of  passive  congestion. 

For  the  physical  signs  of  stenosis  of  the  cardia  see  page  566. 
The  condition  of  appetite  and  thirst  is  variable.  Generally,  the 
patients  complain  of  great  hunger  and  excessive  thirst. 

Diagnosis. — The  physical  inspection  of  the  abdomen  is  sugges- 


DIAGNOSIS  OF  STENOSIS  OF  THE  CARDIA.  655 

tive.  As  no  food  can  pass  the  stenosis,  the  stomach  and  the  intestine 
having  been  empty  for  a prolonged  period,  the  abdominal  walls  are 
very  much  retracted  and  sunk  in  beneath  the  level  of  the  costal 
arch.  In  attempting  to  locate  the  stenosis  by  introducing  an  esopha- 
geal sound,  a very  soft  instrument  should  at  first  be  used,  in  order  to 
avoid  injury  to  a possible  esophageal  or  gastric  ulcer  or  carcinoma. 
In  the  chapter  on  the  Technics  of  the  Stomach-tube  we  have  re- 
ferred to  a case  from  Penzoldt’s  clinic,  in  which  the  stomach  should 
have  been  washed  out  in  the  morning,  but,  for  some  reason,  this 
was  postponed  until  the  evening.  On  the  same  afternoon  the 
patient  died  of  rupture  of  an  aortic  aneurysm  into  the  esophagus. 
Stenosis  of  the  cardia  might  possibly  be  due  to  an  aortic  aneurysm, 
and  sounding  of  the  esophagus  may  lead  to  rupture  of  the  sac. 

The  constriction  is  generally  located  by  means  of  the  tube  as 
being  about  forty  centimeters  from  the  point  where  the  incisor 
teeth  touch  the  introduced  sound.  This  is  only  an  approximate 
figure,  as  the  length  of  the  esophagus  will  vary  with  the  height  of 
the  person.  In  one  case  of  carcinoma  of  the  cardia  in  our  experi- 
ence, the  tube  could  be  introduced  for  fifty  centimeters  before  it 
struck  the  stenosis.  (For  rules  to  determine  the  length  of  the 
esophagus  in  any  individual,  see  Hemmeter,  “ New  York  Medical 
Journal,”  December  28,  1895,  quoted  on  p.  1 1 5 of  this  volume.) 
In  case  of  carcinoma  patient  research  will  eventually  result  in  the 
discovery  of  a fragment  of  the  neoplasm  which  in  these  cases  is 
generally  found  in  the  eye  of  the  tube.  Cardiospasm  occurs 
mainly  in  neuropathic  individuals.  It  differs  from  the  organic 
stenosis  of  the  cardia  from  the  fact  that  the  obstruction  is  not 
constant,  but  intermittent.  Large  sounds  will  pass  as  readily 
as  small  ones  after  a little  practice  in  the  introduction,  and  the 
stenosis  will  disappear  entirely  under  anesthesia. 

Prognosis. — Though  dependent  on  the  fundamental  alteration 
causing  the  stenosis,  it  is  generally  unfavorable,  except  in  cardio- 
spasm. Prognosis  is  absolutely  hopeless  in  carcinoma.  When  the 
stenosis  is  due  to  cicatricial  contraction,  the  orifice  may  remain 
patent  sufficient  to  carry  on  nutrition,  and  for  a long  time  the 
narrowing  process  may  appear  stationary. 

Treatment. — The  treatment  is,  in  the  main,  the  same  as  for 
carcinoma  of  the  cardia  (vide).  Nutritive  enemata  are,  in  my  ex- 
perience, best  used  as  soon  as  the  diagnosis  of  obstruction  is 
certain,  even  if  a limited  amount  of  food  can  be  introduced  through 
the  mouth.  Stenosis  due  to  cicatricial  contraction  can  be  succes- 


656 


MOTOR  INSUFFICIENCY. 


fully  treated  by  gradual  dilation  of  the  constriction  by  means  of 
sounds  of  greater  and  greater  thickness. 

Sometimes  the  cardiospasm  is  due  to  an  ulcer  that  has  been 
healing  very  slowly,  or  possibly  to  a small  erosion  due  to  the 
passing  violence  of  some  sharp  body  in  the  food.  In  one  case  of 
dysphagia,  which  was  due  to  ulcer  of  the  cardia,  we  relieved  the 
pain  and  made  swallowing  possible  by  a kind  of  local  treatment. 
A small  sponge,  saturated  with  a four  per  cent,  solution  of  cocain, 
was  placed  in  the  end  of  a stomach-tube  that  had  only  a side 
opening,  the  lower  end  of  the  tube  being  bluntly  closed ; when 
the  lateral  opening  had  reached  the  stenosis,  the  cocain  solution 
was  pressed  out  by  a wire  which  terminated  in  a small  round  ball 
resting  upon  the  sponge,  and  emptied  the  cocain  on  the  painful 
surface. 

Patients  with  stenosis  of  the  cardia  fear  starvation,  and  justly 
so.  The  moral  effect  of  sufficient  nutrition  is  a great  one.  I 
am  in  the  habit  of  feeding  all  patients  into  whom  a tube 
can  be  passed  at  least  three  times  daily  with  food  represent- 
ing a caloric  value  beyond  what  is  really  required.  Benign 
strictures  of  the  lower  end  of  the  esophagus  and  of  the  cardia 
have  been  cured  by  the  patients  themselves,  after  they  had  ac- 
quired the  technic  of  sounding  and  dilation.  The  longer  the 
sound  remains  in  position  after  it  has  passed  the  stenosis,  the 
more  effective  will  be  the  widening  process.  Leyden  has  suc- 
cessively employed  permanent  cannulas,  which  remain  in  situ  for 
several  days.  He  has  even  employed  them  in  carcinomatous  con- 
strictions in  the  lower  end  of  the  esophagus.  These  cannulas  can 
be  introduced  by  the  aid  of  the  stomach-tube.  They  are  from 
six  to  eight  centimeters  long,  and  are  attached  by  means  of  strong 
cords  to  the  ear  or  around  the  neck.  The  diet  should  consist  of 
raw  eggs,  milk,  thin  chocolate,  meat  powder,  somatose,  gelatin  ; 
also  ice-cream  and  frozen  custard  may  be  allowed,  but  must  be 
warmed  in  the  mouth  and  eaten  slowly.  Egg-nog  should  not  con- 
tain too  much  brandy.  Not  much  should  be  expected  from  medici- 
nal treatment.  Morphin  or  codein  can  not  be  avoided  for  the  relief 
of  pain.  For  the  pain  of  cancer  of  the  cardia  we  have  found  chloral 
hydrate  (gr.  xv,  t.  i.  d.)  especially  effective.  Iodid  of  potassium 
and  sodium,  methylene-blue,  and  arsenic  have  been  recommended 
for  cancerous  stricture.  Personally,  I have  no  faith  in  these 
medications.  The  iodids  should  be  tried,  however,  if  there  is  a 
suggestion  or  evidence  of  syphilis  about  the  case.  When  a dila- 


OBSTRUCTION  OF  THE  PYLORUS. 


657 


tion  of  the  esophagus  has  formed  above  the  constriction,  it  is 
well  to  wash  out  the  pouch  every  morning,  as  one  would  wash  out 
a dilated  stomach.  This  will  prevent  a septic  esophagitis.  The 
mouth,  nose,  and  throat  should  be  kept  disinfected  by  antiseptic 
sprays  and  gargles. 

Gastrostomy  will  prolong  life  if  performed  early  enough.  In 
our  experience  even  if  the  stenosis  is  due  to  a carcinoma,  it  will 
not  progress  so  rapidly  when  it  is  kept  free  from  food,  and  disin- 
fected daily  by  lavage  from  above.  But  when  gastrostomy  is  un- 
dertaken in  benign  stenosis,  it  not  only  makes  possible  the  proper 
feeding  of  the  patient,  but  the  stenosis  can  be  dilated  after  the 
operation  by  intubation  from  the  gastric  end  of  the  esophagus. 

Exploratory  laparotomy  may  reveal  the  fact,  unknown  before  the 
operation,  that  although  the  stenosis  of  the  cardia  was  due  to  a 
carcinoma,  this  neoplasm  was  sufficiently  below  the  diaphragm  to 
be  entirely  removed.  The  recent  success  of  Brigham  and  Schlatter 
after  a total  extirpation  of  the  stomach  makes  it  conceivable  that 
large  portions  of  the  cardiac  end  and  fundus  can  be  removed,  and 
the  remainder  of  the  healthy  stomach  or  the  jejunum  attached  to 
the  stump  of  the  esophagus.  (See  section  on  Surgical  Treatment 
of  Organic  Diseases.) 

Obstruction  of  the  Pylorus. 

Stenosis  of  the  pylorus  is,  in  the  majority  of  cases,  a consequence 
of  organic  disease.  Idiopathically  it  occurs  very  rarely  in  chil- 
dren in  the  form  of  congenital  atresia.  Meltzer  and  Adler  each 
reported  one  such  case  to  the  meeting  of  the  Association  of 
American  Physicians  in  May,  1898.  Maier  has  collected  thirty-one 
cases  of  this  kind  (“  Virchow’s  Archiv,”  Bd.  cn).  The  stenosis 
due  to  pylorospasm  is  described  in  chapter  IX.  The  pylorus  may 
become  obstructed  by  a swallowed  foreign  body  that  may  become 
lodged  in  it,  by  a gall-stone,  or  a gastrolith.  Hypertrophic  pyloric 
stenosis  has  been  considered  in  a special  chapter.  Obstruction  due 
to  benign  tumors  is  exceedingly  rare  ; such  abnormalities  are  not 
discovered  except  at  autopsies.  Dr.  W.  S.  Thayer,  of  the  Johns 
Hopkins  Hospital,  has  related  to  the  writer  a case  in  his  experience 
in  which  obstruction  of  the  pylorus  had  been  caused  by  a fibroma. 
For  further  information  concerning  benign  tumors,  foreign  bodies, 
gastroliths,  etc.,  the  reader  is  referred  to  chapter  vi,  of  part  in. 
Scar  tissue  may  develop  in  the  neighborhood  of  the  outlet  of  the 
stomach  as  a result  of  the  destructive  action  of  corrosive  poison. 


658 


MOTOR  INSUFFICIENCY. 


This  is  also  a rare  occurrence,  since  chemicals  that  are  swallowed 
in  sufficient  quantity  to  destroy  the  pyloric  tissue  would,  most  prob- 
ably, cause  death  by  the  injury  they  inflict  on  the  esophagus  and 
portions  of  the  stomach.  The  outlet  of  the  stomach  may  be  com- 
pressed by  tumors  developing  in  its  vicinity,  such  as  pancreatic 
cysts,  malignant  tumors  of  the  pancreas,  liver,  and  omentum,  fecal 
concretions  in  the  colon.  The  lodgment  of  a large  gall-stone  in 
the  common  bile-duct  or  in  the  duodenum  has  been  known  to  have 
the  same  effect. 

Perigastritis  and  peritonitis  may  effect  stenosis  of  the  pylorus  by 
constricting  bands  of  fibrous  tissue.  The  author  has  reported  a 
case  of  persistent  gastralgia  in  a negro,  operated  upon  on  his 
advice  by  Dr.  John  D.  Blake.  The  stomach  was  bound  down  to 
the  liver,  diaphragm,  and  transverse  colon  by  numerous  adhesions. 
Those  going  to  the  liver  had  produced  an  absolute  stenosis  of  the 
pylorus. 

Syphilitic  and  tubercular  ulcers  (see  chapter  devoted  to  this  sub- 
ject) are  very  rare  in  the  stomach.  In  one  case  of  tubercular 
ulceration  extending  through  the  pylorus  into  the  duodenum  the 
author  found  this  orifice  normally  permeable. 

A number  of  the  causes  enumerated  may  also  bring  about 
duodenal  stenosis  and  obstruction,  which  is  often  clinically  indis- 
tinguishable from  pyloric  obstruction. 

Peptic  ulcer  may  effect  constriction  of  the  outlet  of  the  stomach 
in  three  ways:  (1)  The  induration  inflammatory  thickening  of  the 
edges  of  the  ulcer  may  encroach  upon  the  lumen  of  the  pylorus  ; 

(2)  the  pain  and  irritation  of  the  ulcer  may  cause  pylorospasm  ; 

(3)  in  healing  the  contraction  of  the  cicatrix  may  effect  a deformity 
of  the  pyloric  canal.  The  most  frequent  cause  of  pyloric  obstruc- 
tion is  cancer.  From  the  tables  referred  to  previously,  it  is  evident 
that  ulcer  affects  the  pylorus  in  12  per  cent,  of  793  cases  collected 
by  Welch  ; and  carcinoma  occurred  in  the  pyloric  region  in  60.8 
per  cent,  of  1300  cases  of  cancer  collected  by  the  same  author. 

Symptomatology. — The  symptoms  of  pyloric  stenosis  may  be 
arranged  under  three  headings — compensation,  stagnation,  and 
retention — which  represent  degrees  and  phases  of  the  conse- 
quences of  the  obstruction.  This  classification  of  the  symptoms 
has  been  ingeniously  followed  out  by  Van  Valzah  and  Nisbet 
(“  Diseases  of  the  Stomach,”  p.  584).  Not  all  cases  present  these 
three  degrees,  for  whenever  the  stenosis  is  malignant,  the  stage  of 
compensation  does  not  occur.  The  results  of  stenosis  are  familiar 


SYMPTOMS  OF  PYLOKIC  OBSTRUCTION.  659 

from  the  analogies  with  stenosis  of  other  hollow  muscular  organs, 
such  as  the  heart  and  the  bladder.  When  the  pylorus  is  nar- 
rowed, the  stagnating  ingesta  may  influence  the  musculature  in  two 
diagonally  opposite  ways.  They  may  effect  a stretching  and  dila- 
tation, or  constitute  an  incentive  to  the  gastric  musculature  bring- 
ing on  increased  contraction  and  peristaltic  unrest.  The  result 
that  will  be  produced  depends  upon  the  state  of  nutrition  of  the 
musculature  at  the  time  the  stenosis  occurs.  We  exclude  malignant 
tumors  as  agents  causing  the  increase  of  gastric  musculature  by 
hyperplasia  of  the  normal  tissues.  If  the  gastric  muscular  fiber  is 
well  nourished,  new  formation  of  muscle-fibers  and  increased  con- 
traction will  result.  This  constitutes  the  stage  of  compensation. 
But  if  they  are  badly  nourished,  a dilation  of  the  stomach  will 
result,  leading  to  stagnation  and  retention,  so  that  development 
of  dilation  on  one  hand  or  hypertrophy  on  the  other,  depends 
largely  upon  the  state  of  nutrition  of  the  gastric  muscle.  But 
if  the  obstruction  persists,  which  it  does  as  a rule,  the  distention 
of  the  gastric  wall  and  consequent  permanent  dilation  will 
eventually  supervene,  although  compensation  had  been  for  a time 
established.  In  case  the  constriction  be  moderate  and  remains 
so,  and  overburdening  of  the  gastric  wall  be  carefully  avoided,  a 
normal  volume  of  the  hypertrophic  stomach  will  persist  for  a long 
time.  There  are  three  factors  that  control  the  advent  of  stagna- 
tion and  retention — (i)  the  width  of  the  outlet,  (2)  the  bulk  and 
weight  of  the  ingesta,  and  (3)  the  neuromuscular  energy  of  the 
expulsive  force.  Thus,  stagnation  and  retention  may  be  caused  by 
gastric  atony  or  myasthenia,  because  the  expulsive  force  is  not 
sufficient  to  expel  the  contents.  It  may  occur  after  excessive  bur- 
dening of  the  stomach  by  ingesta,  because  the  weight  on  the  gas- 
tric contents  is  too  heavy  for  the  musculature. 

Hyperacidity  and  supersecretion  may  cause  stagnation  and 
retention  of  food  by  producing  a secondary  pyloric  spasm.  The 
tonic  contractions  of  the  pylorus  in  excessive  secretion  of  acid 
gastric  juice  appears  to  be  a precaution  to  prevent  undue  acidifica- 
tion of  the  duodenal  digestive  juices.  A small  quantity  of  free 
HC1  has  little  or  no  retarding  influence  on  the  diastatic  action  of 
pancreatic  juice  (Rachford),  but  a very  acid  gastric  chyme  renders 
the  ferments  of  the  pancreatic  juice  inoperative.  As  a rule,  the 
dilation  of  the  stomach  is  secondary  to  the  stenosis;  but  there 
are  very  rare  and  curious  cases  in  which  the  stenosis  is  caused 
by,  and  secondary  to,  the  dilatation.  (See  chapter  on  Motor 


66o 


MOTOR  INSUFFICIENCY. 


Insufficiency.)  When  distention  and  dilation  have  been  caused 
by  overburdening  the  stomach,  hypertrophy  of  the  musculature 
may  counteract  stagnation  and  retention  ; but  if  the  musculature 
is  incapable  of  resistance  of  further  development,  the  overdis- 
tention of  the  stomach  may  distort  the  lumen  of  the  pylorus,  pro- 
ducing a secondary  stenosis.  I have  reported  a number  of  cases 
in  which  the  stomach  was  of  normal  size  when  empty,  but  showed 
all  the  evidences  of  dilation  when  filled  with  food.  At  the  opera- 
tion a rather  sharp  bend  in  the  duodenum  just  beyond  the  pylorus 
was  discovered  by  the  author.  This  kinking  of  the  duodenum 
was  effected  by  traction  when  the  stomach  was  overdistended. 
Kussmaul  (“  Peristalt.  Unruhe  d.  Magens,”  Volkmann’s  Vortrage, 
Nr.  1 8 1 ) has  described  a similar  condition  in  the  duodenum  pro- 
duced secondarily  by  dilated  stomachs,  and  reproduced  the  ab- 
normality experimentally  in  the  cadaver.  Stenosis  of  the  pylorus, 
as  far  as  the  relation  between  (i)  expulsive  power  and  (2)  bulk  of 
gastric  chyme  are  concerned,  may  be  ( a ) absolute  or  ( b ) relative. 
(See  p.  477.)  In  such  conditions  of  secondary  stenosis,  although  the 
constriction  may  not  be  absolute,  yet  it  may  be  relative  because 
it  may  not  suffice  for  the  exit  of  the  large  quantity  of  the  gastric 
contents ; or,  again,  even  when  the  contents  are  not  excessive,  the 
width  of  the  outlet  may  be  relatively  too  small  for  the  contractile 
power  of  the  musculature. 

Congenital  Pyloric  Stenosis. — The  subject  of  congenital  hy- 
pertrophic stenosis  of  the  pylorus  in  infants  has  been  ably  reviewed 
in  an  article  by  S.  J.  Meltzer  (“  New  York  Medical  Record,”  Aug. 
20,  1898),  in  which  he  adds  a new  case  to  the  literature  of  this  sub- 
ject. A histological  examination  of  the  stomach,  after  the  autopsy, 
was  made  by  T.  Mitchell  Prudden,  showing  the  thickening  of  the 
pylorus  to  have  been  largely  due  to  the  presence  of  dense  fibrous 
tissue  in  the  submucosa,  and  to  a hyperplasia  of  the  inner  mus- 
cular layer,  especially  of  the  proximal  half  of  the  pyloric  portion. 
The  moderate  thickening  of  the  wall  of  the  gastroduodenal  valve, 
which  could  be  seen  as  a prominence  when  viewed  from  the  duo- 
denal side,  was  almost  wholly  due  to  fibrous  hyperplasia  in  the 
submucosa.  At  the  proximal  end  of  the  pyloric  portion  the  thick- 
ening was  due  to  increase  in  the  submucosa  and  inner  muscular 
layer.  The  external  muscular  layer  presented  no  abnormality. 
Like  others  who  have  considered  this  subject,  Meltzer  divides  the 
life-history  of  this  stomach  into  three  phases — (1)  the  phase  of 
simple  insufficiency,  (2)  of  attempted  compensation,  and  finally  (3) 


CONGENITAL  PYLORIC  STENOSIS. 


66 


the  phase  of  atony  and  dilation.  The  stomach  of  this  neonatus 
when  completely  filled  for  the  first  time  was  not  able  to  empty  it- 
self thoroughly  in  the  interval  before  the  second  feeding;  only  a 
part  of  its  contents  could  be  evacuated  into  the  intestines.  A por- 
tion remained  behind  in  the  stomach,  and  was  present  there  when 
the  second  feeding  took  place.  This  same  partial  retention  occur- 
ring with  every  feeding  finally  led  to  overdistention,  which,  in 
turn,  evoked  the  increased  contractility  of  the  muscularis,  followed 
by  a somewhat  greater  quantitative  expulsion  of  the  contents  into 
the  intestine.  But  as  the  accumulation  of  remnants  in  the  stomach 
had  been  proportionately  greater  before  this  extraordinary  mus- 
cular effort  took  place,  the  balance  remaining  in  the  stomach  was, 
notwithstanding,  greater  now  than  in  the  foregoing  interval. 
Finally,  a stage  will  come  when  the  muscular  fibers  make  their 
extremest  effort  upon  the  accumulation  of  the  several  balances  in 
the  stomach ; this  extreme  effort  results  in  the  expulsion  of  the 
entire  contents  by  vomiting.  This  stage  is  that  of  insufficiency. 
The  stomach  is  unable  to  empty  its  contents  entirely  into  the  in- 
testine, but  it  is  not  yet  in  a state  of  dilation.  The  muscularis 
still  retains  its  tonicity.  The  constant  overdistention  in  the  method 
I have  previously  described  causes  the  development  of  a varied 
degree  of  muscular  hypertrophy,  which,  when  once  accomplished, 
causes  the  stomach  to  respond  even  to  moderate  overdistention 
with  very  powerful  contraction,  so  that  the  entire  gastric  contents 
may  be  expelled  through  the  cardiac  orifice.  The  frequent  repeti- 
tion of  this  form  of  evacuation  may  then  bring  on  insufficiency  of 
the  cardia.  Frequent  vomiting  generally  starts  with  the  develop- 
ment of  the  compensating  hypertrophy  of  the  gastric  muscularis. 
The  unnecessarily  strong  contraction  effects  a partial  dilation  of 
the  pyloric  stenosis  in  a similar  manner  as  it  overcomes  the  nor- 
mal contraction  of  the  cardia.  It  is  also  instrumental  in  the  ab- 
normal distention  of  the  fundus,  for  in  this  portion  the  muscularis 
is  very  thinly  developed,  and  does  not  take  part  in  the  hypertrophy 
that  is  so  prominent  toward  the  pyloric  end.  During  the  power- 
ful contraction  of  the  hypertrophied  pyloric  portion  the  gastric 
contents  are  driven  into  the  fundus,  which  is  incapable  of  much 
resistance,  and  gradually  becomes  distended  and  dilated.  As  it  is 
impossible  for  the  contracting  pyloric  portion  to  evacuate  all  of  the 
chyme,  a considerable  portion  must  remain  in  the  most  dilatable 
portion  of  the  stomach.  This  is  the  fundus.  As  the  accumulated 
balances  of  many  feedings  become  larger  and  larger,  in  proportion 
44 


662 


MOTOR  INSUFFICIENCY. 


to  the  increased  size  of  the  fundus,  the  hypertrophied  pyloric  end 
finally  exhausts  itself  in  its  efforts  to  overcome  the  obstruction : it 
loses  its  contractility,  the  muscular  fibers  may  become  degener- 
ated through  overexertion,  and  eventually  the  third  phase,  that  of 
gastrectasis,  is  reached. 

The  body  is  insufficiently  nourished  long  before  this  ; in  the  phase 
of  compensation  it  begins  to  suffer,  and  though  with  the  increased 
pressure  within  the  stomach  a greater  transmission  of  food  into 
the  intestine  takes  place,  the  amount  passed  is  inadequate  for  the 
nutrition  of  the  body. 

This  detailed  description  of  the  mechanism  of  pyloric  insuffi- 
ciency and  the  consequent  stages  of  compensation  and  dilation 
was  considered  necessary  because  it  represents,  in  rough  outlines, 
exactly  what  occurs  in  every  case  of  pyloric  stenosis,  excepting, 
perhaps,  those  cases  due  to  carcinoma.  Here  the  carcinomatous 
invasion  and  the  consequent  putrefaction  and  gastrectasis  prevent 
the  stage  of  compensation. 

Diagnosis. — In  the  first  stage  the  greediness  which  the  child 
displays  in  taking  the  nursing-bottle  and  the  constant  crying 
should  suggest,  the  possibility  of  congenital  stenosis  of  the  pylorus. 
A catheter  should  be  introduced  into  the  stomach  about  two  hours 
after  feeding,  and  the  organ  evacuated.  The  amount  of  the  pre- 
vious feeding  must  be  known.  If  there  is  a residual  balance  in  the 
stomach,  it  is  evident  that  an  insufficiency  is  present.  In  the 
second  stage  Meltzer  places  reliance  on  the  following  symptoms: 
The  change  of  the  area  of  percussion  with  the  degree  of  filling  of 
the  stomach ; the  appearance  of  peristaltic  waves  over  the  region 
of  the  stomach  ; palpation  of  the  contracted  stomach  in  an  empty 
state.  In  the  stage  of  compensated  hypertrophy  the  frequent 
vomiting  immediately  after  drinking,  the  absence  of  vomiting  at 
any  other  time,  the  absence  of  bile  from  the  vomit,  and  its  non- 
catarrhal  appearance  are  characteristic  symptoms.  The  diagnosis 
of  the  last  stage,  the  gastrectasis,  should  offer  no  difficulty.  The 
stomach  may  be  filled  with  air  or  water,  when  palpation  and 
percussion  will  give  evidence  of  the  dilation.  When  air  is 
blown  into  the  partly  filled  stomach,  a gurgling  sound  can  be 
localized  at  an  abnormally  low  level  by  means  of  the  stetho- 
scope. Simple  inspection  will  reveal  the  bulging  upper  part  of 
the  abdomen,  while  the  lower  part  is  in  a collapsed  state.  W. 
Soltau  Fenwick  (“  Disorders  of  Digestion  in  Infancy  and  Child- 
hood ”)  was  able  to  examine  the  contents  of  such  an  infant 


TREATMENT  OF  CONGENITAL  STENOSIS.  663 

stomach,  after  a test-meal,  and  found  that  the  secretion  of  HC1 
was  normal. 

Prognosis. — The  disease  usually  proves  fatal  within  the  first 
three  months  of  infant  life,  very  frequently  within  a few  weeks. 
Few  children  having  congenital  stenosis  of  the  pylorus  live  to  attain 
adult  life.  It  seems  that  the  disease  is  not  necessarily  fatal 
within  itself,  but  becomes  so  because  it  is  not  recognized.  With 
an  early  diagnosis  and  proper  treatment  the  lives  of  some  of  these 
infants  might  be  saved.  Four  children  are  on  record  as  having 
been  kept  alive  by  these  means — three  cases  published  by  Heub- 
ner (/.  c.)  and  one  by  Henschel  (/.  c.). 

Treatment. — The  palliative  treatment  consists  in  regulation  of 
the  feeding,  and  frequent  washing  of  the  stomach.  The  advice  of 
Meltzer  to  give  a slightly  larger  amount  of  milk  than  the  normal 
capacity  of  the  stomach  in  the  first  stage  of  the  trouble — in  order 
to  bring  out  better  contraction  of  the  muscular  tissue,  and  drive 
more  food  into  the  intestines,  and  thereby  effect  dilation  of  the  py- 
lorus— seems  to  me  a doubtful  procedure.  Overburdening  of  the 
gastric  walls  can  do  nothing  but  harm,  and  the  expected  increase 
of  muscular  contraction  may  not  take  place.  We  can  not  tell  the 
condition  of  the  nutrition  of  the  muscular  layer.  Washing  the 
stomach  with  a one-half  of  a one  percent,  solution  of  Carlsbad  salts 
is  recommended  by  Heubner.  A very  small  piece  of  tenacious 
mucus  or  a coagulum  of  milk  sticking  in  the  pylorus  may  be  suf- 
ficient to  make  this  passage  absolutely  impenetrable.  Hence  the 
utility  of  lavage.  Massage  of  the  stomach  has  been  recommended. 
Rectal  enemata  of  milk  and  egg-albumen  will  support  the  strength 
of  the  little  patient.  But  the  only  curative  procedure  is  opera- 
tion. There  have  been  cases  when  the  infant  lived  a number 
of  years  without  operation  ; but  in  view  of  the  rapid  advances  of 
gastric  surgery,  and  the  positive  and  permanent  relief  accruing 
from  a successful  gastro-enterostomy,  operation  should  be  urged 
whenever  the  diagnosis  can  be  clearly  established. 


LITERATURE  ON  CONGENITAL  HYPERTROPHIC  STENOSIS  OF 
THE  PYLORUS  IN  INFANTS. 

1.  Ashby,  H.,  “Archives  of  Pediatrics,”  1897. 

2.  Finkelstein,  “ Jahrbuch  f.  Kinderheilk.,”  vol.  vm,  1896,  p.  105. 

3.  Thompson,  “On  Congenital  Gastric  Spasm,”  “The  Scottish  Med.  and 
Surg.  Jour.,”  1897. 

4.  Henschel,  “ Archiv  f.  Kinderheilk.,”  vol.  xm,  1891,  p.  32. 


664 


MOTOR  INSUFFICIENCY. 


5.  Schwyzer,  “ New  York  Med.  Jour.,”  1897. 

6.  Rolleston  and  Haynes,  “British  Med.  Jour.,”  April  23,  1898,  p.  1070. 

7.  Williamson,  “ London  and  Edinburgh  Monthly  Jour,  of  Med.  Sciences,” 
1841,  p.  23. 

8.  Davoski,  “Caspar’s  Wochenschrift,”  1842,  No.  7. 

9.  Hirschsprung,  “ Jahrbuch  f.  Kinderheilk.,”  vol.  xxvm,  1888,  p.  61. 

10.  Gran,  “Jahrbuch  f.  Kinderheilk.,”  vol,  xliii,  1896,  p.  118. 

11.  Landerer,  “ Ueber  angeborene  Stenose  des  Pylorus,”  Dissert.,  Tubingen, 
1879. 

12.  Maier,  Rud.,  “Virchow’s  Archiv,”  vol.  cil,  1885,  p.  413. 

13.  Meltzer,  S.  J.,  “ N.  Y.  Med.  Rec.,”  Aug.,  1898. 

14.  Huebner,  Quoted  by  Finkelstein. 

15.  Peden,  “ Glasgow  Med.  Jour.,”  1889,  p.  416. 

16.  Pitt,  “Trans.  Path.  Soc.,”  London,  1889,  p.  63. 

17.  De  Bruin  Kops,  “ Nederlandsch.  Tijdschrift  voor  Geneeskunde,”  1896, 
No.  19.  (After  Thomson.) 

18.  Thomson,  “ Edin.  Hosp.  Reports,”  vol.  iv,  1896,  p.  116. 

19.  Schwyzer,  “ New  York  Med.  Jour.,”  Nov.  21,  1896. 

20.  Fenwick,  “The  Disorders  of  Digestion  in  Infancy  and  Childhood,” 
London,  1897. 

21.  Loesschaft,  “ Jahrbuch  f.  Kinderheilk.,”  vol.  xxii,  p.  164. 

22.  Brandt,  “ Die  Stenose  des  Pylorus,”  Dissert.,  Jena,  1851. 


For  Obstruction  of  the  Pylorus  Caused  by  Cicatrices,  Pep- 
tic Ulcer,  or  Carcinoma,  see  the  chapters  devoted  to  these  sub- 
jects. 

Various  Symptoms  After  Different  Causes  of  Obstruction. 
— The  stages  of  (1)  insufficiency,  (2)  compensation,  and  (3)  atony 
and  dilation  with  the  attendant  stagnation  and  retention,  are 
present  in  all  forms,  except,  perhaps,  a rapidly  developing  pyloric 
carcinoma.  In  the  benign  stenoses  the  first  period  is  generally 
overlooked  ; but  dietetic  errors  bring  on  attacks  of  gastric  pain  of 
increasing  severity,  which  are  generally  relieved  by  vomiting. 
The  vomited  food  contains,  in  most  cases,  more  liquid  than  has 
been  swallowed,  which  is  explained  by  the  investigations  of  von 
Mering,  who  demonstrated  that  when  the  stomach  contained 
absorbable  substances  (alcohol,  salts,  sugar,  dextrin,  peptone)  and 
their  transition  into  the  intestine  is  prevented,  absorption  takes 
place  more  or  less  in  the  stomach  itself,  but  simultaneously  with 
it  an  excretion  of  water  occurs  into  the  stomach.  This  liquid 
can  not  find  an  outlet  through  the  pylorus,  and  is  expelled  during 
the  attacks  of  vomiting.  The  vomit  under  such  conditions  con- 
tains an  abundance  of  mucus,  and  often  an  excess  of  free  and  com- 
bined HC1.  After  the  emesis  the  pain  subsides.  It  may  happen 


EFFECTS  OF  VARIOUS  FORMS  OF  STENOSIS.  665 

that  the  very  next  meal  may  pass  the  pylorus,  because  perfect 
compensation  has  been  established.  There  is  invariably  a persistent 
constipation.  At  the  onset  the  intermissions  between  the  attacks 
extend  for  months,  in  which  there  is  perfect  freedom  from  pain 
and  vomiting;  but  as  the  stage  of  atony  and  dilation  is  ap- 
proached, the  stenosis  meanwhile  having  become  more  absolute, 
the  attacks  occur  more  frequently,  until  they  finally  take  place 
regularly  after  every  large  meal. 

When  the  period  of  stagnation  has  become  established,  pain  is 
usually  present  whenever  food  is  taken  into  the  stomach.  The 
vomit  gives  the  chemical  evidences,  and  sometimes  also  the  histo- 
logical evidences,  of  gastritis.  In  the  retention  of  dilation  the 
vomiting  is  not  so  frequent,  but  more  copious.  The  amount 
of  free  and  combined  HC1  gradually  becomes  less  and  less,  even 
when  the  stenosis  is  benign ; this  is  due  to  the  progressing  gas- 
tritis. Now,  the  conditions  favorable  to  the  development  of  lactic 
acid  are  present;  these  are:  (i)  Impaired  gastric  motility;  (2) 
absence  of  HC1;  (3)  reduction  of  albumen  digestion;  (4)  impaired 
absorption ; and  (5)  presence  of  lactic  acid  bacteria.  Acetic  and 
butyric  acids  are  present  if  the  original  substances  from  which 
they  can  develop  were  contained  in  the  food  (alcohol-butter).  The 
gastric  contents  after  being  drawn  separate  into  three  layers ; and 
if  the  stenosis  is  benign,  usually  contain  the  products  of  pepsin 
digestion.  The  quantity  of  urine  is  small,  its  amount  being  in  pro- 
portion to  the  degree  of  the  stenosis  and  retention.  The  appetite 
is  lost,  severe  cachexia  develops,  and  the  case  may  end  fatally  if 
not  properly  treated.  The  foregoing  is  the  usual  course  with  a 
benign  stenosis,  such  as  may  occur  with  hypertrophy  of  the 
pylorus  or  benign  tumor. 

The  symptomatology  after  a stenosis  due  to  gastric  ulcer  may 
present  peculiarities.  If  an  ulcer  is  located  in  the  pylorus,  it  may 
begin  with  its  usual  classical  signs  and  symptoms.  A stenosis 
may  develop  from  the  inflammatory  swelling  and  induration  sur- 
rounding the  ulcer;  or,  later  on,  as  a result  of  cicatricial  contraction 
when  the  ulcer  heals.  Chronic  peptic  ulcer  still  in  its  progressive 
stage  does  not  give  rise  to  hemorrhage  nearly  so  frequently  as 
the  acute  ulcer  located  in  other  parts  of  the  stomach.  When  the 
obstruction  is  developed,  there  is  usually  vomiting,  occurring  from 
one-half  to  three  hours  after  meals  but  occasionally  containing 
food  taken  twelve  hours  previously. 

There  may  be  stagnation,  retention,  and  fermentation,  as  in  sten- 


666 


MOTOR  INSUFFICIENCY. 


osis  caused  by  other  benign  obstructions.  We  have  observed  cases 
in  which  the  symptoms  of  vomiting,  pain,  and  retention  entirely 
disappeared  after  the  ulcer  was  brought  to  healing  by  proper 
treatment.  The  patients  remained  apparently  cured  for  a period 
varying  from  six  months  to  two  years,  when  the  same  symptoms 
and  evidences  of  retention  returned,  which  in  a number  of  our  cases 
were  proved  to  be  due  to  the  contracting  cicatrix  at  the  operation. 
Thus,  the  clinical  history  of  obstruction  due  to  peptic  ulcer  may 
extend  over  as  many  years  as  that  of  hypertrophic  stenosis. 

The  Appetite. — The  appetite  is  absent  in  carcinoma;  it  is 
present  or  exaggerated  in  ulcer  and  benign  hypertrophy ; as  a rule, 
it  will  vary  with  the  state  of  gastric  cleanliness.  In  all  conditions 
when  there  is  much  gastric  fermentation,  the  appetite  is  dimin- 
ished. 

Thirst  is  normal  whenever  compensation  is  perfect;  but  may 
cause  much  suffering  during  retention. 

Fullness,  Distention,  Pressure,  and  Pain. — The  overloaded 
stomach  gives  rise  to  a sense  of  uneasiness.  The  increased  con- 
tractions during  compensation  frequently  cause  distress.  The 
contractions  of  a hypertrophic  or  ulcerated  pylorus  cause  severe 
pain,  which  becomes  most  intense  when  a struggle  occurs  between 
the  antagonistic  contractions  of  the  stomach  and  pylorus. 

Nausea  and  Vomiting. — These  symptoms  as  they  occur  in 
gastritis,  ulcer,  carcinoma,  hyperacidity,  hypertrophic  stenosis, 
congenital  pyloric  stenosis,  and  benign  tumors,  have  been  described 
in  the  chapters  devoted  to  these  subjects.  There  is  nothing  in- 
variably characteristic  in  the  nature  and  chemical  composition  of 
the  vomit  in  these  various  conditions  by  which  a diagnosis  could 
be  arrived  at.  The  chemical  differences,  as  far  as  they  are  of 
diagnostic  value,  have  been  described  in  the  chapters  referred  to. 

Emaciation,  Loss  of  Weight  and  Strength. — These  are  due 
to  the  albuminous  decomposition  brought  about  by  the  possible 
carcinoma,  but  more  frequently  by  the  fact  that  most  of  the  food 
is  vomited  and  can  not  enter  the  intestine.  It  is  possible  that 
autointoxication  may  be  instrumental  in  the  bodily  denutrition. 
It  must  not  be  overlooked  that  the  modern  ideas  of  intestinal 
autointoxication  are  nothing  but  hypotheses,  and  lack  sufficient 
experimental  foundation.  That  there  is  some  truth  in  it  we  do 
not  wish  to  deny,  but  much  hard  and  well-directed  work  is  neces- 
sary before  we  can  admit  of  the  intestinal  autointoxication  theory 
as  an  explanation  of  malnutrition. 


SYMPTOMS  OF  PYLORIC  OBSTRUCTION. 


667 


Tumor. — This  subject  has  been  thoroughly  ventilated  in  the 
chapter  on  Malignant  Neoplasm,  and  the  differentiation  of  gastric 
tumors  from  those  of  other  abdominal  organs  explicitly  stated. 
It  must  be  emphasized  again  that  when  the  pylorus  is  in  its  nor- 
mal position, — under  the  left  lobe  of  the  liver, — it  can  not  be  pal- 
pated, even  when  there  is  a tumor  present.  In  a case  recently 
operated  upon,  by  the  author’s  suggestion,  by  Professor  L.  M. 
Tiffany,  a pyloric  tumor  exceeding  the  size  of  a man’s  fist  was 
firmly  attached  by  adhesions  to  the  under  surface  of  the  liver. 
This  large  cancerous  mass  could  not  be  felt  because  it  was  firmly 
held  under  the  liver  and  out  of  the  way  of  any  possible  palpation. 

The  Cause  of  the  Stenosis  in  the  Duodenum. — When  gastric 
retention  and  dilation  are  caused  by  an  obstruction  in  the  duo- 
denum, the  exact  definition  of  the  diagnosis  is  difficult.  Among 
the  principal  causes  that  act  in  this  manner  are:  (1)  Twisting  and 
torsion  of  the  horizontal  part  of  the  duodenum,  brought  about  by 
partial  rotation  of  the  filled  stomach  when  the  abdominal  walls 
are  very  much  relaxed  (Kussmaul).  (2)  Indurated  ulcers  of  the 
duodenum.  (3)  Carcinoma  of  the  duodenum.  (4)  Carcinoma  of 
adjacent  organs,  liver,  gall-bladder,  pancreas,  colon,  omentum. 
(5)  Gall-stones  projecting  into  the  lumen  of  the  intestine,  and  act- 
ing directly  as  an  obstruction,  or  by  causing  an  adhesive  and 
stenosing  inflammation.  In  a case  described  by  Mikulicz  in  which 
the  stone  was  removed  by  gastrotomy,  this  inflammatory  indura- 
tion had  occurred  immediately  below  the  pylorus.  Among  the 
causes  that  act  externally  to  the  duodenum  we  should  mention 
also,  in  addition  to  the  tumors  of  the  neighboring  organs  referred 
to,  enlarged  lymph-glands  in  the  mesentery.  (6)  Cicatricial  adhe- 
sions after  round  ulcer,  or  purulent  gastritis,  or  former  inflamma- 
tions of  the  peritoneum,  such  as  pericolitis,  or  appendicitis.  (7) 
Traction  and  distortion  of  the  duodenum  and  pyloric  region, 
induced  by  large  herniae,  especially  scrotal  (Rokitansky). 

It  is  very  doubtful  whether  right-sided  floating  kidney  can  com- 
press the  duodenum  sufficiently  to  produce  gastrectasis,  and  Leube, 
Ewald,  Oser,  Nothnagel,  and  Kuttner  have  advanced  convincing 
arguments  against  such  an  assumption.  This  error  was  probably 
due  to  the  confounding  of  dilation  or  gastrectasis  with  atony  and 
particularly  with  gastroptosis.  These  are  affections  that  occur 
simultaneously  with  floating  kidney,  and  are  probably  due  to  com- 
mon causes,  such  as  relaxation  of  the  abdominal  muscles,  stretch- 
ing of  the  peritoneal  folds  known  as  ligaments.  I agree  with 


668 


MOTOR  INSUFFICIENCY. 


Riegel  that  gastroptosis  is  not  rarely  combined  with  gastrectasis, 
but  the  cause  of  this  by  dislocated  kidney  is  not  proved ; it 
is  conceded,  however,  that  a dislocated  right  kidney  which  has 
become  fixed  in  its  abnormal  position,  or  a kidney  that  has  in- 
creased enormously  in  size  may  compress  the  duodenum  and  cause 
a dilation. 

A definite  decision  concerning  the  various  causes  that  may  lead 
to  obstruction  of  the  pylorus  is  very  frequently  not  possible, 
although  every  attainable  diagnostic  moment  is  considered  care- 
fully. With  the  status  of  our  present  knowledge  of  diseases  of  the 
stomach  it  is  impossible  to  recognize  the  beginning  of  pyloric 
stenosis  with  precision,  and  the  practitioner  will  have  to  be  content 
if  he  is  enabled  to  decide  whether  the  dilation  and  retention  are 
due  to  a malignant  or  to  a benign  process.  In  the  writer’s  experi- 
ence all  further  deductions  made  from  the  clinical  phenomena  con- 
cerning the  particular  nature  and  origin  of  the  many  possible 
varieties  of  benign  stenosis  are  largely  conjectural.  The  differen- 
tial points  between  benign  and  malignant  pyloric  stenoses  have 
been  given  in  the  chapters  on  Carcinoma,  Ulcer,  and  Hypertrophic 
Stenosis  ; but  for  the  sake  of  convenience,  we  will  briefly  recapitu- 
late them  here. 

1.  Age. — Refer  to  the  tables  already  stated.  Malignant  tumors 
occur  at  a more  advanced  age,  but  it  must  not  be  overlooked  that 
the  age  of  carcinomatous  patients  is  receding,  and  that  malignant 
tumors  may  occur  at  a very  youthful  age;  therefore  this  moment 
is  of  not  much  utility  in  the  diagnosis. 

2.  Duration. — Benign  stenoses  last  for  many  years;  malignant 
processes  are  short,  generally  from  three  to  six  months,  only 
exceptionally  exceeding  one  year. 

3.  Course  and  Progress. — In  benign  stenosis  these  are  very 
variable.  Periods  of  tolerable  well-being  or  even  of  good  health 
alternate  with  periods  of  severe  sickness ; but  in  malignant  steno- 
sis the  aggravation  of  the  symptoms  is  progressive  and  continuous, 
notwithstanding  rational  treatment. 

4.  Tumor. — The  most  important  deciding  element  for  the  diag- 
nosis of  pyloric  stenosis  will  be  the  demonstration  of  a tumor,  but 
in  the  differentiation  between  benign  stenosis  and  carcinoma  the 
existence  of  tumor  is  of  little  value.  A tumor,  if  present,  may  as 
well  be  a benign  hypertrophy  as  cancer  ; and  if  it  is  absent,  it  does 
not  exclude  the  diagnosis  of  either  of  these  conditions. 


RELATIVE  VALUE  OF  DIAGNOSTIC  FACTORS.  669 

5.  Metastases. — If  these  can  be  palpated  in  other  abdominal 
organs, — for  instance,  in  the  liver  or  in  the  mesenteric  glands, — we 
have  a strong  evidence  in  favor  of  malignant  process.  The  same 
may  be  said  of  swelling  of  the  cervical  lymph-glands  occurring  in 
the  left  supraclavicular  region.  This  complication  is,  in  our  ex- 
perience, a rare  occurrence. 

6.  Edema. — If  other  causes  that  may  bring  on  edema  of  the 
ankles  may  be  excluded,  the  presence  of  this  symptom  is  sugges- 
tive of  a malignant  process,  but  absence  of  this  symptom  does  not 
argue  against  carcinoma.  It  is  a late  symptom. 

7.  Hematemesis. — In  my  experience  blood  is  contained  in  the 
vomit  in  one-half  of  all  cases  of  gastric  cancer.  Large  quantities 
of  blood  are  rarely  vomited,  but  the  characteristic  cofifee-ground 
vomit,  in  consequence  of  stagnation  and  decomposition  of  the 
blood,  is  diagnostically  important.  The  more  copious  the  effu- 
sions of  blood  into  the  stomach,  the  quicker  do  they  cause  vomit- 
ing; for  that  reason  the  abundant  hemorrhages  in  ulcer  are  often 
vomited  uncoagulated  and  very  little  altered,  whereas  the  smaller 
amounts  of  blood  in  carcinoma  and  gastritis  remain  in  the  stomach 
a longer  time,  and  then  show  the  characteristic  coffee-ground  ap- 
pearance. But  large  hemorrhages  may  occur  in  cancer,  and  small 
hemorrhages  may  occur  in  ulcer ; and  I have  seen  cases  of  coffee- 
ground  vomiting  in  ulcer  repeatedly. 

8.  Chemistry  of  the  Gastric  Contents. — This  has  been  dwelt 
upon  in  the  chapters  on  Ulcer  and  Carcinoma.  Hyperchlorhydria 
or  hyperacidity  is  suggestive  of  a cicatrix  or  cicatricial  tumor 
formed  from  an  ulcer.  It  also  occurs  in  the  ulcus  carcinoma- 
tosum,  the  carcinomatous  degeneration  of  the  peptic  ulcer.  Ab- 
sence of  free  HCl  may  be  present  in  benign  as  well  as  malignant 
stenosis.  Pepsin  and  chymosin  are  present  in  the  benign  cases,  but 
show  a very  variable  condition  proportionate  to  the  degree  of 
destruction  of  the  mucosa  in  malignant  conditions. 

9.  Lactic  acid  is  very  rare  in  benign  stenosis,  and  was  present 
in  eighty-two  per  cent,  of  all  cases  of  gastric  cancer  coming  to  the 
author’s  clinic.  It  is  a valuable  though  not  an  early  diagnostic  sign . 

10.  Hydrogen  Sulphid. — This  is  said  to  occur  frequently  in 
benign,  and  rarely  in  malignant,  stenosis.  In  the  author’s  opinion 
this  sign  is  not  reliable. 

11.  Bacteriological  Evidences. — These  organisms  were  present 
in  fifty-three  out  of  fifty-five  cases  of  gastric  carcinoma,  and  are  of 
great  diagnostic  significance.  In  our  experience  they  have  not  been 


6yo 


MOTOR  INSUFFICIENCY. 


found  in  benign  stenosis,  though  Lindner  and  Kuttner  assert  that 
they  do  occur  in  such.  Sarcinae  occur  more  frequently  and  in 
greater  abundance  in  the  benign  stenosis. 

12.  The  presence  of  large  numbers  of  cells  in  a state  of  atyp- 
ical mitosis  is,  in  the  writer’s  opinion,  diagnostically  important. 
We  have  not  been  able  to  find  them  in  the  contents  of  eighteen 
cases  of  gastric  ulcer  and  a much  larger  number  of  cases  of  chronic 
gastritis,  which  were  especially  examined  with  regard  to  this 
factor.  The  study  of  karyokinesis  in  cells  obtained  from  the 
human  stomach  is  as  yet  very  incomplete.  It  should  be  carried 
out  in  a large  number  of  gastric  diseases  other  than  cancer.  Cells 
in  a state  of  atypical  mitosis  are  early  signs  of  cellular  proliferation, 
and  very  suggestive  of  malignant  disease.  So  far,  very  few  cases 
of  gastric  cancer  have  been  diagnosed  by  this  method. 

13.  Fragments  of  Neoplasm. — While  these  clinch  the  diag- 
nosis of  carcinoma,  they  are  not  early  signs.  If  they  are  found  in 
the  wash-water  without  any  special  effort  having  been  made  to  de- 
tach them,  they  come  from  tumors  that  are  in  a state  of  disinte- 
gration, and,  in  my  experience,  often  were  found  to  have  already 
induced  glandular  metastases. 

The  differential  diagnosis  between  benign  and  malignant  stenoses 
is  not  always  clear,  even  after  a pyloric  tumor  can  be  palpated.  But 
when  no  tumor  can  be  palpated,  judgment  is,  indeed,  difficult,  and 
is  possible  only  after  frequent  and  prolonged  observations ; in 
rare  instances,  in  the  author’s  experience,  the  diagnosis  could  not 
positively  be  made  even  after  exploratory  laparotomy. 

The  differential  diagnosis  between  motor  insufficiency  due  to 
obstruction  and  that  due  to  myasthenia  can  be  decided  in  favor 
of  the  former  whenever  a tumor  can  be  palpated.  All  symp- 
toms of  stagnation,  retention,  etc.,  have  no  differentiating  value  ; 
neither  has  the  chemistry  of  the  stomach  in  the  two  conditions. 
These  and  other  distinguishing  points  are  given  in  the  chapter  on 
Motor  Insufficiency.  The  author  has  devised  a method  by  which  a 
tube  can  be  passed  from  the  mouth  through  the  stomach  and  py- 
lorus into  the  duodenum  (Hemmeter,  “ Intubation  des  Deode- 
num,”  Boas,  “ Archiv  f.  Verdauungskrankh.,”  Bd.  11,  Seite  85  ; see 
first  part  of  this  volume).  This  method  is,  in  a fair  proportion  of 
the  cases,  available  for  the  determination  for  the  permeability  of  the 
pylorus.  Similar  methods  have  been  described  by  Dr.  Fenton  B. 
Turck  and  F.  Kuhn.  Efforts  of  this  kind  to  sound  the  pylorus  give 
promise  of  diagnostic  aid  and  of  enlarging  the  means  of  treatment. 


CONTINUED  SUPERSECRETION  AND  PYLORIC  OBSTRUCTION.  67  I 

Hyperacidity,  whenever  it  prolongs  gastric  digestion  and  causes 
distention,  does  so  by  causing  indigestion  of  the  carbohydrates,  or 
reflex  spasm  of  the  pylorus.  In  simple  hyperacidity  these  symp- 
toms can  be  relieved  by  internal  use  of  the  alkalies,  or  washing  the 
stomach  with  alkaline  solutions.  In  retention  due  to  obstruction 
the  alkaline  treatment  will  give  no  benefit.  As  a rule,  in  our  ex- 
perience, the  motility  of  the  stomach  is  well  preserved  in  hyper- 
acidity. 

Continued  Supersecretion  and  Pyloric  Obstruction. — Gastro- 
succorrhea  chronica  and  dilation  of  the  stomach  occur  together 
very  frequently.  This  dilation  may  be  of  the  so-called  atonic 
or  myasthenic  variety,  or  it  may  be  due  to  pyloric  obstruction  ; but 
there  are  dilations  without  chronic  continued  supersecretion,  and, 
on  the  other  hand,  this  secretory  anomaly  may,  according  to  Riegel 
and  Reichmann,  occur  without  dilation.  The  origin  of  the  atonic 
dilation  from  a continued  supersecretion  of  gastric  juice  is  ex- 
plainable by  the  following  facts : The  permanent  presence  of  gas- 
tric juice,  the  acidity  of  which  may  increase  with  every  addi- 
tion of  food,  constitutes  an  inhibition  to  carbohydrate  digestion. 
The  starchy  foods  are  retained  abnormally  long.  Then,  again,  if  a 
continued  secretion  of  gastric  juice  is  assumed,  the  stomach,  of 
course,  is  never  entirely  empty,  and  therefore  never  obtains  abso- 
lute rest,  and,  finally,  the  hyperacid  contents  may  cause  a pyloric 
spasm,  preventing  the  exit  of  the  gastric  chyme.  In  this  manner 
gastrosuccorrhea  may  cause  obstruction  and  retention.  Reversely, 
pyloric  stenosis  may  keep  up  a kind  of  continued  gastric  flow  by 
holding  back  the  food  within  the  stomach.  It  is  almost  impossible 
to  decide  in  such  cases  whether  the  pyloric  stenosis  was  primary, 
or  whether  it  was  superadded  to  an  already  existing  continued 
supersecretion.  The  author  has  been  able  to  observe  a number  of 
cases  from  their  very  incipiency,  and  concludes  that  both  varieties 
occur  clinically.  Even  among  those  who  devote  special  attention 
to  the  abnormalities  of  secretion  there  is  confusion  with  regard  to 
the  terms  hyperacidity  and  hyperchlorhydria  on  the  one  hand,  and 
chronic  continued  supersecretion  and  gastrosuccorrhea  on  the 
other.  We  may  have  retention  and  dilation  together  with  hyper- 
acidity ; we  may  even  have  a pyloric  stenosis  together  with  hyper- 
acidity ; and  yet  there  will  be  no  sign  of  chronic  continued  secre- 
tion. Hyperacidity  means  an  increased  secretion  of  gastric  juice, 
or  rather  of  HC1,  during  digestion.  The  stimulus  to  this  increased 
secretion  is  the  normal  presence  of  food  in  the  stomach.  Hyper- 


672 


MOTOR  INSUFFICIENCY. 


secretion  or  continued  secretion  of  the  gastric  juice  is  an  abnormal 
condition  in  which  the  gastric  mucosa  secretes  continuously,  even 
when  the  digestive  stimulation  is  absent  and  the  stomach  contains 
no  food.  This  condition  may  be  intermittent  and  periodical,  or  it 
may  be  continuous. 

It  is  a generally  accepted  fact  that  hyperacidity  predisposes  to 
gastric  ulcer,  but  continued  hypersecretion  renders  a patient  much 
more  liable  to  the  development  of  ulcer  than  hyperacidity,  since 
in  the  continued  secretion  the  stomach  is  never  free  from  gastric 
juice  which  is  as  highly  acid  as  that  which  occurs  in  hyperacidity. 
The  development  of  dilation  from  continuous  hypersecretion 
may  be  explained  by  the  presence  of  an  ulcer  in  the  pylorus, 
which  may  have  resulted  in  the  formation  of'  a stenosing  cicatrix. 
Thus,  a primary  continued  secretion  may  give  rise  to  an  ulcer, 
cicatricial  stenosis,  and  a consequent  secondary  dilation. 

Hyperacidity  represents  a lesser  degree  of  irritation,  and  con- 
tinued secretion  a higher,  more  intensely  irritated  state  of  the  se- 
creting gland-cells.  Undoubted  cases  have  occurred  in  which 
hyperacidity  was  intensified  and  developed  into  chronic  continued 
hypersecretion.  In  the  cases  in  which  the  dilation  and  reten- 
tion was  the  primary  condition  and  the  hypersecretion  was  recog- 
nized later  on,  it  is  not  absolutely  certain  that  the  dilation  caused  the 
hypersecretion;  undoubted  and  long-observed  cases  of  this  char- 
acter, with  careful  and  repeated  chemical  and  physical  analyses, 
have,  in  our  experience,  not  been  published.  It  is  more  rational  to 
assume  that  in  such  cases  the  dilation  was  consequent  upon  an 
ulcer  in  the  pylorus,  which  ulcer  had  arisen  on  the  basis  of  a pro- 
longed hyperacidity.  After  the  dilation  had  developed,  the  hy- 
peracidity was  intensified  into  a chronic  continued  hypersecretion. 
A pronounced  stagnation  of  the  ingesta  consequent  upon  a dila- 
tion may  very  much  resemble  a continued  hypersecretion.  To 
distinguish  between  these  two  conditions,  it  is  necessary  to  examine 
and  analyze  the  gastric  contents  in  the  morning  before  any  food 
has  been  taken.  In  continued  secretion  the  jejune  stomach  should 
always  contain  active  gastric  juice  in  quantities  from  150  to  300 
c.c.  This  gastric  juice  should  be  free  from  food  remnants.  This 
can  not  occur  in  simple  dilation — it  should  not  even  occur  in 
dilation  with  hyperacidity,  for  in  both  of  these  cases  we  will  find 
food  remnants,  particularly  undigested  carbohydrates.  The  diagno- 
sis between  the  two  conditions  can  be  definitely  settled  by  washing 
out  the  stomach  thoroughly — until  the  lavage  water  comes  out 


TREATMENT  OF  PYLORIC  OBSTRUCTION. 


673 


absolutely  clear  and  shows  no  signs  of  acid.  This  must  be  done 
in  the  evening.  The  patient  must  not  eat  anything  in  the  mean 
while.  The  next  morning,  before  food  is  taken,  the  gastric  contents 
are  drawn  by  the  expression  method,  and  if  100  c.c.  or  more  of 
gastric  juice  without  any  traces  of  food  remnants  can  be  gained,  it 
is  a case  of  continued  hypersecretion.  The  differentiation  between 
dilation  with  continued  hypersecretion  or  supersecretion  and  dila- 
tion with  simple  hyperacidity  hinges  upon  the  presence  or  absence 
of  food  in  the  stomach  when  it  is  prepared  as  just  described.  If 
the  presence  of  food  is  necessary  to  bring  out  the  secretion  of 
gastric  juice  in  the  stomach  in  the  morning,  it  is  a dilation  with 
hyperacidity;  but  if  the  stimulus  of  food  is  not  necessary,  it  is  a 
dilation  with  continued  hypersecretion. 

The  degree  of  the  obstruction  can  be  determined  by  the 
amount  of  our  double  test-meal,  or  of  the  test-meals  of  Herschell, 
Riegel,  or  Leube,  that  remains  in  the  stomach  after  a certain  time. 
During  compensation  the  stomach  succeeds  in  emptying  itself  in 
perhaps  one  hour  longer  than  the  normal  time.  During  stagnation 
the  stomach  requires  from  six  to  eight  hours  to  empty  itself  of  a 
Riegel  dinner;  but  when  the  stagnation  is  advanced,  the  stomach 
is  not  empty  except  perhaps  before  breakfast.  In  retention  the 
stomach  is  never  empty.  The  degree  of  the  retention  can  be 
measured  by  the  methods  given  in  the  chapter  on  Motor  Insuffi- 
ciency. In  benign  stenosis  the  degree  of  the  obstruction  may  be 
gaged  by  the  author’s  method  of  duodenal  intubation. 

Prognosis. — The  prognosis  will  vary  with  the  cause.  It  is  grave 
in  malignant  obstruction  ; and  even  in  benign  obstruction,  such  as 
peritonitic  adhesions,  ulcer  of  the  duodenum,  impacted  gall-stone, 
corrosive  gastritis,  etc.,  the  prognosis  is  grave.  If  the  stenosis  is 
due  simply  to  kinking  of  the  pylorus  or  duodenum  by  a primary 
atonic  dilation,  the  prognosis  is  also  bad,  because  not  even  surgical 
aid  can  be  depended  upon  to  relieve  this  condition  permanently. 

Treatment. — The  maxim  of  all  treatment  in  these  cases  should 
be : “ In  pyloric  obstruction  beware  of  wasting  valuable  time  with 
purely  medical  treatment.”  The  medical  treatment  is  given  in  the 
chapter  on  Motor  Insufficiency.  It  is  very  much  to  be  regretted 
that  the  literature  of  the  subject  shows  no  well-observed  cases  in 
which  undoubted  benign  stenosis  was  cured  by  purely  medical 
means.  The  plan  that  promises  the  best  results  is  to  decide 
rapidly  upon  an  operation,  exclude  all  medicines  and  food  from  the 
stomach,  maintain  the  patient’s  strength  by  rectal  alimentation, 


674  MOTOR  INSUFFICIENCY. 

and  administer  ^ of  a grain  of  strychnin  hypodermically  four 
times  a day.  During  the  period  of  complete  compensation,  par- 
ticularly if  the  obstruction  is  benign,  the  patients  will  rarely  con- 
sult the  physician.  During  this  stage,  when  the  periodical  attacks 
of  vomiting  and  stagnation  begin,  the  diet  should  be  that  of  motor 
insufficiency  of  the  first  degree.  It  is  very  difficult  to  convince 
the  patient  of  the  necessity  of  operation  during  this  stage,  and 
even  during  the  stage  of  stagnation.  The  physician  is  unfortu- 
nately, therefore,  frequently  compelled  to  persist  in  purely  medical 
treatment,  notwithstanding  his  convictions  to  the  contrary. 

Lavage. — I prefer  to  carry  out  lavage  during  stagnation  in  the 
evening,  according  to  Riegel’s  plan.  The  last  meal  is  given  be- 
tween four  and  five  o’clock  in  the  afternoon,  consisting  of  some 
food  that  will  readily  pass  the  pylorus,  even  though  it  may  be  par- 
tially constricted.  Milk,  koumiss  or  matzoon,  the  whites  of  four 
eggs,  egg  beaten  up  in  hot  beef  bouillon  with  four  grams  of  soma- 
tose  added,  custard,  meat  pulp,  cream,  Zwieback  or  cake,  cerealin, 
strained  oatmeal,  strained  breakfast  wheat,  well-boiled  rice,  soft- 
boiled  eggs,  corn-meal  mush,  are  suggested  as  possible  articles  of 
diet.  Great  solubility  and  fluidity  of  the  food,  and  minute  sub- 
division in  its  preparation  are  desiderata  in  the  process  of  cooking. 
Whenever  possible,  the  food  should  be  strained  or  passed  through 
a colander.  Soup  made  of  sweetbread  in  beef  bouillon  has  a high 
caloric  value.  After  such  a meal  the  patient  must  lie  down  and 
submit  to  gastric  massage.  With  this  aid,  and  in  the  recumbent 
position,  the  liquid  diet  is,  as  a rule,  out  of  the  stomach  in  five 
hours ; if  it  is  not,  there  is  no  need  of  further  experimentation  with 
dietetic  and  medicinal  treatment.  After  the  meal  can  be  presumed 
to  be  out  of  the  stomach,  the  organ  is  thoroughly  washed  out  with 
medicated  solutions  that  are  varied  according  to  the  condition  of 
the  gastric  chemistry.  If  no  HC1  is  present,  it  is  well  to  use  first 
sodium  chlorid,  one  teaspoonful  to  the  quart  of  warm  water,  and 
toward  the  end  of  the  operation  a solution  of  dilute  HC1,  say  a 
3 to  4:1000  solution.  If  the  gastric  contents  show  persistent 
hyperacidity,  I prefer  to  wash  out  the  stomach  with  sodium  bi- 
carbonate, one  teaspoonful  to  the  quart,  followed  by  a solution 
of  nitrate  of  silver,  1 : 1000,  or  a one-half  of  one  per  cent,  solution 
of  tannin.  If  gastric  ulcer  is  suspected,  a suspension  of  subnitrate 
or  subgallate  of  bismuth  may  be  used  with  advantage,  one  dram  to 
the  quart  of  warm  water,  and  permitted  to  run  in  during  constant 
agitation  of  the  suspension  of  the  bismuth. 


LITERATURE. 


675 


In  addition  to  fine  subdivision  of  the  food,  the  next  most  im- 
portant dietetic  principle  is  to  assure  one’s  self  that  the  stomach  is 
always  empty  before  a meal  is  permitted.  To  ascertain  this,  it  is 
necessary  to  learn  the  time  in  which  the  patient’s  stomach  will 
evacuate  itself,  by  passing  a stomach-tube  from  four  to  five  hours 
after  a meal  like  the  Riegel  dinner,  or  by  employing  our  double 
test-meal. 

The  stool  should  be  watched  and  sufficient  food  introduced  to 
cover  the  caloric  requirements  of  the  patient.  It  is  not  an  easy 
matter  to  gage  the  proper  amount  of  food  to  be  introduced  into 
these  weak  stomachs.  The  danger  of  overburdening  is  very 
great.  It  is,  therefore,  advisable  to  give  two,  perhaps  three,  nutri- 
tive enemata  a day,  which  will  permit  of  considerable  reduction  in 
the  amount  of  food  necessary  to  be  given  by  the  mouth. 

Dilation  of  Benign  Pyloric  Stenosis  by  Sounding. — This  method 
has  been  employed  by  the  author  in  obstruction  due  to  hyper- 
trophic stenosis  of  the  pylorus,  when  operation  was  refused.  The 
cases  were  markedly  relieved  for  a time,  but  permanent  cure  of 
the  obstruction  by  this  method  seems  doubtful.  Nevertheless,  the 
technics  of  this  procedure  should  be  perfected  to  be  available  in 
the  efforts  to  dilate  cicatricial  and  hypertrophic  stenosis  whenever 
operation  is  impossible  or  refused.  (Concerning  the  indications 
and  methods  of  operation,  see  the  chapter  devoted  to  Surgery  of 
the  Stomach,  or  the  Cartwright  lectures  on  “ Surgery  of  the 
Stomach,”  by  W.  W.  Keen,  LL.D.,  “ Philadelphia  Medical  Jour- 
nal,” volume  1,  pages  829,  927,  1053,  and  1104.) 

LITERATURE 

ON  DILATION  OF  THE  STOMACH. 

1.  Abrams,  A.,  “ Gastrectatic  Dyspnea,”  “Pacific  Rec.  M.  and  S.,”  San 
Francisco,  1898-’ 99,  xm,  39-42. 

2.  Alex,  “ Stenose  du  pylore  d’origine  biliaire,”  “ These  de  Lyon,”  97. 

3.  Anderson,  “British  Med.  Jour.,”  May  10,  1890. 

4.  Von  Anrep,  “Du  Bois’  Archiv,”  1881. 

5.  Armstrong,  W.,  “Gastric  Dilation,”  “Brit.  Med.  Jour.,”  Lond.,  1898, 
I,  949. 

6.  Ashby,  H.,  “A  Case  of  Congenital  Stenosis  of  the  Pylorus,”  “Arch. 
Pediat.,”  New  York,  1897,  xiv,  498-505. 

7.  Aufrecht,  “ Centralbl.  f.  klin.  Med.,”  1893,  Nr.  23. 

8.  Bardet,  “ Bull.  Gen.  de  Therap.,”  1884,  329. 

9.  Bartels,  “ Berl.  klin.  Wochenschr.,”  1877,  Nr.  30. 

10.  Von  Basch,  “Berl.  klin.  Wochenschr.,”  1889,  Nr.  19,  S.  433. 


6y6 


MOTOR  INSUFFICIENCY. 


11.  Bauermeister,  I naug.- Dissert.,  Halle,  1890. 

12.  Baum,  “Wien.  med.  Presse,”  Nr.  17,  1873. 

13.  Beau,  “ Gaz.  Med.  de  Paris,”  No.  5,  i860. 

14.  Beaumetz,  D.,  et  D.  Ettinger,  “ Union  Medicale,”  29  Janvier,  1884. 

15.  Beaumont,  “ Experiments  on  the  Gastric  Juice,”  1838. 

16.  Benedict,  A.  L.,  “ Diagnosis  of  the  Gastric  Conditions  Producing  Ischo- 
chymia  (Atony,  Gastroptosis,  Atonic  Dilation,  Obstructive  Dilation),”  “ Med. 
Age,”  Detroit,  1898,  xvi,  386-392. 

17.  Beurmann,  “Gaz.  Hebd.,”  No.  14,  1889. 

18.  Bettmann,  H.  W.,  “Acute  Dilation  of  the  Stomach,”  “Cincin.  Lancet- 
Clinic,”  1897,  N.  S.,  xxxviii,  569-575. 

19.  Bettmann,  H.  W.,  “Motor  Insufficiency  of  the  Stomach,”  “Cincin. 
Lancet-Clinic,”  1897,  xxxviii,  517-522,  Discussion,  525;  also,  “ Tr.  Acad. 
Med.,”  Cincin.,  i897~’98. 

20.  Bircher,  H.,  “ Correspondenzbl.  f.  Schweizer  Aerzte,”  1891,  Nr.  23. 

21.  Boas,  “ Diagnostik u.  Therapie  der  Magenkrankheiten,”  2.  Theil,  S.  in, 
Leipzig,  1893. 

22.  Boas,  “Deutsche  med.  Wochenschr.,”  1893,  Nr.  39,  und  “ Miinchener 
med.  Wochenschr.,”  1893,  Nr.  43. 

23.  Boas,  “ Hypertrophic  Stenosis  of  the  Pylorus  and  jts  Treatment,”  “ Arch, 
d.  Verdauungskrankh.,”  Apr.  1,  1898. 

24.  Bokai,  A.,  “ Wirkung  des  Quassin  betr.,”  “ Pester  med.-chirurg.  Presse,” 
1893,  Nr.  45. 

25.  Bouveret,  “Stenose  du  pylore  adherent  a la  vesicule  calculeuse,” 
“Revue  de  Med.,”  Jan.,  1896. 

26.  Bouveret,  “ Sur  le  diagnose  de  l’estomac  biloculaire  par  l’insufflation,” 
“ Lyon  Medical.,”  2,  11,  1896. 

27.  Bouveret  et  Devic,  “ Revue  de  Medec.,”  1892,  H.  1 und  11. 

28.  Boyd,  M.  A.,  “ A Clinical  Lecture  on  the  Significance  of  Dilation  or 
Gastrectasia  in  Functional  and  Organic  Diseases  of  the  Stomach,”  “ Brit.  Med. 
Jour.,”  London,  1897,  II,  265,  266. 

29.  Broadbent,  W.  H.,  “Dilation  of  the  Stomach,”  “Practitioner,”  Lon- 
don, 1898,  lx,  11-28. 

30.  Brown,  R.  Hill,  “Case  of  Dilation  of  the  Stomach  Complicated  by 
Fatal  Tetany,”  “ Lancet,”  21,  in. 

31.  Bruhl,  “Gaz.  des  Hopitaux,”  1891. 

32.  Bugge,  “ Tidshrift  f.  pract.  Med.,”  Nr.  10,  1881. 

33.  Buist,  S.  Somers,  “ Amer.  Jour,  of  Med.  Sciences,”  Oct.,  1870. 

34.  Carr,  W.,  “ A Case  of  Dilation  of  the  Stomach  Associated  with  Per- 
ipheral Neuritis,”  “ Lancet,”  London,  1897,  11,  721. 

35.  Carrel,  “ L’estomac  biloculaire  (presentation  de  la  piece),”  Soc.  des 
Science  Med.  de  Lyon,  Mai,  1896. 

36.  Cautley,  E.,  “Congenital  Hypertrophic  Stenosis  of  the  Pylorus,” 
“Lancet,”  London,  1898,  11,  1264. 

37.  Cecchini,  S.,  “ Rassegna  di  Scienza  mediche,”  1886. 

38.  Chauffard,  “ Stenose  pylorique;  gastroenteroanastomose,  etat  du  malade 
trois  mois  apres  l’operation,  Presentations  de  malade,”  Soc.  Med.  des  Hop., 
22  Oct.,  1896. 

39.  Chauffard,  A.,  “Stenose  pylorique  et  vaste  dilatation  de  l’estomac ; 


LITERATURE.  677 

application  au  diagnostic  de  l’6clairage  61ectrique  intra  stomacal,”  “ Bull,  et 
Mem.  Soc.  Med.  d.  Hop.  de  Par.,”  1897,  3 S.,  xiv,  979-982. 

40.  Chiari,  “ Wiep.  med.  Blatt,”  Nr.  3,  1881. 

41.  Chomel,  “ Des  Dyspepsies,”  Paris,  1857. 

42.  Comby,  J.,  “Dilatation  de  l'estomac  chez  les  nourrissons,”  “Bull,  et 
M6m.  Soc.  M6d.  d.  Hop.  de  Par.,”  1897,  3 S.,  850-857. 

43.  Comby,  “Dilatation  de  l’estomac  chez  le  enfants,”  Soc.  Med  des  Hop., 
18  Juin,  1897. 

44.  Comby,  “Arch.  Gen.  de  Med.,”  Aout,  1884. 

45.  Cordier,  A.  H.,  “ Gastro-jejunostomy  in  Gastrectasis,”  “Med.  Record,” 
25,  ix,  1897. 

46.  Coyon,  A.,  “ Stenoses  du  pylore,”  “ Gaz.  d.  hop.,”  Paris,  1898,  lxxi, 
9 17>  945- 

47.  Debove,  Soc.  Med.  des  Hopit.,  12  Dec.,  1886. 

48.  Dehio,  “ Verhandlungen  d.  Cong.  f.  innere  Med.,”  1888. 

49.  Deiters,  Inaug.-Dissert.,  Greifswalde,  1889. 

50.  Donkin,  “The  Lancet,”  Sept.  27,  1890. 

51.  Duchon-Doris,  “These  de  Paris,”  1887. 

52.  Dujardin-Beaumetz,  “ Berl.  klin.  Wochenschr.,”  1890,  Nr.  31. 

53.  Dunin,  “ Resultate  der  Gastroenterostomie  bei  narb.  Pylorusstenose,” 

“ Centralbl.  f.  Chirurg.,”  1893,  Nr.  36. 

54.  Einhorn,  V.,  “ Ueber  elektr.  Magen-  und  Darmdurchleuchtung,” 

“ Therap.  Monatshefte,”  1892,  S.  128. 

55.  Einhorn,  “ Berl.  klin.  Wochenschr.,”  1891,  Nr.  23. 

56.  Einhorn,  M.,  “A  Further  Contribution  to  our  Knowledge  of  Ischochy- 
mia,”  “ Med.  Rec.,”  New  York,  1877,  li,  865-873. 

57.  Erdmann,  “Virchow’s  Archiv,”  Bd.  xliii,  S.  295. 

58.  Ewald,  “Berl.  klin.  Wochenschr.,”  1890,  Nr.  12. 

59.  Ewald,  “Therap.  Monatshefte,”  August,  1887. 

60.  Fagge,  Hilton,  “ Guy’s  Hosp.  Rep.,”  xvm  ; “ Virchow’s  Jahresb.,”  1873, 
B.  H.,  S.  155. 

61.  Fleiner,  “ Ueber  die  Behandl.  einiger  Reizerschein.  u.  Blut.  des  Magens,” 
“Verhandlungen  d.  Cong.  f.  innere  Med.,”  1894,  S.  309. 

62.  Francois,  L.,  “ Sur  une  volumineuse  dilation  stomacale,”  “ Marseille 
Med.,”  1897,  xxxiv,  372-374. 

63.  Francon,  “Lyon  Med.,”  7 Aout,  1887. 

64.  Von  Frankl-Hochwart,  “ Die  Tetanie,”  Berlin,  1891. 

65.  Friedenwald,  J.,  “ Two  Interesting  Cases  of  Dilation  of  the  Stomach,” 

“ Maryland  Med.  Jour.,”  Baltimore,  1897 -’98,  xxxvm,  1 53—1 55. 

66.  Galliard,  Assoc.  Fran9aise,  Congres  de  Rouen,  1883. 

67.  Galvagin,  E.,  “ Gastrectasia  da  stenosi  pilorica,”  “ Gazz.  d.  osp.,” ' 
Milano,  1898,  xix,  777-779. 

68.  Garcia,  E.  L.,  “ Dilatacion  del  estomago  sin  estinosis  pilorica,”  Cron, 
med.  Lima,”  1897,  xiv,  393  ; 41 1,  1898  ; xv,  6,  25,  61. 

69.  Garcia,  Duarte  R.,  “ De  la  gastro-ectasia,”  “ Gac.  med.  de  Granada,” 
1898,  XVI. 

70.  Gerhardt,  “ Berl.  klin.  Wochenschr.,”  S.  74,  Januar,  1888. 

71.  Gillet,  A.,  “ Dyspepsie  et  dilatation  gastro-intestinale  chez  d’enfant,” 

“ Rev.  gen.  de  Clin,  et  de  Therap.,”  Paris,  1897,  xi,  325-327. 

45 


6yS 


MOTOR  INSUFFICIENCY. 


72.  Grundzach,  “Wien.  med.  Presse,”  Nr.  28,  1891. 

73.  Hamill,  S.  McC.,  “Dilated  Stomach  from  Pyloric  Obstruction;  Con- 
tracted Kidneys,”  “ Tr.  Path.  Soc.  of  Phila.,”  1898,  xviii, 75-78. 

74.  Hayem,  G.,  “ Note  sur  les  variations  de  la  capacite  stomacale  dans  les 
stenoses  pyloriques,  ” “ Bull,  et  Mem.  Soc.  Med.  d.  Hop.  de  Paris,”  1897,  3 S., 
xiv,  1322-1325. 

75.  Hayem,  “ Stenose  pylorique,”  “ Presse  Med.,”  20  Novembre,  1897. 

76.  Hayem,  “ Stenose  sous  pylorique  incomplete.,”  “Med.  Moderne,”  9 
fevrier,  1898. 

77.  Heynsius,  “Weekblad  van  het  Nederlandsch.  Tydschrift  voor  Genesk.,” 
Nr.  37,  1874. 

78.  Hirschberg,  “These  de  Paris,”  1889. 

79.  Hochenegg,  J.,  “A  Case  of  Hour-glass  Stomach  Cured  by  Gastroanas- 
tomosis,”  “Wien.  klin.  Wochenschr.,”  July  16,  1898. 

80.  Hofmann,  “ Anzeiger  d.  Ges.  d.  Aerzte  in  Wien,”  Nr.  12,  1881. 

81.  Hoppe-Seyler,  “Deutsches  Archiv  f.  klin.  Med.,”  Bd.  l,  C.  S.  82. 

82.  Huber,  “ Deutsches  Archiv  f.  klin.  Med.,”  Bd.  xlvii. 

83.  Hufschmidt,  “Wien.  klin.  Wochenschr.,”  1893,  Nr.  3. 

84.  Hunter,  “New  York  Med.  Record,”  p.  273,  1889. 

85.  Jacobson  und  Ewald,  “ Ueber  Tetanie,”  “ Verhandlungen  d.  Congr.  f. 
innere  Medizin,”  1895,  S.  298. 

86.  Jago,  “ Med.  Times  and  Gaz.,”  Oct.  12,  1872. 

87.  Jaworski,  “Wien.  med.  Wochenschr.,”  No.  16,  1888. 

88.  Jobin,  A.,  “ Un  cas  de  dilatation  aigue  de  l’estomac,”  “ Rev.  Med.,” 
Quebec,  1897,  1,  177. 

89.  Von  Johann,  Peter  Frank,  “ De  cur.  horn.  morb.  epit.,”  lib.  V,  pars.  6, 

p.  666. 

90.  Jiirgensen,  Th.  v.,  “ Tod  unter  schweren  Hirnerscheinungen  bei  hoch- 
gradiger  Erweiterung  des  Magens,”  “ Archiv  f.  klin.  Med.,”  Bd.  lx,  p.  327. 

91.  Kansche,  “ Unters.  fiber  die  funkt.  Resultate  von  Operat.  am  Magen.” 

92.  Kelynack,  T.  N.,  “ Gastrectasis  Secondary  to  Malignant  Stricture  of  the 
Pylorus,”  “Med.  Press  and  Circ.,”  London,  1898,  N.  S.,  lxv,  5. 

93.  Kern,  Inaug.-Dissert.,  Berlin,  1891. 

94.  Klemperer,  “ Ein  Fall  geheilter  Magenerweiterung,”  “ Deutsche  med. 
Wochenschr.,”  1889,  Nr.  9. 

95.  Krasnobayeff,  T.  P.,  “ Three  Cases  of  Stricture  of  the  Pyloric  Portion  of 
the  Stomach  in  Childhood,”  “ Dietsk.  med.  Mosk.,”  1898,  ill,  195-204. 

96.  Kuckein,  R.,  “A  Case  of  Latent  Tetany,  with  Dilation  of  the  Stomach, 
in  Consequence  of  Carcinomatous  Stenosis  of  the  Pylorus,”  “ Berl.  klin. 
Wochenschr.,”  Nov.  7,  1898. 

97.  Kuhn,  “ Zeitschr.  f.  klin.  Med.,”  1892,  Heft  5 u.  6. 

98.  Kuhn,  “ Deutsche  med.  Wochenschr.,”  1892,  Nr.  49  u.  52. 

99.  Kussmaul,  “ Zur  peristalt.  Unruhe  des  Magens,”  “Volkm.  klin.  Vor- 
trage,”  Nr.  181. 

100.  Kuttner  und  Jacobson,  “ Berl.  klin.  Wochenschr.,”  1892,  Nr.  39  u.  40. 

101.  Landau,  “ Die  Wanderniere  der  Frauen,”  Berlin,  1881. 

102.  Landerer,  Inaug.-Dissert.,  Freiburg,  1879. 

103.  Laprevotte,  “These  de  Paris,”  1884. 

104.  Lefevre,  “ Archiv  Gen.  de  Med.,”  tome  xiv  et  xv,  1842. 


LITERATURE.  679 

105.  Leichtenstern,  “ Ziemssen’s  Handbuch,”  2.  Aufl.,  Bd.  vn,  2,  S.  411- 
418. 

106.  Leo,  “ Diagn.  der  Krankh.  d.  Verdauungsorgane,”  p.  41,  Berlin,  1892. 

107.  Lepoil,  " Th&se  de  Paris,”  1881. 

108.  Leube,  “ Archiv  f.  klin.  Med.,”  Bd.  xvm,  S.  207. 

109.  Lindemann,  E.,  “ Demonstration  von  Rontgenbildern  des  normalen 
•und  erweiterten  Magens,”  Deutsche  med.  Wochenschr.,”  1897,  xxm,  266. 

no.  Litten,  “ Verhandlungen  des  VI.  Congr.  f.  innere  Med.,”  1887. 
hi.  Lyman,  H.  M.,  “Dilation  of  the  Stomach,”  “Jour.  Amer.  Med. 
Assoc.,”  1897,  xxviii. 

1 1 2.  Maier,  R.,  “Congenital  Pyloric  Stenosis,”  “Virchow’s  Archiv,” 
Bd.  cii. 

1 13.  Malibran,  “These  de  Paris,”  1885. 

1 14.  Marten,  “Lancet,”  April  2,  1890,  p.  230. 

1 1 5.  Mattheides,  Inaug. -Dissert.,  Erlangen,  1890. 

1 16.  Maynard,  E.  F.,  “Chronic  Dilation  of  the  Stomach  Associated  with 
Chronic  Gastric  Catarrh,”  “ Brit.  Med.  Jour.,”  London,  1898,  II,  1126. 

1 17.  Mazotti,  Luigi,  “ Rivista  Clinica  di  Bologna,”  Aout  et  Sept.,  1824. 

1 18.  McKendrick,  John  S.,  “ Case  of  Tetany  with  Dilation  of  the  Stomach  ; 
Death,”  “ Lancet,”  Sept.  24,  1898. 

1 19.  McNaught,  “Dilation  and  Eructation  of  Inflammable  Gas,”  “Brit. 
Med.  Jour.,”  1890. 

120.  Von  Mering,  “ Ueber  die  Funktion  des  Magens,”  “ Verhandl.  d.  Congr. 
f.  innere  Med.,”  1893. 

121.  Meltzer,  S.  J.,  “On  Congenital  Hypertrophic  Stenosis  of  the  Pylorus  in 
Infants,”  “Med.  Rec.,”  New  York,  Aug.  20,  1898. 

122.  Meyer,  “Virchow’s  Archiv,”  Bd.  cxv,  S.  326. 

123.  Michalis,  Walter,  “Ueber  die  Erweiterung  des  Antrum  pylori  und  ihre 
Beziehung  zu  der  motorischen  Insufficienz  des  Magens,”  “ Zeitschr.  f.  klin 
Med.,”  Bd.  xxxiv,  S.  241. 

124.  Moncorvo,  Rio  de  Janeiro,  broch.,  1883. 

125.  Montaya,  “These  de  Paris,”  1881. 

126.  Montprofit,  “Obstruction  du  pylore  par  un  calculi  biliare,”  “ Soc.  anat. 
Bullet.,”  de  Mai-Juin,  1897. 

127.  Monyour,  “Dilatation  de  l’estomac  par  stenose  du  pylore;  gastro- 
enterostomie  par  le  procede  G.  Dubourg,  guerison,”  Soc.  d’Anat.  et  de  Phys.  de 
Bordeaux,  4 Octob.,  1897. 

128.  Moritz,  “Gastric  Motility  with  Regard  to  Liquids  and  Semi-liquids,” 
“Verhandl.  d.  Naturforsch.-Versamml.,”  Wien,  1894. 

129.  Muller,  F.,  “ Charite  Annalen,”  p.  283,  1888. 

130.  Mueller-Warnek,  “ Berl.  klin.  Wochenschr.,”  Nr.  30,  429,  1877. 

1 31 . Naunyn,  “ Gastric  Fermentation  and  Motor  Insufficiency,”  “ Deutsch. 
Arch.  f.  klin.  Med.,”  Bd.  xxxi,  82. 

132.  Nauwerk,  D.,  “ Archiv  f.  klin.  Med.,”  Heft  5 u.  6,  vol.  XXI,  p.  573,  1878. 

133.  Neumann,  “ Deutsche  Klinik,”  Nr.  2 u.  3,  1861. 

134.  Newmann,  “ Lancet,”  Dec.  5,  1868. 

135.  Oppolzer,  “ Magenerweiterung,”  “Wien.  med.  Wochenschr.,”  1893. 

136.  Oser,  Artikel,  “Magenerweiterung”  in  Eulenburg’s  “ Realencyclo- 
padie.” 


68o 


MOTOR  INSUFFICIENCY. 


137.  Pacanowski,  “ Zur  physikal.  Diagnostik  d.  mechan.  Insuff.  d.  Magens.” 

138.  Parker,  R.,  “A  Series  of  Operations  for  Dilated  Stomach,”  “ Liverpool 
Med.-Chir.  Jour.,”  1898,  xvm,  274-282. 

139.  Patek,  A.  J.,  “Atony  of  the  Stomach,”  “ Med.  News,”  New  York,  1898, 
LXXIII,  584-587. 

140.  Penzoldt,  “ Die  Magenerweiterung,”  Erlangen,  1875.  (History  of  the 
subject.) 

141.  Penzoldt  (in  Penzoldt  und  Stintzing’s  “ Handbuch  d.  speciellen  Ther- 
apie  innerer  Krankheiten,”  Bd.  iv). 

142.  Penzoldt-Faber,  “Berl.  klin.  Wochenschr.,”  1882,  Nr.  21. 

143.  Pepper,  “ Phila.  Med.  Times,”  May  1,  1871. 

144.  Pepper,  W.,  and  Alfred  Stengel,  “ Diagnosis  of  Dilation  of  the  Stom- 
ach,” “ Amer.  Jour.  Med. ’.Sciences,”  Tan.,  1898. 

145.  Perret,  “ L’estomac  biloculaire,”  “ These  de  Lyon,”  1896. 

146.  Pertick,  “ Archiv  f.  path.  Anat.  u.  Phys.,”  cxiv,  1888,  Heft  3,  S.  98. 

147.  Petriquin,  “ Bulletin  de  Therap.,”  X,  p.  239. 

148.  Phaundler,  M.,  “ So-called  Congenital  Stenosis  of  the  Pylorus  and  its 
Treatment,”  “Wien.  klin.  Wochenschr.,”  Nov.  10,  1898. 

149.  Plempius,  et  suivants,  cites  par  D.  Beaumetz,  “ Traitement  des  mal  de 
PEstomac,”  Paris,  1893. 

150.  Poensgen,  “ Motor- Verricht.  d.  menschl.  Magens,”  Strassburg,  1882. 

1 5 1.  Pope,  C.,  “A  Clinical  Lecture  on  Gastric  Dilation,”  “Charlotte, 
N.  C.,  Med.  Jour.,”  1897,  xi,  171-176. 

152.  Popoff,  “ Berl.  klin.  Wochenschr.,”  1870,  Nr.  38  u.  40. 

153.  Preble,  R.  B.,  “ Gastrectasis,  with  a Tetanoid  Condition  and  the  So- 
called  Pulmonary  Hypertrophic  Osteoarthritis  of  Marie,”  “Jour.  Amer.  Med. 
Assoc.,”  1898,  xxx,  217-219. 

154.  Purjesz,  Sigmund,  “Deutsches  Arch.  f.  klin.  Med.,”  Bd.  xxm,  S.  554, 
1879. 

155.  Quincke,  “Dilation  with  Rupture  into  Colon,”  “ Correspondenzbl.  f. 
Schweizer  Aerzte,”  1874. 

156.  Reed,  B.,  “Dilation  of  the  Stomach,  with  Reports  of  Cases  Treated 
by  Diet,  Massage,  and  Intragastric  Electricity,”  “Jour.  Amer.  Med.  Assoc.,” 
1898,  xxxi,  220-223. 

157.  Reed,  W.  W.,  “Report  of  a^Case,  with  Remarks  upon  the  Diagnosis 
of  Pyloric  Stenosis,”  “Colorado  Med.  Jour.,”  Denver,  1898,  iv,  139-144. 

158.  Reichmann  und  Heryng,  “Ueber  Gastrodiaphanie,”  “Berl.  klin. 
Wochenschr.,”  1892,  Nr.  51. 

159.  Remond  (de  Metz),  “ Gaz.  des  Hopit.,”  14  Nov.,  1891. 

160.  Revilliod,  “ Revue  de  Med.  de  la  S.  Romande,”  No.  1,  1885. 

161.  Riegel,  “ Zur  Diagnose  u.  Behandlung  der  Magenerweiterung,” 
“ Deutsche  med.  Wochenschr.,”  1886,  Nr.  37. 

162.  Riegel,  “Ueber  Diagnostik  u.  Therapie  der  Magenkrankheiten,” 
“ Volkmann’s  klin.  Vortrage,”  Nr.  289. 

163.  Robson,  A.  W.  Mayo,  “ Tetany  and  Tetanoid  Spasms  Associated  with 
Gastric  Dilatation  Treated  Surgically,”  “ Lancet,”  Nov.  26,  1898. 

164.  Rosenbach,  “ Berlin,  klin.  Wochenschr.,”  Nr.  51,  S.  742,  1876. 

165.  Rosenheim,  “Ueber  d.  Verhaltn.  d.  Magenfunkt.  nach  Resekt.  des 
carcinomat.  Pylorus,”  “Deutsche  med.  Wochenschr.,”  1892,  Nr.  40. 


LITERATURE. 


68  I 

1 66.  Rosenheim,  F.,  “ Ueber  motorische  Insufificienz  des  Magens,”  “ Berlin, 
klin.  Wochenschr.,”  1897,  xxiv,  228,  252  ; Discussion,  256. 

167.  Rosenthal,  “ Magenneurosen  und  Magenkatarrh,”  Wien,  1886,  S.  181. 

168.  Rosenthal,  A.,  “ Preliminary  Note  on  Disorders  of  Mobility  of  the 
Stomach,  Myasthenia,  Atony,  and  Ectasia,”  “Chicago  Med.  Recorder,”  1898, 
xv,  176. 

169.  Rossler,  A.,  “ Ueber  die  Ausschaltung  der  Ernahrung  durch  den  Magen 
bei  Dilatatio  ventriculi,”  “Wien.  klin.  Wochenschr.,”  1893,  Nr.  40. 

170.  Rousseau,  G.,  “ De  la  dilatation  d’estomac  chez  les  nourrissons,” 
These  de  Paris,  25,  xi,  1896. 

1 7 1 . Rupstein,  “ Archiv  f.  Anat.  u.  Physiol.,”  1874. 

172.  Rydygier,  “ Zur  Magendarmchirurgie,”  “Wien.  klin.  Wochenschr.,” 

1894,  Nr.  10. 

173.  Saundby,  “ Deutsche  med.  Wochenschr.,”  Nr.  42,  1896. 

174.  Schliep,  “ Deutsches  Archiv  f.  klin.  Med.,”  Bd.  xm,  S.  445. 

175.  Schmidt,  “Berlin,  klin.  Wochenschr.,”  1886,  No.  33. 

176.  Schmidt-Monnard,  “ Hour-glass  Stomach,”  “ Munch,  med.  Woch- 
enschr.,” 1893. 

177.  Schreiber,  “Archiv  f.  Verdauungskrankh.,”  Bd.  11,  S.  423. 

178.  Schwyzer,  T.,  “ A Case  of  Congenital  Hypertrophy  and  Stenosis  of  the 
Pylorus,”  “ N.  Y.  Med.  Jour.,”  21,  xi,  1897. 

179.  See,  G.,  et  A.  Mathieu,  “ Rev.  de  Med.,”  10  Mai  et  18  Sept.,  1884. 

180.  Senator,  “Ueber  einige  neuere  Arzneimittel,”  “ Berl.  klin.  Woch- 
enschr.,” 1885,  Nr.  1. 

1 8 1 . Senator,  “On  Autointoxications,  etc.,”  “ Zeitschr.  f.  klin.  Med.,”  Bd. 
vii,  1884. 

182.  Sievers,  R.,  “On  tetanie  vid  dilatation  of  magsaken,”  “ Finska  lak. 
sallsk.  handl.,”  Helsingfors,  1898,  XL,  18-39. 

183.  Sittmann,  “ Miinch.  med.  Wochenschr.,”  1893,  Nr.  29. 

184.  Stockton,  C.  G.,  “ Gastrectasis  from  Pyloric  Spasm,”  “ Internat.  Clin.,” 
Phila.,  1898,  8 S.,  1,  126-128. 

185.  Stoker,  “Hour-glass  Contract.  Stomach,”  “Med.  Press  and  Circ.,” 
March  3,  1869. 

186.  Talma,  “ Indicat.  z.  Magenoperationen,”  “Berl.  klin.  Wochenschr.,” 

1895. 

187.  Tappeiner,  “ Zeitschr.  f.  Biol.,”  Bd.  v,  471. 

188.  Thiebaut,  These  de  Nancy,  1884. 

189.  Tilger,  “ Traction  Diverticulum  of  Pyloric  Region,  Caused  by  Disloca- 
tion of  the  Gall-bladder,”  “Virchow’s  Archiv,”  Bd.  cxxxm,  Heft  2;  the 
same  author,  “ Congenital  Stenosis  of  the  Pylorus  ” (/.  c.). 

190.  Traube-Kundrat,  “ Handbuch  d.  Kinderkrankh.,”  Bd.  iv. 

191.  Traube,  “ Gesammelte  Abhandlungen,”  1871. 

192.  Thorowgood,  “Lancet,”  17  Fev.,  1872. 

193.  Wagner,  “Berl.  klin.  Wochenschr.,”  Nr.  16,  S.  229,  und  Nr.  25,  S.  361, 
18  April  und  20  Juni,  1881. 

194.  Wegele,  “ Die  diatet.  u.  medicament.  Behand.  d.  Magendarmerkrank.,” 
Jena,  1896. 

195.  Weiss,  H.,  “ Der  Sanduhrmagen,”  “ Mittheil.  a.  d.  Grenzgeb.  d.  Med. 
u.  Chir.,”  Jena,  1897-8,  1,  393-398. 


682 


HEMORRHAGE  FROM  THE  STOMACH. 


196.  Winternitz,  “Deutsche  Medicinalzeitung,”  1891,  Nr.  38. 

197.  Winternitz  und  Baum,  “Wien.  med.  Presse,”  1873,  Nr.  17. 

198.  Zabludowski,  “ Zur  Massagetherapie,”  “ Berl.  klin.  Wochenschr.,”  1886, 
Nr.  26  ff.  u.  36. 

199.  v.  Ziemssen,  “ Ueber  physik.  Behandl.  chron.  Magendarmerkrankimg," 
Leipzig,  1888. 


CHAPTER  VIII. 

HEMORRHAGE  FROM  THE  STOMACH  (GASTRORRHAGIA). 

This  symptom  as  it  occurs  in  consequence  of  gastric  ulcer  and 
carcinoma  has  already  been  described  in  the  chapters  devoted  to 
these  subjects.  Hematemesis,  or  vomiting  of  blood,  is  not  a syn- 
onymous term  with  gastric  hemorrhage,  for  the  vomited  blood 
may  have  had  its  origin  in  the  respiratory  passages,  and  have  been 
swallowed.  It  may  have  come  from  the  esophagus  or  from  the 
duodenum.  Then,  again,  there  may  be  undoubted  gastric  hemor- 
rhage without  hematemesis. 

The  cause  of  the  gastric  hemorrhage  may  be  found  in  injurious 
influences  coming  from  without,  or  developing  within,  the  stomach. 

Etiology. — 1.  Gastric  Ulcer. — This  is  the  most  frequent  cause 
of  hemorrhage.  Tuberculous,  syphilitic,  or  typhoid  ulcers  of  the 
stomach  are  extremely  rare;  and  even  in  those  cases  that  are 
reported  they  are  seldom  mentioned  as  causes  of  hemorrhage. 
Professor  William  Osier  described  a case  of  profuse  gastric  hemor- 
rhage to  the  author  which  was  caused  by  a typhoid  ulcer  of  the 
stomach  occurring  at  the  Johns  Hopkins  Hospital.  Erosions  of 
the  stomach,  as  such,  do  not,  in  my  experience,  cause  hemorrhage, 
but  when  they  are  digested  out  by  hyperacidity  or  supersecretion, 
they  may  break  into  the  walls  of  a blood-vessel ; then,  however,  we 
can  no  longer  speak  of  an  erosion  : it  has  become  a peptic  ulcer. 

2.  Malignant  Tumors  of  the  Stomach. — Carcinoma  and  sarcoma. 

3.  Be7iig7i  Tumors  of  the  Stomach. — These  are  rare  causes  of 
hemorrhage. 

4.  Mecha7iical,  Chemical , and  Theri7iic  Causes. — (a)  Acting  from 
without,  such  as  direct  traumatism,  or  injury  to  the  abdomen; 
penetrating  wounds  of  the  abdomen  affecting  the  stomach.  ( b ) 
Acting  from  within:  swallowed  foreign  bodies,  such  as  fish-bones, 


ETIOLOGY  OF  GASTKORRH  AGIA. 


683 


pins,  etc.  ( c ) Corrosive  chemical  poison,  such  as  mineral  acids  and 
caustic  alkalies;  poisons  swallowed  by  mistake  or  with  suicidal 
intent,  (d)  Exceedingly  hot  substances.  ( e ) The  HC1  itself  in  a 
state  of  hyperacidity  or  supersecretion  may  erode  small  blood- 
vessels in  places  where  the  circulation  is  abnormal,  where  there  are 
blood  extravasations,  emboli,  or  thrombi.  (/)  Injury  caused  by 
the  stomach-tube. 

5.  Disease  of  the  Gastric  Blood-vessels. — ( a ) Galliard  found  mil- 

iary aneurysms  of  the  arteries  of  the  stomach  as  a cause  of  fatal 
hemorrhage,  (b)  The  gastric  veins  may  be  affected  by  varices, 
this  condition  being  generally  associated  with  chronic  passive 
congestion  of  the  stomach.  Recently,  Lancaster  has  reported  a 
case  of  fatal  gastric  hemorrhage  in  a woman  aged  thirty-three 
years.  At  the  autopsy  varicose  dilatation  of  several  branches  of  the 
gastro-epiploic  vein  in  the  greater  omentum  and  in  the  submucosa 
of  the  stomach  were  found.  The  largest  ones  of  these  varices 
showed  a rupture  as  large  as  a pin  (“  Miinchen.med.  Wochenschr.,” 
1896,  Nr.  45).  ( c ) Fatty  atheromatous  and  amyloid  degenera- 

tion of  the  gastric  blood-vessels.  No  reliable  autopsy  reports 
could,  however,  be  found  in  which  gastric  hemorrhage  was  due 
to  amyloid  degeneration  of  the  blood-vessels.  Gastric  hemorrhage 
in  phosphorus-poisoning  is  attributed  to  fatty  degeneration  of  the 
arteries. 

6.  Active  congestion  of  the  stomach  usually  is  a result  of  intense 
acute  inflammation,  which  inevitably  brings  on  inflammatory  altera- 
tions in  the  vessel  walls.  W.  H.  Welch  assigns  the  so-called 
vicarious  hemorrhages  from  the  stomach  to  active  congestion.  As 
a result  of  a large  experience  in  cases  of  gastric  hemorrhage,  the 
author  can  confirm  that  periodic  gastric  hemorrhages  occur  simulta- 
neously with  the  menstrual  period.  In  amenorrhea  one  occasionally 
observes  periodic  gastric  hemorrhages.  Sometimes,  when  a young 
female  is  afflicted  with  a gastric  ulcer,  the  hemorrhages  may  coincide 
with  the  menstrual  terms.  Whether  such  hemorrhages  are  “ vicari- 
ous ” or  not  is  difficult  to  decide.  This  term  means  “ substitutive ,” 
and  is  applied  to  the  assumption  of  functions  of  one  organ  by 
another.  In  our  opinion  gastric  hemorrhage  can  hardly  substi- 
tute the  physiological  process  of  menstruation.  It  has  been 
assumed  that  suppressed  hemorrhoidal  hemorrhage  and  epistaxis 
may  be  substituted  by  a gastric  hemorrhage — a very  hypothetical 
suggestion. 

7.  Passive  congestion  of  the  stomach , resulting  from  some  obstruc- 


684 


HEMORRHAGE  FROM  THE  STOMACH. 


tion  to  the  portal  circulation.  Such  obstruction  can  occur  (a)  in 
the  portal  vein  itself  or  in  its  branches  within  the  liver,  as  in  cir- 
rhosis of  the  liver,  neoplasms,  echinococcus-cysts  pressing  on  the 
portal  vein  ; also  in  pylethrombosis,  and  cholecystitis.  Obstruc- 
tion to  the  flow  of  bile,  and  consequent  dilatation  of  the  bile-ducts  in 
the  liver,  and  pigment  deposits  in  melanemia  may  cause  occlusion 
of  the  capillaries  in  a similar  way.  ( b ) The  obstruction  may  occur 
from  failure  of  compensation  in  valvular  and  other  diseases  of  the 
heart.  ( c ) In  the  pulmonary  blood-vessels  caused  by  emphysema, 
chronic  pleurisy,  and  fibroid  indurations  of  the  lungs.  During 
violent  acts  of  vomiting  gastric  hemorrhage  is  occasionally  ob- 
served, and  may  be  explained  by  the  venous  congestion  of  the 
mucous  membrane  of  the  stomach.  Such  hemorrhages  have  been 
observed  by  the  author  during  vomiting  of  pregnancy  and  sea- 
sickness. The  veins  in  the  muscular  layer  of  the  stomach  are 
much  more  likely  to  be  compressed  during  the  violent  contractions 
of  the  gastric  muscularis  than  are  the  arteries.  Obstruction  to  the 
pulmonary  or  cardiac  circulation  is  not  so  frequent  a cause  of  gas- 
tric hemorrhage  as  obstruction  in  the  portal  vein  or  the  liver. 
Next  to  ulcer  and  cancer  of  the  stomach,  cirrhosis  of  the  liver  is 
the  most  frequent  cause  of  gastric  hemorrhage. 

8.  Acute  Infectious  Diseases. — The  manner  and  process  by  which 
gastric  hemorrhage  is  brought  about  in  these  diseases  are  not  well 
understood.  It  is  usually  explained  by  the  dissolution  of  the 
blood-corpuscles  and  alterations  in  the  walls  of  the  blood-vessels. 
In  a few  instances  only  was  the  hemorrhage  found  to  be  due  to 
plugging  of  the  vessels  with  bacteria.  The  gastrorrhagia  in  acute 
yellow  atrophy  of  the  liver  has  been  attributed  to  the  simultaneous 
action  of  a variety  of  causes — for  instance,  dissolution  of  the 
blood  by  bacteria  or  bile  constituents,  together  with  obstruction  of 
portal  circulation  due  to  disease  and  occlusion  of  the  hepatic 
capillaries.  The  infectious  diseases  that  are  generally  assigned  as 
causes  of  gastric  hemorrhage  are  yellow  fever,  acute  yellow  atrophy 
of  the  liver,  malaria,  relapsing  fever,  cholera,  typhoid  fever,  typhus 
fever,  erysipelas,  diphtheria,  small-pox,  measles,  and  scarlet  fever. 

g.  Certain  Constitutional  Affections.  — ( a ) Scorbutus,  purpura, 
hematophilia,  and  other  affections  inducing  a hemorrhagic  diathe- 
sis. ( b ) Various  forms  of  anemias  ; progressive  pernicious  anemia, 
chlorosis,  leukocythemia,  and  pseudoleukocythemia.  (< c ) Malaria. 
The  author  has  lived  in  the  malarious  regions  of  Virginia  and 
Maryland  along  the  Chesapeake  Bay,  and  can  assert  from  exten- 


NEPHRITIS — M ELENA. 


685 


sive  experience  that  this  disease  is  capable  of  causing  hemorrhage 
from  the  stomach.  Not  only  are  the  hemorrhages  cured  by  quinin, 
but  the  malarial  organism  has  been  found  by  the  writer  in  the 
vomited  blood.  Hans  Herz  in  his  new  contribution,  “ Die  Stor- 
ungen  des  Verdauungsapparates  als  Ursache  und  Folge  anderer 
Erkrankungen,”  admits  the  influence  of  malaria  in  bringing  about 
these  gastric  affections.  We  may  distinguish  (1)  the  periodical 
malarial  gastric  hemorrhage  (curable  by  quinin);  (2)  the  pernicious 
malarial  gastric  fever ; (3)  gastric  hemorrhages  due  to  extreme 
anemia  brought  about  by  malarial  cachexia;  (4)  cholemia.  This  is 
attributed  to  dissolution  of  the  blood-corpuscles  by  biliary  con- 
stituents. 

10.  Nephritis. — In  very  rare  instances  hemorrhage  from  the 
stomach  has  been  reported  in  connection  with  contracted  kidneys. 
Wm.  H.  Welch  found  the  cause  of  a fatal  gastric  hemorrhage  in 
one  such  case  to  be  due  to  the  bursting  of  a miliary  aneurysm  of 
a smalt  artery  in  the  submucous  coat,  and  he  considers  that  all 
similar  hemorrhages  occurring  in  such  cases  are  referable  to 
disease  of  the  vessel  walls  (Pepper’s  “ System  of  Medicine,”  vol.  11, 
P.  582). 

11.  Melcena  Neonatorum. — An  extravasation  of  blood  into  the 
stomach  and  intestines  of  the  new-born  infant,  occurring  most 
often  in  the  first  few  hours  of  life.  Large  quantities  of  blood  are 
lost  by  the  intestinal  evacuations  or  by  vomiting.  The  origin  of 
this  disease  is  very  obscure.  In  some  cases  it  seems  to  be  an 
infection ; in  others,  scorbutus  or  hemophilia  seems  to  lie  at  the 
foundation.  In  rare  cases  gastric  and  duodenal  ulcers  have  been 
found.  Landau  (“  Ueber  Malaena,  Habilitationschrift,”  Breslau, 
1875)  and  others  have  ascribed  it  to  embolism  of  the  umbilical 
veins.  They  presume  that  thrombi  become  detached  from  this 
vein  and  the  ductus  arteriosis,  and  reach  the  gastric  or  intestinal 
arteries.  W.  Soltau  Fenwick  (“  Disorders  of  Digestion  in  Infancy 
and  Childhood  ”)  reports  a case  in  which  postmortem  examination 
failed  to  explain  the  origin  of  the  bleeding,  but  when  the  vessels 
of  the  stomach  were  subsequently  injected,  a large  vein  was  dis- 
covered close  to  the  cardiac  orifice,  through  an  aperture  in  which 
the  injection  poured  out  in  great  quantities.  Fenwick  correctly 
suggests  that  in  many  cases  the  cause  of  the  bleeding  is  not 
detected  because  postmortem  contraction  of  the  mucous  mem- 
brane may  have  obliterated  the  signs  of  rupture  of  some  varicose 
vein  in  the  stomach  or  bowel.  Among  twenty  cases  recorded  by 


686 


HEMORRHAGE  FROM  THE  STOMACH. 


Rilliet  and  Barthez  (“  Trait,  des  Malad.  de  l’enfance,”  2d  edition, 
vol.  ii,  pp.  295-310),  nine  exhibited  melena  within  thirty-six  hours, 
and  seventeen  before  the  sixth  day.  Silbermann  (“  Gerhardt’s 
Handbuch,”  iv,  S.  415)  reported  thirty-seven  cases,  in  twenty-seven 
of  which  the  hemorrhage  occurred  within  the  first  two  days.  The 
clinical  picture  of  this  fatal  infantile  disease  is,  in  brief,  about  as 
follows  : The  child  is  very  anemic,  the  evacuations  consist  of  thick, 
dark  blood,  and  are  followed  by  collapse  or  great  restlessness.  The 
stools  succeed  one  another  in  rapid  succession,  and  soon  consist 
entirely  of  bright  blood.  The  hemorrhage  from  the  bowels  con- 
tinues for  about  twenty-four  hours ; hematemesis  is  not  so  fre- 
quent. If  the  loss  of  blood  is  excessive,  the  infant  succumbs  to 
heart  failure;  but  even  in  the  less  severe  cases,  in  which  it  gradu- 
ally improves,  it  will  remain  anemic  for  many  weeks,  or  eventually 
die  of  some  acute  gastrointestinal  disease.  The  mortality  of 
melena  is  variously  stated  at  from  sixty  to  seventy-five  per  cent. 

E.  von  Preuschen  (“  Centralbl.  f.  Gynakol.,”  xviii,  9,  1894)  bases 
his  explanation  on  the  fact  that  blood  extravasations  were  found 
in  the  brains  of  the  infants  simultaneously  with  melena.  Accord- 
ingly, he  regards  the  brain  lesion  as  the  cause  of  the  disease. 
Suffice  it  to  say  that  frequently  no  blood  extravasation  has  been 
found  in  the  brain  in  these  cases,  and  that  it  may  also  rationally  be 
interpreted  as  the  contemporaneous  expression  of  the  same  severe 
constitutional  disturbances.  F.  Gartner  (“  Archiv  f.  Gynakol.,” 
xlv,  1893)  claims  to  have  discovered  the  cause  of  an  infectious  dis- 
ease in  infants  analogous  to  melena.  In  fact,  he  calls  this  organism 
the  bacillus  of  melena.  His  researches  have,  as  yet,  not  been  con- 
firmed. Grynfelti  (“Arch,  de  Tocol.  et  Gynecol.,”  Bd.  xix.  Nr.  6) 
compares  melena  to  the  disencumbering  discharge  of  blood  occur- 
ring through  the  hemorrhoidal  veins  in  chronic  diseases  of  the 
liver.  It  is  not  impossible  that  the  sudden  closure  of  the  um- 
bilical artery  may  cause  a collateral  overfilling  of  the  other  abdom- 
inal organs.  L.  Fischer  (“  Munch,  med.  Wochenschr.,”  xliv,  1897) 
suggests  that  such  an  excess  of  blood  may  be  caused  by  a late 
ligation  of  the  umbilical  cord,  but  all  of  these  explanations,  although 
very  interesting,  are  conjectural. 

12.  Nej'vous  Conditions. — The  experiments  of  Schiff,  Brown- 
Sequard,  Ebstein,  and  Ewald  make  it  probable  that  injury  to  the 
cerebral  peduncles — optic  thalami,  corpus  striatum,  the  crura,  and 
the  anterior  corpora  quadrigemina — may  cause  gastric  hemor- 
rhages and  formation  of  peptic  ulcers.  This  is  a justifiable  deduc- 


I D I OPAT H I C HEMORRHAGE. 


687 


tion  when  we  are  dealing  with  physiological  experiments,  but  there 
is  no  evidence  that  gastric  hemorrhage  sufficient  to  be  of  clinical  im- 
portance can  be  caused  by  lesions  of  the  central  nervous  system. 
A number  of  the  most  conservative  authors  hold  that  gastric  hem- 
orrhages occur  in  hysterical  women.  Personally,  I have  had  no 
opportunity  to  observe  an  unmistakable  case  of  hemorrhage  from 
the  stomach  in  a hysterical  woman  that  could  not  be  explained  in 
some  other  way.  I do  not  wish  to  deny  that  it  occurs,  but  the 
chance  of  deception  by  crafty  patients  is  great.  It  should  be  men- 
tioned in  this  connection,  that  in  patients  suffering  from  undoubted 
gastric  ulcers  hemorrhages  are  liable  to  occur  after  psychical  and 
emotional  excitement.  Hemorrhages  from  the  stomach,  which 
have  been  reported  to  occur  in  locomotor  ataxia,  in  tubercular 
meningitis,  in  epilepsy,  and  in  progressive  paralysis  of  the  insane, 
may  be  classified  under  this  heading,  but  are  largely  attributable  to 
other  causes. 

ij.  The  Rupture  of  Abscesses  or  of  Aneurysms  from  Adjacent 
Organs  into  the  Stomach. 

i/f.  Idiopathic  Gastric  Hemorrhage. — Wm.H.  Welch  (/.  c.)  assigns 
a place  to  hemorrhage  attributed  to  this  cause,  quoting  from 
Flint  (“  Principles  and  Practice  of  Medicine,”  5th  edition,  p.  513); 
“ Hemorrhage  sometimes  occurs  from  the  stomach,  as  from 
the  bronchial  tubes,  the  Schneiderian  membrane,  and  in  other 
situations,  without  any  apparent  pathological  connections,  neither 
following  nor  preceding  any  appreciable  morbid  conditions.  It  is 
then  to  be  considered  as  idiopathic.”  Apparently  healthy  persons, 
it  is  claimed,  suddenly  have  profuse  gastric  hemorrhages,  which 
are  followed  only  by  symptoms  immediately  referable  to  the 
bleeding.  They  develop  no  further  symptoms,  and  often  have  no 
other  hemorrhage. 

Personally,  we  consider  that  so-called  idiopathic  causes  should 
have  no  place  in  the  etiology  of  gastric  hemorrhage.  The  sources 
of  error  are  too  great  to  be  eliminated  by  a microscopic  examina- 
tion of  the  stomach.  We  have  already  referred  to  the  cases  of 
Lancaster  and  Soltau  Fenwick  of  fatal  hemorrhages  resulting 
from  pin-point  openings  in  gastric  vessels.  Orth  and  Chiari  have 
reported  similar  cases.  Capillary  hemorrhages  can  very  often  not 
be  demonstrated  at  all.  One  must  not  overlook  the  fact  that  hem- 
orrhage from  the  stomach  is  not  the  only  cause  of  hematemesis. 
The  source  of  the  blood,  which  may  have  gained  access  to  the 
stomach,  may  be  in  the  mouth,  nose,  throat,  bronchial  tubes, 


688 


HEMORRHAGE  FROM  THE  STOMACH. 


esophagus,  or  the  duodenum.  Ewald  (“  Real-Encyklopadie,”  3. 
Aufl.,  xiv,  “ Magenkrankheiten,”  p.  288)  reports  a case  of  fatal 
gastric  hemorrhage  with  absolutely  no  lesion  in  the  stomach  or 
anywhere  in  the  digestive  tract.  A.  Frankel  (“  Deutsch.  Med. 
Wochenschr.,”  1894)  reported  a case  of  fatal  gastric  hemorrhage 
in  an  anemic  patient  due  to  slight  capillary  erosions. 

Pathology. — It  can  not  be  considered  the  object  of  this  work 
to  describe  the  manifold  lesions  that  are  found  after  death  from 
gastric  hemorrhage.  It  is  sometimes  very  difficult  to  find  the  source 
of  fatal  gastric  hemorrhage.  Often  it  has  proved  fruitless.  In  such 
cases  writers  have  overcome  the  difficulty  by  assigning  the  cause  of 
the  hemorrhage  to  diapedesis,  and  not  to  rupture  of  a blood-vessel. 
In  most  cases  of  gastrorrhagia  the  outpouring  of  blood  is  very  sud- 
den and  profuse,  and  the  conception  of  diapedesis  does  not  justify 
the  belief  that  the  red  corpuscles  can  escape  through  the  unrup- 
tured walls  of  blood-vessels  with  that  combined  rapidity  and 
abundance  that  is  necessary  to  explain  the  typical  gastric  hemor- 
rhage (Welch,  /.  c.).  In  Welch’s  case  of  bursting  of  a miliary 
aneurysm,  over  an  hour  of  continuous  searching  was  required  to 
find  the  pin-hole  perforation  in  the  bottom  of  which  lay  the  small 
aneurysm.  The  erosion  in  Chiari’s  case  (“  Prag.  med.  Wochenschr.,” 
82,  Nr.  50)  was  not  larger  than  a hemp-seed.  The  more  pains- 
taking and  careful  the  search  after  the  source  of  the  hemorrhage 
is  made,  the  more  frequently  will  a definite  anatomical  lesion  be 
found  as  the  cause.  Injection  of  the  gastric  vessels  with  some 
highly  colored  fluid  aids  in  finding  the  ruptured  vessel. 

Symptomatology. — There  are  cases  of  undoubted  gastric 
hemorrhage  that  present  no  symptoms  whatever.  Very  small 
amounts  of  blood  do  not  lead  to  vomiting,  and  are  not  sufficient 
to  produce  visible  alterations  in  the  stools.  As  a rule,  patients  do 
not  observe  the  character  of  their  stools.  Very  frequently  the 
stools  are  not  even  observed  by  the  attending  physician.  It  fol- 
lows that  it  is  possible  for  large  gastric  hemorrhages  to  escape 
detection  when  the  blood  escapes  exclusively  by  way  of  the  intes- 
tines. In  cases  of  sudden  pallor  and  weakness,  as  occur  in  patients 
suffering  from  gastric  diseases,  and  even  in  such  as  have  hitherto 
presented  no  history  of  gastric  disease,  the  stools  should  by  all 
means  be  examined.  The  symptoms  that  lead  up  to  gastric 
hemorrhage  are  described  in  the  chapters  on  Ulcer  and  Carci- 
noma. The  symptoms  that  are  directly  brought  about  by  the  loss 
of  blood  are,  in  severe  cases,  fainting,  unconsciousness,  and  con- 


SYMPTOMATOLOGY  OF  GASTKORKH AGIA.  689 

vulsion ; but  when  the  hemorrhage  has  not  been  profuse,  the 
patient  feels  a progressive  weakness  and  languor.  Sometimes  a 
giddiness,  vertigo,  tinnitus,  and  flashes  before  the  eyes  are  com- 
plained of.  In  copious  bleeding,  nausea  and  vomiting  are,  as  a 
rule,  produced;  but  whether  the  bleeding  was  copious  or  not,  the 
symptoms  of  anemia  sooner  or  later  become  evident.  The  appear- 
ance of  the  vomited  blood  will  vary  according  to  the  time  it  has 
remained  in  the  stomach  prior  to  emesis,  according  to  the  source 
of  the  hemorrhage, — that  is,  whether  it  be  arterial  or  venous, — 
and  the  condition  of  the  gastric  juice,  and  whether  remnants  of 
food  were  in  the  stomach  at  the  time  the  rupture  of  the  vessel 
occurred.  Food  that  has  remained  in  the  stomach  for  a longer 
time  assumes  a dark  brown  or  chocolate  color  or  the  appearance  of 
coffee-grounds  under  the  action  of  the  gastric  juice.  The  quantity 
may  vary  from  thirty  grams  to  one  liter  or  more.  It  is  sometimes 
difficult  to  estimate  the  total  quantity  of  blood  that  has  been  lost, 
because  a certain  portion  of  the  blood  is  invariably  lost  by  the 
stools.  In  certain  cases  the  entire  quantity  of  blood  lost  by  rup- 
ture of  a gastric  blood-vessel  passes  into  the  intestines;  larger 
admixtures  of  blood  to  the  stool  can  be  easily  recognized  when 
the  administration  of  iron  or  of  bismuth  can  be  excluded.  Smaller 
quantities  can  not  be  recognized  by  inspection.  In  this  case  some 
of  the  tests  described  in  chapter  xm  will  have  to  be  gone 
through. 

Although  a hemorrhage  has  been  very  copious,  it  may  be  re- 
peated several  times — at  short  intervals. 

Rise  of  Temperature  After  Gastric  Hemorrhage . — After  a copious 
loss  of  blood,  rise  of  temperature  can  be  experimentally  produced 
in  animals.  This  fever,  which  has  been  termed  anemic  fever,  is 
not  peculiar  to  gastric  hemorrhages,  but  occurs  in  a similar  manner 
from  hemorrhages  from  other  organs.  It  was  first  emphasized  by 
Leichtenstern  that  a mild  or  a high  fever  is  a frequent  and  even 
regular  phenomena  of  gastric  hemorrhage  caused  by  peptic  ulcer. 
This  does  not  signify  that  fever  indicates  that  the  hemorrhage  has 
come  from  an  ulcer;  it  is  frequently  observed  in  hemorrhages  from 
carcinoma,  and  even  from  the  hemorrhage  resulting  from  passive 
congestion  in  certain  forms  of  chronic  gastritis.  It  is  quite  well 
known  that  fever  usually  follows  venesection.  The  term  anemic 
fever  merely  suggests  that  it  occurs  with  various  hemorrhages 
leading  to  anemia.  The  intensity  of  the  febrile  reaction  is  largely 
influenced  by  two  factors — viz.,  the  rapidity  and  the  quantity  of  the 


690 


HEMORRHAGE  FROM  THE  STOMACH. 


hemorrhage.  Small  hemorrhages  are,  as  a rule,  not  followed  by 
elevation  of  temperature.  The  pathological  physiology  of  this 
fever  is  very  obscure.  In  advanced  anemia  the  blood  stagnates  in 
the  internal  organs,  while  the  peripheral  parts  become  deficient  in 
blood  and  cooler,  and  the  rate  of  the  blood-current  is  considerably 
reduced;  thus  the  loss  of  heat  from  the  surface  is  diminished,  and 
the  heat  of  the  internal  parts  is  increased.  In  the  author’s  opinion 
this  is  the  most  probable  explanation.  Other  theories  explain  the 
fever  by  an  invasion  of  bacteria  through  the  ruptured  blood-vessel ; 
by  the  resorption  of  putrefying  blood-masses  from  the  intestine; 
and  by  the  assumption  that  advanced  anemia  stimulates  the  heat 
centers  in  the  medulla. 

This  fever  may  last  several  days,  and  is  accompanied  by  marked 
acceleration  of  the  pulse.  The  rate  of  the  beat  can  frequently  be 
determined  only  by  auscultation  over  the  heart,  the  radial  pulse 
being  frequently  imperceptible.  Notwithstanding  this,  the  impulse 
of  the  apex-beat  may  appear  intensified. 

The  Disturbances  of  Sight — Blindness  After  Gastric  Hemorrhages. 
— These  are  extraordinary  and  rare  complications  of  copious  loss 
of  blood  from  the  stomach,  and  are  known  to  occur  after  hemor- 
rhages from  other  organs.  But  although  hemorrhages  from  other 
organs  are  frequent,  disturbances  of  sight,  as  a consequence,  occur 
only  exceptionally.  It  has  been  argued  that  in  uterine  hemor- 
rhages the  slowness  of  the  effusion,  and  in  traumatic  hemorrhages 
the  otherwise  healthy  condition  of  the  patient,  prevents  a develop- 
ment of  eye  phenomena.  It  is  well  known  that  copious  hemor- 
rhages from  the  lungs  in  phthisical  patients  are  not  followed  by 
optic  phenomena.  Blindness  has,  however,  been  observed  after 
very  violent  attacks  of  vomiting  unaccompanied  by  any  evidence 
of  hemorrhage,  which  suggests  that  perhaps  the  act  of  emesis  may 
be  instrumental  in  the  production  of  these  eye  symptoms. 

These  disturbances  of  sight  may  occur  immediately  after  the 
hemorrhage,  but,  as  a rule,  they  do  not  appear  until  from  the  fifth 
to  the  eighth  day,  but  they  have  been  observed  as  late  as  the 
twenty-fourth  day.  Slight  attacks  of  amaurosis,  amblyopia,  or  even 
transient  blindness,  are  sometimes  overlooked  because  other  graver 
symptoms  step  to  the  foreground,  and  when  the  strength  of  the 
patient  is  very  much  spared,  owing  to  extreme  prostration,  there  is 
little  opportunity  for  using  and  testing  the  eyesight.  Fortunately, 
the  disturbances  of  sight  disappear  in  the  majority  of  cases,  but  in 
others  permanent  blindness  of  one  or  both  eyes  may  result.  The 


§ 


DIAGNOSIS  OF  GASTKOKKH AGI A. 


69 


usual  result  is  recovery  with  a slight  defect  of  sight,  such  as  irreg- 
ularities in  the  visual  field,  color-blindness,  etc.  Forster  has 
observed  extravasations  in  the  retina  and  grayish  clouding  around 
the  papilla  immediately  after  the  hemorrhage.  In  some  cases  these 
changes  did  not  produce  any  symptoms  whatever  in  other  cases 
they  led  to  atrophy  of  the  optic  nerve.  According  to  Knies, 
ophthalmoscopical  examination  is  often  entirely  negative  ; at  other 
times  he  found  merely  a pale  papilla  and  very  narrow  blood-ves- 
sels, and  finally  complete  atrophy  of  the  optic  nerve  such  as  occurs 
in  retrobulbar  neuritis.  In  a few  cases  he  claims  to  have  observed 
complete  choked  disc,  and  finally  in  a number  of  cases  an  entirely 
normal  fundus  and  papilla. 

The  cause  of  the  eye  affection  is  not  known.  Gowers  attributes 
it  to  an  influence  in  the  nature  of  shock  on  the  nerve  elements  of 
the  retina.  Forster  supposed  that  malnutrition  of  the  nerve-fibers, 
swelling,  and  clouding  occurred  through  absorption  of  water  from 
the  vitreous  substance.  Ziegler  demonstrated  fatty  degeneration 
in  the  optic  nerve  and  retina,  particularly  in  the  neighborhood  of 
the  lamina  cribrosa;  results  which  he  attributes  to  ischemia. 
Ulrich  assumes  a circulatory  disturbance  at  the  edges  of  the  papilla 
where  the  retinal  vessels  are  bent  in  a sharp  angle;  this  compels 
the  intraocular  pressure  to  remain  unchanged,  while  the  general 
blood  pressure  rapidly  sinks.  Knies  locates  the  changes  in  the 
optic  nerve  itself,  not  in  the  retina. 

There  are  disturbances  of  sight  after  gastric  hemorrhages  which 
appear  to  be  of  cerebral  origin.  They  are  usually  not  permanent, 
but  clinically  they  are  distinguishable  from  those  previously  de- 
scribed. The  reaction  of  the  pupil  is  preserved ; there  may  be 
total  blindness,  or  hemianopia. 

Diagnosis. — In  all  cases  of  hematemesis  it  will  be  necessary 
first  to  decide  whether  the  material  vomited  is  really  blood,  because 
a color  more  or  less  resembling  that  of  altered  blood  may  be  pro- 
duced in  the  vomit  by  iron,  bismuth,  claret,  fruits, — such  as  black- 
berries, mulberries,  cranberries, — and  bile.  One  or  other  of  the 
tests  for  blood  in  the  stomach-contents  given  in  chapter  xm  will 
here  become  necessary.  We  recommend  the  modification  of  Van 
Deen’s  method,  suggested  by  H.  Weber.  And,  secondly,  it  must 
be  ascertained  whether  the  blood  is  really  from  the  stomach,  and 
not  from  the  nose,  throat,  or  the  esophagus.  Here  a careful  ex- 
amination of  the  respiratory  passages,  of  the  mouth  and  nose,  will 
generally  reveal  the  source  of  the  bleeding.  The  differential  diag- 


692  HEMORRHAGE  FROM  THE  STOMACH. 

nosis  between  hematemesis  and  hemoptysis  is  given  in  the  chapter 
on  Gastric  Ulcer.  In  doubtful  cases  the  microscope  may  reveal 
tubercle  bacilli  in  case  the  hemorrhage  came  from  the  lungs. 

The  differential  diagnosis  between  these  two  causative  conditions 
presents  difficulties  when  there  are  indications  of  pulmonary 
tuberculosis  simultaneously  with  those  of  gastric  ulcer.  Hemor- 
rhages that  come  from  the  esophagus,  especially  the  lower  portion 
of  it,  can  hardly  be  distinguished  from  genuine  gastric  hemor- 
rhages. Several  cases  have  been  reported  of  fatal  hemorrhage 
from  varices  of  the  esophagus,  and  the  esophagoscope  has  been 
suggested  as  a means  for  differential  diagnosis.  In  recent  hem- 
orrhages from  the  stomach  and  esophagus,  however,  the  use  of 
so  rigid  and  annoying  an  instrument  to  the  patient  as  the  eso- 
phagoscope is  unjustifiable.  A microscopic  examination  of  vomited 
matter  may  often  reveal  intact  red  blood-corpuscles,  making  the 
diagnosis  definite.  It  has  been  suggested  that  in  hemorrhages  from 
the  esophagus  the  blood,  as  a rule,  is  not  mixed  with  food 
remnants;  but  in  stenosis  of  the  esophagus  the  ingesta  accumu- 
lates above  the  constriction,  and  may  therefore  be  vomited  up 
mixed  with  blood;  but  the  food  in  esophageal  vomiting  is  alkaline, 
undigested,  mixed  with  mucus,  saliva,  and  perhaps  blood ; food 
brought  up  from  the  stomach  is  more  or  less  digested,  has 
an  acid  reaction,  and  contains  products  of  peptic  digestion.  Vom- 
iting of  blood  occurs  in  about  fifty  per  cent,  of  all  cases  of  gastric 
ulcer.  The  next  most  frequent  cause  is  carcinoma.  But  there 
is  a variety  of  other  abnormal  conditions  of  the  stomach  which 
may  bring  forth  this  symptom  ; these  are  : (1)  Acute  and  chronic 

gastritis.  Teissier  reported  a case  of  an  alcoholic  subject  suffering 
from  chronic  gastritis  who  showed  frequent  vomiting  of  food  and 
blood.  The  autopsy  showed  a simple  chronic  inflammation  of  the 
stomach  with  hypertrophy.  (2)  The  gastric  hemorrhages  occur- 
ring periodically  and  associated  with  abnormal  conditions  in  other 
organs.  We  have  considered  these  possibilities  in  the  etiology. 
DaCosta  mentions  vicarious  gastric  hemorrhage  in  patients  suffer- 
ing from  hemorrhoids.  The  author  has  never  seen  a case  of  this  sort. 

The  gastric  hemorrhages  that  occur  from  ischemia  due  to  per- 
sistent vomiting  are  at  times  puzzling.  During  a voyage  to 
Bremen  in  1896,  the  author  had  occasion  to  study  a case  of  this 
kind.  A healthy  young  man,  age  twenty-two,  suffered  intensely 
from  seasickness.  For  the  first  three  days  he  vomited  every- 
thing he  ate,  and  when  his  stomach  was  empty,  the  nausea  would 


HEMATEMESIS  NOT  DUE  TO  ULCER.  693 

continue,  although  nothing  but  a little  mucus  was  forced  up,  under 
painful  exertions.  On  the  seventh  day  of  the  voyage  he  vomited 
half  a liter  of  blood,  and  on  the  eighth  day  about  ^ of  a liter. 
After  that  he  was,  by  the  author’s  suggestion,  kept  constantly 
under  narcotics.  The  hypodermic  injections  of  morphin  proved 
most  effective  in  allaying  the  vomiting,  ice-bags  were  placed  over 
the  epigastrium,  and  the  patient’s  strength  kept  up  by  nourishing 
enemata.  Although  he  vomited  blood  on  three  other  occasions 
after  that,  the  amount  was  small.  After  our  arrival  in  Bremen  he 
recovered  entirely,  and  could  eat  almost  the  regular  hotel  menu. 
This  patient  had  never  previous  to  this  voyage  suffered  from  any 
gastric  disease,  and  his  vomiting  of  blood  could  be  attributed  only 
to  the  persistent  emesis  caused  by  the  sea-sickness. 

I have  observed  a number  of  cases  similar  to  this  in  hospital 
and  consultation  practice  where  hematemesis  was  brought  on  by 
uncontrollable  vomiting  of  pregnancy.  One  case  of  death  from 
vomiting  in  pregnancy,  in  which  one  pint  of  blood  was  vomited 
the  day  before  the  fatal  termination,  the  stomach  showed  numerous 
hemorrhagic  infarcts.  Extravasations  of  blood  had  occurred  in 
the  submucosa,  and  under  the  columnar  epithelium,  lifting  it 
from  the  glandular  layer.  The  death  of  this  patient  was  due  to  ex- 
haustion, because  not  even  rectal  enemata  could  be  retained,  and 
operative  evacuation  of  the  uterine  cavity  had  been  refused. 

In  chlorotic  and  anemic  patients  that  present  hematemesis  it  is 
wise  to  be  reserved  in  the  diagnosis  of  gastric  ulcer.  In  all  such 
cases  a careful  blood-count  should  be  made,  and  a prolonged  course 
of  iron  and  arsenic  undertaken  before  the  diagnosis  of  gastric 
ulcer  should  be  determined  upon.  The  diet  of  such  cases  should 
be  that  of  ulcer. 

The  following  is  an  example  of  how  puzzling  cases  of  gastric 
hemorrhage  may  be  clinically  : A male  patient  in  the  author’s 
private  sanatorium  had  been  complaining  for  two  years  of  intense 
gastric  pains,  which  recently  had  become  so  aggravated  as  to  cause 
refusal  of  food,  and  consequent  rapid  emaciation.  The  test-meals 
showed  a slight  excess  of  free  HC1,  equal,  on  the  average,  to  38 
degrees,  normal  NaOH.  One  morning,  while  the  patient  was 
being  examined  by  the  author,  he  began  to  vomit  his  breakfast,  and 
after  the  food  had  all  been  evacuated,  about  one  pint  of  pure  blood 
was  vomited.  The  pain  in  the  epigastrium  was  somewhat  more 
severe  for  several  days  after  this  attack,  and  on  this  account  an 
exploratory  laparotomy  was  advised.  At  the  operation,  which 

46 


694  HEMORRHAGE  FROM  THE  STOMACH. 

was  done  by  Dr.  J.  M.  T.  Finney,  the  stomach  was  found  entirely 
normal,  it  was  not  enlarged,  presented  no  abnormalities  of  any 
kind.  There  were  a number  of  enlarged  mesentery  glands,  one  of 
which  was  excised  by  the  surgeon,  but  on  histological  examina- 
tion it  showed  nothing  characteristic.  The  patient  recovered  from 
the  laparotomy,  and  under  a very  carefully  selected  diet  and  use 
of  external  heat  to  the  epigastrium  with  rest  in  bed  the  pain  was 
cured.  He  was  kept  under  observation  for  six  weeks,  and  dis- 
charged apparently  cured.  Three  months  after  the  operation  he 
was  reported  as  doing  very  well. 

Prognosis. — We  do  not  wish  to  refer  here  to  the  prognosis  of 
the  fundamental  disease  causing  the  hematemesis,  which  is  spoken 
of  in  other  chapters,  but  merely  of  the  hemorrhage  itself.  This 
prognosis  depends  upon  the  quantity  of  the  blood  lost.  The  most 
abundant  hemorrhages  are  observed  in  gastric  ulcer,  but  even 
larger  hemorrhages,  are,  as  a rule,  not  dangerous  to  life.  We  have 
repeatedly  observed  recovery  from  gastric  hemorrhage  that  had 
led  to  collapse  with  disappearance  of  the  radial  pulse.  The  dan- 
ger of  gastric  hemorrhage  exists  in  an  early  and  rapid  repetition 
of  the  loss  of  blood ; though  we  have  seen  one  case  of  profuse 
gastric  hemorrhage  which  led  to  death  in[a  very  short  time — we 
should  conjecture  about  fifteen  minutes. 

Treatment. — The  treatment  of  this  symptom  has  been  given 
under  the  heading  of  Gastric  Ulcer.  Here  we  wish  to  repeat  once 
more  the  necessity  of  absolute  rest,  of  moral  encouragement  from 
the  physician, — assuring  his  patient  that  the  symptom  is  entirely 
free  from  danger,  and  will  be  recovered  from, — total  abstention 
from  any  food  or  medicine  by  the  stomach,  and  substitution  of 
rectal  feeding.  Internal  medication  during  the  bleeding  is  danger- 
ous. The  author  favors  a hypodermic  injection  of  ergotin  or 
ergotol,  of  the  latter  thirty  minims.  Whenever  there  is  danger 
of  collapse  from  very  profuse  loss  of  blood,  subcutaneous  or  intra- 
venous injection  of  normal  salt  solution  is  strongly  recommended. 
A solution  of  0.6  to  0.75  per  cent,  of  sodium  chlorid  is  used  for 
this  purpose.  We  prefer  the  subcutaneous  injection  to  the  intra- 
venous, because  it  requires  less  apparatus,  is  rapidly  executed,  and 
free  from  danger.  About  200  c.c.  of  this  salt  solution  may  be  in- 
jected into  the  subcutaneous  connective  tissue  of  the  breast  in 
this  manner,  and  with  the  aid  of  massage  it  is  generally  rapidly 
absorbed.  The  subsequent  treatment  is  that  of  simple  anemia  and 
of  the  causative  condition. 


HISTORY  AND  PATHOGENESIS  OF  ENTEROPTOSIS. 


695 


CHAPTER  IX. 

ENTEROPTOSIS— GASTROPTOSIS. 

CONCERNING  THE  HISTORY  AND  PATHOGENESIS  OF  ENTERO- 
PTOSIS. 

The  term  enteroptosis  comes  from  the  two  Greek  words,  tvTepov, 
bowel  or  intestine,  and  nruxTiq,  fall.  It  refers  to  a dislocation  of  the 
abdominal  organs.  Splanchnoptosis  is  a synonymous  term.  Entero- 
ptosis is  a disease  in  which  the  liver  and  the  kidneys  have  descended 
from  their  normal  positions,  and  are  movable.  The  stomach  is 
often  found  descended  and  to  have  assumed  a vertical  position, 
which  induces  an  atony  of  the  gastric  wall  with  motor  and  secre- 
tory disturbances.  The  transverse  colon,  particularly  the  hepatic 
side  of  it,  is  found  descended.  Generally  only  one  kidney,  the  right, 
is  dislocated  or  very  movable.  The  terms  hepatoptosis,  nephro- 
ptosis, gastroptosis,  and  coloptosis  refer  to  the  particular  organ 
which  has  become  displaced.  The  oldest  description  resembling 
such  a clinical  picture  is  found  in  Aberle’s  work  (/.  c.) ; and 
similar  instructive  anatomical  accounts  are  found  in  the  works  of 
Becquet,  Rollet,  Rayer,  Oppolzer,  and  Chrobak,  referring  to  the 
relation  between  hysteria  and  movable  kidney.  The  causes  as- 
signed by  these  various  older  writers  to  the  production  of  movable 
kidney  are  manifold,  and  some  of  them  are  even  at  the  present 
time  still  considered  factors  in  the  etiology  of  enteroptosis;  one  of 
the  earliest  explanations  is  contusion  of  the  renal  region.  Various 
other  traumatisms  are  accused  of  bringing  about  this  effect ; par- 
ticularly severe  coughing  attacks,  such  as  occur  in  pertussis, 
bronchitis,  and  pleurisy,  which  exert  their  pernicious  effect  espe- 
cially when  rapid  emaciation  has  occurred,  as  in  phthisis,  producing 
disappearance  of  the  fat  in  the  adipose  capsule  surrounding  the 
kidney;  or  when  a pleuritic  exudate  brings  about  descent  of  the 
diaphragm,  and  thereby  of  the  liver  and  kidney. 

In  the  opinion  of  Cruveilhier,  Chapotot,  and  Valker  the  corset  is 
an  important  cause  in  the  development  of  this  disease,  and  although 
Ebstein  denied  this,  Weisker  and  Meinert  have  recently  sup- 
ported this  explanation.  Becquet  considers  that  the  floating 
kidney  is  intimately  connected  with  the  sexual  life  of  woman, 
and  explains  it  by  the  congestion  of  the  kidneys  which  occurs 


696 


ENTEROPTOSIS GASTROPTOSIS. 


during  menstruation,  as  a result  of  the  intimate  connection  be- 
tween the  ovarian  and  renal  plexus.  He  also  associates  the  trouble 
with  frequent  births,  uterine  diseases,  and  pendulous  abdomen.  I 
have  seen  a liver  in  an  autopsy  on  a young  woman,  age  twenty- 
four,  who  died  from  intestinal  perforation  in  typhoid  fever,  which 
showed  very  marked  grooves  evidently  produced  by  tight  lacing. 
The  transverse  colon,  stomach,  and  the  right  kidney  were  dis- 
placed, and  the  lower  portion  of  the  thorax  compressed  in  a funnel- 
shaped  manner.  Opolzer  believes  that  rapid  emaciation  in  wasting 
diseases  is  a cause.  Dietl  has  observed  movable  kidney  in  four 
cases  after  severe  malarial  and  typhoid  fever.  He  believes  that  in 
these  infectious  diseases  marked  change  in  volume  in  the  abdominal 
organs  occurs.  Rollet  argues  in  favor  pf  rapid  emaciation,  and  adds 
the  pressure  created  by  large  neighboring  organs,  especially  hepatic 
and  splenic  tumors.  He  suggests  the  possibility  of  inherited  pre- 
disposition. In  experiments  on  cadavers  Heller  could  not  confirm 
the  view  that  traction  made  upon  the  kidneys  by  dislocations  of 
the  female  sexual  organs  could  effect  renal  displacement. 

In  1881  Landau  published  a very  complete  monograph  on  float- 
ing kidney.  In  explaining  the  etiology  of  the  disease  he  empha- 
sized three  factors:  (1)  Rapid  disappearance  of  the  fat  in  the  adi- 
pose embedding  of  the  kidney,  and  laxity  of  the  peritoneum.  The 
disappearance  of  the  fat  must  be  rapid,  because  Landau  considered 
it  possible  that  an  accommodation  might  be  effected  through  the 
elasticity  of  the  capsule.  (2)  Disease  of  the  abdominal  walls, 
which  are  subjected  to  considerable  changes  in  their  elasticity, 
density,  and  resistance  by  pregnancy  and  abdominal  tumors.  In 
rapidly  consecutive  pregnancies  the  condition  known  as  pendulous 
abdomen  may  be  developed.  Normally,  there  is  a uniform  pres- 
sure on  all  abdominal  organs,  but  in  cases  of  pendulous  abdomen 
this  is  converted  into  the  opposite  condition,  and  the  intestines  that 
hang  into  the  relaxed  abdominal  bag  exert  a traction  upon  the  super- 
imposed organs.  (3)  The  numerous  displacements  of  the  genito- 
urinary organs,  which  exert  a direct  traction,  upon  the  kidneys  by 
way  of  the  ureters. 

Among  forty-two  observations  by  Landau,  only  two  were  nulli- 
parae, and  one  of  these  had  been  operated  on  for  an  ovarian 
tumor. 

Litten  was  the  first  to  distinguish  between  congenital  and  ac- 
quired dislocation  of  the  kidney,  and  also  between  dislocated 
kidney  with  and  without  movability.  His  differentiation  between 


OBSERVATIONS  ON  GASTROPTOSIS.  697 

a movable  kidney  and  a floating  kidney  that  has  developed  its  own 
mesentery  is  a masterpiece  of  clinical  diagnosis,  containing  also  a 
description  of  the  possibilities  of  respiratory  movements  that  are 
imparted  to  the  right  kidney,  particularly  by  the  diaphragm  and 
the  liver,  thus  explaining  the  predisposition  of  the  right  kidney 
to  abnormal  movability.  Kuttner  argues  that  a kidney  that  has 
become  loose  in  its  adipose  capsule  follows  the  movements  of  the 
diaphragm  in  a more  extensive  manner.  He  explains  the  more 
frequent  movability  of  the  right  kidney  by  assuming  that  the  upper 
end  of  this  organ  gradually  glides  under  the  lower  surface  of  the 
liver,  and  is  thereafter  completely  dislocated  by  the  hepatic  pres- 
sure to  which  the  respiratory  movements  are  superadded.  James 
Israel  first  observed  the  respiratory  movements  of  the  kidney 
during  an  operation  in  which  the  lumbar  regions  had  been  opened. 
Bartels  observed  dilation  of  the  stomach  together  with  movable 
kidney,  and  was  one  of  the  first  to  describe  the  simultaneous  dis- 
location of  several  abdominal  organs.  This  author  and  his  pupil, 
Muller-Warneck,  advance  a theory  explaining  the  production  of 
dilation  of  the  stomach  by  a floating  kidney  : — the  right  kidney, 
which  has  become  dislocated,  according  to  their  conception, 
presses  on  the  descending  portion  of  the  duodenum,  which  is  firmly 
attached  to  the  posterior  abdominal  wall  by  the  peritoneum.  The 
exit  of  the  gastric  chyme  is  prevented  by  compression  of  the 
duodenum,  and  gastrectasia  is  the  consequence. 


OBSERVATIONS  ON  GASTROPTOSIS. 

J.  E.  Meckel  first  observed  in  autopsies  the  so-called  vertical 
position  of  the  stomach,  and  also  that  this  occurred  more  fre- 
quently in  females,  but  occasionally  also  in  men.  Kussmaul  gave 
the  first  clinical  description  of  the  vertical  position  of  the  stomach, 
of  which  he  distinguished  two  kinds, — the  first  was  congenital, 
and  represented  an  arrest  at  a fetal  stage  of  development,  and  the 
second  was  acquired,  caused  by  the  pressure  of  lacing.  The 
movable  pyloric  portion  of  the  stomach  is  forced  downward  and 
toward  the  left  by  the  descending  liver,  and  the  cardia  is  held 
in  its  position  near  the  median  line.  Kussmaul  observed  that  a 
stomach  of  normal  size  which  had  been  forced  into  vertical  position 
became  displaced  beneath  the  umbilicus.  This  occurs  when  the 
pylorus  is  moved  to  the  left  nearer  the  spinal  column  while  the 
cardiac  portion  with  the  fundus  is  moved  to  the  right  and  down- 


ENTEROPTOSIS — GASTROPTOSIS. 


ward.  When  the  cardia  and  pylorus  are  approximated  in  this 
manner,  the  lesser  curvature  is  converted  into  an  acute  angle. 
The  descending  arm  of  this  angle  becomes  shorter  and  shorter, 
while  the  ascending  arm  becomes  longer,  the  stomach  thereby 
assuming  the  form  of  an  intestinal  loop,  and  gradually  sinking 
below  the  umbilical  line.  (See  illustration  in  chapter  on  Motor 
Insufficiency.)  In  one  of  the  cases  described  by  Kussmaul  the 
wearing  of  the  corset  was  blamed  for  the  production  of  the  con- 
dition, because  of  very  evident  and  deep  furrows  on  the  lower 
thorax  which  were  undoubtedly  due  to  lacing. 

A similar  view  is  held  by  von  Ziemssen,  who  credits  the  so-called 
vertical  position  of  the  stomach  as  being  productive  of  many  ail- 
ments, and  occurring  principally  in  women.  He  believes  the  con- 
dition is  most  generally  acquired  during  youth  by  excessive  con- 
striction of  the  waist  in  lacing.  As  a consequence  of  this,  the 
stomach  can  only  escape  in  a downward  direction,  because  the 
lacing  compresses  the  region  of  the  lower  ribs,  and  the  epigas- 
trium offers  no  space  when  the  stomach  is  filled  with  food.  The 
pyloric  part,  which  is  the  most  movable,  makes  the  most  extensive 
excursions,  and  gradually  assumes  the  lowest  position.  At  the 
same  time,  the  duodenum  is  drawn  down  under  strong  tension  of 
the  hepatoduodenal  ligament.  According  to  Meinert,  the  normal 
position  of  the  stomach  in  the  female  sex  is  the  exception.  Ac- 
cording to  him,  gastroptosis  is  a drawing  out  of  the  pyloric  portion 
mainly — connected  with  dislocation.  He  does  not  think  that  it 
usually  involves  the  entire  stomach,  and  seeks  its  cause  in  patho- 
logical changes  of  the  liver,  or  in  the  pyloric  portion  of  the  stomach 
itself.  The  most  frequent  cause,  according  to  Meinert,  is  a patho- 
logical change  of  form  of  the  thorax.  When  these  deformities  of 
the  thorax  and  their  causes — such  as  pressure  caused  by  cloth- 
ing, or  peculiarities  of  profession,  and  rachitis — have  influenced  a 
series  of  generations,  they  are,  in  Meinert’s  opinion,  capable  of 
being  transplanted  by  inheritance  upon  both  sexes.  They  are  then 
not  congenital,  but  developmental,  abnormalities. 

Historical  Observations  on  Dislocation  of  the  Colon. — 
We  shall  presently  refer  to  Virchow’s  contribution  to  our  knowl- 
edge of  coloptosis,  to  which  he  concedes  great  importance  as  a 
primary  factor  in  the  dislocation  of  the  abdominal  organs.  He 
asserts  that  abnormal  flexures  occur  in  the  majority  of  adults,  the 
most  frequent  abnormality  being  a descent  of  the  transverse  colon, 


HISTORY  OF  COLON  AND  LIVER  DISLOCATIONS.  699 

the  next  most  frequent  being  a descent  of  the  hepatic  flexure,  and, 
lastly,  of  the  splenic  flexure.  The  simultaneous  existence  of 
floating  kidney  and  dislocated  colon  is  described  in  the  autopsy 
protocols  of  Sandifort  and  Aberle.  Leichtenstern  describes  ab- 
normal position  of  the  colon,  and  attributes  it  to  abnormal 
conditions  of  growth  and  position  dating  from  the  fetal  period. 
He  also  suggests  that  a defective  development  of  the  muscular 
ligaments  of  the  colon  and  incomplete  descent  of  the  cecum,  also 
abnormally  developed  colon,  and  abnormal  length  of  the  mesen- 
teries, are  possible  causes.  Rosenheim  holds  very  similar  views. 
Landau  describes  the  descent  of  the  hepatic  and  splenic  flexures 
of  the  colon  as  quite  constant  accompaniments  of  floating  kidney. 

Historical  Observations  on  Dislocation  of  the  Liver. — The 
liver  may  become  displaced  in  two  manners — (i)  temporarily,  by 
pressure  from  above,  such  as  is  caused  by  lacing  or  by  pleural 
effusions;  (2)  permanent  displacement,  caused  by  disease  of  the 
liver  itself,  increasing  the  volume  of  the  organ,  and  causing  descent 
by  its  augmented  weight.  The  oldest  article  on  dislocation  of  the 
liver  is  by  Cantani,  published  in  1866.  There  is  much  diversity  of 
opinion  as  to  the  frequency  of  dislocated  liver.  Meisner  thinks 
the  hepatic  dislocation  is  caused  by  lengthening  of  the  suspensory 
ligament  of  the  liver,  forming  a peritoneal  fold  analogous  to  that 
attached  to  the  right  hepatic  lobe  in  many  animals,  and  known  as 
the  “ mesohepar.”  The  direct  cause  of  the  dislocation  he  finds  in 
traumatism.  According  to  Winkler,  the  stretching  of  the  ligament 
is  passive  and  secondary;  the  first  cause,  in  his  opinion,  being  the 
sinking  of  intra-abdominal  pressure.  The  other  causes,  which  are 
accentuated  repeatedly,  are  relaxation  of  the  abdominal  walls, 
physical  overexertion,  repeated  overexertion  of  the  abdominal 
muscles,  and  rapid  emaciation.  L.  Landau  holds  that  the  fixation 
of  the  liver  is  effected  through  pressure  of  the  abdominal  muscles 
on  the  viscera  and  by  the  elasticity  of  the  lungs,  which  arch  up  the 
diaphragm.  The  so-called  ligaments  of  the  liver  are  insufficient 
to  retain  the  organ  in  position.  The  only  anatomical  attachment 
of  importance  is  that  of  the  liver  to  the  inferior  vena  cava,  by 
means  of  the  hepatic  vein.  This  attachment  explains  why  descent 
of  the  organ  as  a whole  does  not  occur  more  frequently  than  do 
partial  dislocations  of  the  anterior  margin  or  of  the  right  lobe ; 
under  such  conditions  a partial  rotation  of  the  liver  around  its 
frontal  or  sagittal  axis  occurs. 

To  this  condition  Landau  has  given  the  name  of  “ twisted,” 


700 


ENTEROPTOSIS GASTROPTOSIS. 


“ rotated,”  or  “ torsion,  liver.”  He  has  observed  it  almost  always  in 
connection  with  floating  kidney  and  descent  of  the  transverse  colon, 
a combination  practically  identical  with  the  clinical  picture  of  en- 
teroptosis. 

Historical  Views  on  General  Enteroptosis. — These  were  the 
views  held  concerning  the  etiology  of  the  dislocations  of  the  vari- 
ous abdominal  organs  when  Glenard’s  first  publication  appeared  in 
1885.  The  writings  of  Ewald  and  Meinert,  which  have  already 
been  quoted,  were  published  after  those  of  Glenard.  The  ideas  of 
the  latter  are  dwelt  upon  in  another  portion  of  this  article.  For  the 
sake  of  context,  it  may  be  repeated  that  a descent  of  the  right  or 
hepatic  flexure  of  the  colon,  followed  by  dislocation  of  the  trans- 
verse colon,  is  the  primary  disturbance  in  enteroptosis,  according  to 
this  author.  That  portion  of  the  mesocolon  that  approaches  the 
right  flexure  of  the  colon  he  calls  the  hepatocolic  ligament,  and  con- 
siders that  it  is  naturally  very  weak,  and  can  be  loosened  and 
stretched  by  the  weight  of  the  transverse  colon,  particularly  when 
this  is  burdened  with  stagnating  feces.  The  same  condition  may, 
according  to  him,  also  be  caused  by  exhausting  and  emaciating  dis- 
eases, by  loss  of  tonicity  of  the  abdominal  muscles,  by  repeated 
pregnancies,  by  gastrointestinal  autointoxication,  by  exhausting 
hemorrhage,  or  when  the  abdominal  muscles  are  permanently  dam- 
aged by  pressure  of  the  clothing. 

When  the  hepatic  flexure  of  the  colon  has  sunk,  the  right 
half  of  the  transverse  colon  follows,  up  to  the  place  where  it  is 
connected  with  the  pyloric  end  of  the  stomach  by  the  tense 
gastrocolic  ligament ; here  the  colon  becomes  kinked,  whereby 
stagnation  of  the  contents  results.  The  colon  becomes  dilated  in 
front  of  the  constriction,  but  beyond  this  it  contracts  so  that  it  can 
be  felt  as  a tense  cord.  After  the  transverse  colon  has  descended, 
the  remaining  abdominal  viscera  follow  as  their  ligaments  become 
loosened.  The  stomach  is  drawn  down  by  the  traction  on  the 
gastrocolic  ligament.  Then  follow  the  liver  and  the  kidneys. 
Ewald  has  confirmed  the  observations  of  Glenard,  but  he  did  not 
confirm  his  views  regarding  the  primary  factor  in  the  causation  of 
the  splanchnoptosis.  The  contracted  portion  of  the  colon  beyond 
the  constriction,  which  Glenard  had  designated  as  the  “ corde 
colique  transverse,”  is  considered  by  Ewald  to  be  the  pancreas.  He 
also  denies  that  a simple  kinking  of  the  colon,  uncomplicated  by 
peritonitic  adhesions  or  by  stenosing  neoplasms,  can  lead  to  stag- 
nation of  feces.  Similarly  to  authors  previously  quoted,  Ewald  does 


PATHOGENESIS  OF  ENTEROPTOSIS. 


701 


not  assign  a distinct  cause  for  this  visceral  anomaly,  simply  empha- 
sizing the  fact  that  long-standing  dyspepsias  and  bodily  overexer- 
tions may  create  altered  relations  of  pressure  and  tension,  and 
thereby  lead  to  enteroptosis. 

Ebstein,  Litten,  and  Rollet  inclined  to  the  view  that  floating 
kidney  was  a congenital  abnormality.  They  based  their  conclusions 
on  the  presence  of  a mesonephron.  The  vertical  position  and 
descent  of  the  stomach  was  considered  by  Kussmaul  a congenital 
abnormality,  and  Leichtenstern  held  the  same  view  regarding  dis- 
placement of  the  colon.  Drummond  held  the  opinion  that  a 
congenital  relaxation  of  the  peritoneal  covering  was  the  condition 
under  which  the  kidney  became  movable.  Ewald,  Lindner,  and 
Kuttner, — comparatively  recent  writers  on  the  subject, — realizing 
that  all  explanations  made  hitherto  were  more  or  less  hypothet- 
ical, have  inclined  also  to  the  theory  of  inherited  predisposition  ; 
but  Landau  considers  a cbngenital  predisposition  improbable. 

Although  partial  dislocations  of  individual  viscera,  and  even 
of  two  or  three  of  these  organs  at  the  same  time,  have  been 
observed  and  described  by  other  authors  quoted,  the  first  com- 
plete clinical  representation  must  be  credited  to  Glenard.  But 
one  can  not  fail  to  be  impressed  with  the  fact  that  the  explana- 
tions of  the  etiology  given  by  Glenard  himself,  as  well  as  by  writers 
antedating  and  succeeding  him,  are  widely  divergent.  It  is  appar- 
ent from  the  writings  of  these  authors  that  the  order  of  displace- 
ment and  the  new  abnormal  position  of  the  dislocated  organs  are 
very  variable.  Throughout  all  of  these  writings,  however,  there 
is  a general  agreement  that  these  dislocations  are-  pathological. 

Pathogenesis  of  Enteroptosis. — Most  of  the  hypotheses  pre- 
sented in  the  foregoing  in  explanation  of  the  etiology  of  enteropto- 
sis can  not  be  controlled  experimentally.  Glenard’s  hypothesis 
also  evades  critical  investigation.  The  view  of  Landau  that  the  prin- 
cipal and  primary  cause  is  disease  of  the  abdominal  walls  is  not  ap- 
plicable to  a large  number  of  cases;  for  enteroptosis  occurs  in  all 
ages,  in  men  as  well  as  in  women.  Personally,  I have  observed 
two  cases  in  young  girls,  aged  ten  and  twelve  years  respectively, 
and  one  case  in  a boy  aged  eleven.  Gastroptosis,  movable  right 
kidney,  and  dislocation  of  the  colon  have  been  observed  in  men 
with  strong  abdominal  muscles,  and  also  in  women  who,  although 
they  had  given  birth  to  one  child,  showed  no  relaxation  of  the 
abdominal  muscles.  Therefore,  the  explanation  of  Landau  is  not 
universally  applicable.  Meinert’s  views  do  not  explain  the  exist- 


7 02 


ENTEROPTOSIS GASTROPTOSIS. 


ence  of  enteroptosis  in  men  and  children,  and,  in  order  to  escape 
from  this  dilemma,  he  conceived  a theory  of  inheritance  of  acquired 
malformations  of  the  thorax.  Langerhans  (“  Archiv  fiir  Verdau- 
ungs-Krankheiten,”  Bd.  in,  1897)  recognizes  five  causes,  all  of 
which  are  more  or  less  familiar  to  us : (1)  Relaxation  of  the  abdo- 
minal muscles;  such  cases  developing  after  childbirth  he  designates 
as  Landau’s  enteroptosis.  (2)  Hereditary  enteroptotic  predisposi- 
tion. Stiller,  who  adheres  to  this  view  (“Archiv  fur  Verdauungs- 
Krankheiten,”  Bd.  11,  p.  289),  claims  to  have  found  a pathognomonic 
sign  for  enteroptosis.  This  is  the  fluctuating  tenth  rib , which  is  not 
firmly  fixed  into  the  cartilaginous  costal  arch,  together  with  the 
sixth,  seventh,  eighth,  and  ninth  ribs,  but  floats,  like  the  eleventh 
and  twelfth.  The  tip  of  the  tenth  rib,  if  it  is  floating,  can  be  felt  in 
the  prolongation  of  the  mammillary  line.  Stiller  asserts  that  when- 
ever the  tenth  rib  is  mobile,  there  must  be  a movable  kidney  and 
an  atonic  dilated  stomach.  (This  does  not  mean  gastroptosis.)  The 
reverse  is  not  always  true.  Not  in  all  cases  of  enteroptosis  did  he 
find  a floating  tenth  rib.  He  suggests  that  it  may  be  a distinguish- 
ing sign  between  congenital  and  acquired  enteroptosis.  (3)  The 
pressure  of  clothing,  as  tight  belts  and  corsets.  (4)  Chlorosis.  These 
cases  Langerhans  designates  as  Meinert’s  enteroptosis.  (5)  Nervous 
dyspepsia.  The  author,  in  accepting  these  five  factors  mentioned 
by  Langerhans  as  undoubtedly  active  in  the  pathogenesis  of  dislo- 
cated kidney  in  its  various  types,  would  add  the  following : 

(6)  Displacements  of  the  female  genito-urinary  organs,  produc- 
ing traction  upon  the  kidney  by  means  of  the  ureters.  (7)  Curva- 
tures of  the  spine.  (8)  Enlargement  and  increase  in  weight  of  the 
organ  by  neoplasms,  cysts,  etc.,  and,  perhaps,  (9)  traumatism — direct 
violence. 

The  most  recent  contribution  to  the  pathogenesis  of  enteroptosis 
is  by  Joseph  Rosengart  (“  Zeitschr.  fiir  diatetische  und  physi- 
kalische  Therapie,”  Bd.  1,  p.  220).  The  views  of  this  author,  which 
are  based  on  sound  anatomical  and  embryological  investigations, 
are  the  following : Enteroptosis  is  a disposition  of  the  abdominal 
viscera  in  such  situations  as  are  found  in  the  fetal  organism  ; it  is  a 
pathological  reversion  to  an  embryonic  state.  This  arrangement 
of  the  viscera,  which  is  normal  during  fetal  life,  becomes  still  more 
developed  during  the  first  period  of  extrauterine  life  : i.  e.}  for  a 
time  after  birth  the  abdominal  organs  are  in  a more  progressed 
state  of  enteroptosis,  from  which  the  normal  position  of  the  viscera 
is  very  gradually  developed.  If  an  arrest  of  development  at  a 


REVERSION  TO  EMBRYONIC  STAGE. 


703 


fetal  stage  or  at  a stage  of  very  early  childhood  can  not  be  accepted 
as  an  outright  explanation,  nevertheless  the  manner  and  order  in 
which  the  organs  gradually  rise  into  the  normal  position  in  the 
adult  point  out  the  way  and  the  mechanism  by  which  enteroptosis 
is  developed  from  the  normal  location  of  the  viscera  after  this  is 
once  established.  Rosengart  gives  a fascinating  account  of  a study 
of  a male  fetus  in  the  sixth  month  of  its  history.  The  small  curva- 
ture of  the  stomach  extends  perpendicularly  up  and  down,  and, 
together  with  the  gastrohepatic  (omentum  minus)  and  the  hepato- 
duodenal ligaments,  is  directed  toward  the  right,  and  anteriorly. 
The  ascending  and  the  transverse  colons  extend  in  a straight  line 
from  the  right  lower  inguinal  region  diagonally  upward  through 
the  abdomen.  More  than  one-third  of  the  right  kidney  lies  upon 
the  right  iliac  bone;  the  upper  end  of  the  right  kidney  does  not 
reach  so  high  as  the  left.  The  anterior  surface  of  the  right  kidney 
presents  a sharp  edge  running  from  the  upper  end  to  the  middle 
of  the  outer  margin  of  the  kidney.  Superiorly  and  exteriorly  to 
this  edge  the  kidney  surface  is  flattened,  and  upon  this  portion 
rests  the  liver.  The  lower  portion  of  the  kidney,  extending  down- 
ward and  inward,  is  pressed  upon  by  the  colon.  The  right  kidney 
is  separated  from  the  spinal  column  by  the  descending  portion  of 
the  duodenum.  The  kidney  is  very  movable  under  the  peritoneum, 
which  does  not  cover  the  entire  anterior  surface  of  the  organ.  In 
the  body  of  a child  four  weeks  old  the  transverse  colon  was  simi- 
larly found  to  extend  from  the  lower  right  portion  of  the  inguinal 
region  in  a straight  line  obliquely  upward.  The  course  of  the 
transverse  colon  from  the  right  inguinal  region  to  the  splenic  flexure 
was  a straight  diagonal;  the  lesser  gastric  curvature  was  turned  to 
the  right  side.  The  left  kidney  just  touched  the  edge  of  the  iliac 
bone  with  its  inferior  end  ; but  more  than  one-half  of  the  body  of  the 
right  kidney  lies  on  the  iliac  bone ; its  upper  extremity  does  not 
touch  the  beginning  of  the  diaphragm.  The  position  of  the  stom- 
ach, colon,  liver,  and  kidneys  described  by  Rosengart  corresponds 
very  closely  to  the  anatomical  picture  given  by  W.  Henle  of  the 
abdominal  organs  in  the  child  (“  Topograph.  Anatomie  des  Men- 
schen  ”),  in  which  there  is  complete  vertical  position  of  the  stomach, 
with  corresponding  altered  position  of  the  duodenum,  the  courses 
of  the  ascending  and  transverse  colons  being  merged  into  one 
straight  line ; the  right  kidney  lying  with  its  upper  half  on  the 
quadratus,  psoas,  and  transverse  muscles,  and  with  its  lower  half 
upon  the  concavity  of  the  iliac  bone.  The  under  surface  of  the 


704 


ENTEROPTOSIS GASTROPTOSIS. 


liver,  or,  rather,  what  becomes  the  under  surface  in  the  adult,  is 
turned  completely  posteriorly.  In  comparing  the  anatomical  obser- 
vations on  the  fetus  and  neonatus  with  the  autopsy  reports  on 
cases  of  enteroptosis, — such  as  are  presented  by  Ebstein,  Hayem, 
Aberle,  Sandifort,  Rayer,  Schutze,  Legroux,  Danlos,  Cuilleret,  and 
L.  Krez, — the  impression  will  be  gained  that  the  fetal  situation 
of  the  organs  had  continued  unchanged  during  childhood,  and 
throughout  the  entire  life.  As  has  already  been  stated,  Kussmaul 
regards  the  vertical  position  of  the  stomach  in  the  adult  as  a per- 
petuation of  a fetal  condition,  and  my  observations  on  the  exist- 
ence of  gastroptosis  in  young  children  would  confirm  this  view. 
The  arrest  of  any  one  of  the  abdominal  organs  at  a stage  of  fetal 
development  is  the  condition  necessary  to  create  ptosis.  As 
Rosengart  points  out,  in  order  that  the  right  kidney  shall  reach 
its  correct  position,  and  that  the  ascending  colon  shall  acquire  its 
permanent  location,  it  is  necessary  for  the  colon  to  pass  in  front  ot 
and  over  the  right  kidney.  If  this  is  not  accomplished,  and  the 
colon  remains  in  its  fetal  position,  two  organs  are  already  dis- 
placed, and  in  a position  characteristic  of  enteroptosis.  The 
embryonic  relation  of  the  position  of  the  ascending  colon  and  the 
right  kidney,  and  the  peritoneal  attachment  between  the  two,  are 
of  great  importance  for  the  proper  location  of  the  remaining 
abdominal  viscera.  A loose  attachment  of  the  peritoneum  upon 
the  right  kidney,  and  an  imperfect  transition  of  the  peritoneum 
from  the  kidney  to  the  colon,  without  completely  grasping  and 
encircling  the  latter,  offers  the  condition  necessaryito  pathological 
movability  for  the  right  kidney.  By  means  of  the  gastrocolic 
ligament  the  colon  exerts  a powerful  influence  on  the  position  of 
the  stomach.  Enteroptosis  is  a much  more  frequent  condition  in 
adults  than  in  children,  which  indicates  that  in  the  majority  of 
cases  the  condition  is  acquired  after  the  position  of  the  viscera  has 
approached  that  found  normally  in  the  adult.  But  even  if  that  is 
the  case,  the  primitive  arrangement  in  the  location  of  the  abdominal 
organs  has  an  important  bearing  on  the  later  abnormal  develop- 
ments. 

In  the  development  of  the  position  of  the  viscera  to  that  of  the 
normal  adult  the  liver  plays  a most  important  role.  This  organ 
becomes  relatively  smaller  than  is  found  in  the  fetus  and  neonatus. 
In  the  fetus  the  liver  extends  far  below  the  umbilicus,  but  in  the 
child  several  weeks  old  it  extends  only  to  within  ^ of  an  inch  above 
the  umbilicus.  In  the  fetus  the  anterior  free  margin  of  the  liver  is 


THE  ROLE  OF  THE  LIVER  IN  ENTEROPTOSIS.  /05 

very  much  lower  than  the  posterior.  But  in  the  child  a few  months 
old  this  posterior  margin  of  the  liver  has  descended  still  further,  so 
that  it  touches  the  edge  of  the  ilium,  and  has  pushed  the  right 
kidney  in  front  of  it,  on  to  the  concavity  of  the  ilium.  With  the 
beginning  of  respiration  the  anterior  margin  of  the  liver  begins  to 
rise,  and  the  posterior  margin  descends  somewhat  further.  The 
posterior  and  lateral  sections  of  the  diaphragm  are  the  most  mus- 
cular portions,  which  explains  the  fact  that  the  pressure  exerted 
upon  the  liver  by  the  contracting  diaphragm  is  not  uniformly  equal, 
not  concentric ; for  the  greatest  force  is  brought  to  bear  upon  the 
liver  from  the  rear  and  from  the  sides.  This  effects  a rotation  of 
the  liver  around  a horizontal  axis,  a line  which  we  can  imagine 
as  extending  from  the  right  lateral  to  the  left  posterior  hypochon- 
drium,  and  which  runs  very  close  to  the  anterior  wall  of  the  vena 
cava  posteriorly.  This  rotation  of  the  liver  and  the  diminution  of  its 
size  are  accompanied  by  a rise  of  the  organ  ; and  the  remaining  ab- 
dominal organs,  which  are  attached  to  it  by  peritoneal  folds,  gradu- 
ally follow.  When  the  liver  has  become  fixed  in  the  arching  dome 
of  the  diaphragm,  it  is  held  in  its  position  partly  by  the  aspiration 
of  the  thorax,  and  partly  by  the  hepatic  veins,  which  attach  it  to 
the  vena  cava.  But  the  most  important  support  comes  from  pres- 
sure of  the  abdominal  muscles.  In  the  living  being  the  liver  is 
highly  arched  on  its  convex  surface,  and  its  under  surface  is  not 
turned  backward,  but  forward,  and  arched  up  also  in  a concave 
manner.  This  position  of  the  liver  is  one  of  the  fundamental  con- 
ditions for  the  proper  retention  of  the  other  viscera  in  normal 
situations.  Whenever  the  liver  is  forced  out  of  its  normal  position, 
— in  which  it  is  held  by  the  aspiration  of  the  thorax,  by  its  attach- 
ment to  the  vena  cava,  and  by  abdominal  pressure, — whenever  this 
organ  transiently  or  permanently  descends,  its  volume  increases  at 
the  same  time,  and  it  is  no  longer  possible  for  the  pylorus,  the 
duodenum,  and  the  colon  to  remain  in  normal  positions.  The 
liver  is  the  central  figure  in  the  clinical  picture  of  enteroptosis. 
Rosengart  and  Glenard  hold  this  view,  and  Ewald  reluctantly  ad- 
mits that  the  liver  can  not  be  excluded  from  the  etiology.  All 
causes  that  press  down  the  liver, — whether  they  act  from  the 
thoracic  cavity  upon  the  diaphragm,  or  externally  upon  the  thorax, 
— all  diseases  and  changes  that  cause  relaxation  of -the  abdominal 
muscles,  all  diseases  in  the  liver  itself  that  lead  to  its  enlargement 
and  descent,  will  eventually  lead  to  enteroptosis. 

The  force  by  which  the  liver  is  retained  within  the  arching  dome 


yo6 


ENTEROPTOSIS GASTROPTOSIS. 


of  the  diaphragm  is  a considerable  one.  Luschka  compares  the 
intimate  contact  of  the  two  curved  arches  of  the  diaphragm  and 
the  liver  to  a great  ball-and-socket  joint,  held  together  by  atmos- 
pheric pressure,  and  capable  of  movement  only  in  the  direction  of 
the  two  arched  contact  surfaces.  The  path  that  the  liver  must 
describe  when  it  descends  from  its  normal  position  is  the  same 
that  it  took  when  it  rose  to  it  from  its  fetal  situation.  In  its 
descent  the  liver  goes  through  the  peculiar  axis-rotation  already 
described.  The  direction  of  this  rotation  is  toward  the  anterior 
and  inner  portion  of  the  abdomen.  The  duodenum,  pylorus,  and 
hepatic  flexure  of  the  colon  will,  of  necessity,  for  anatomical 
reasons,  have  to  descend  with  it.  The  posterior  lower  edge  of 
the  liver  rises  during  this  axial  rotation  and  becomes  superim- 
posed on  the  upper  end  of  the  kidney;  and  if  there  has  been  a 
predisposition  to  abnormal  motility,  or  a loose  attachment  of  the 
kidney,  it  will  now  become  completely  dislocated.  In  addition 
to  this  factor  in  nephroptosis  another  important  factor  is  found 
in  the  new  position  of  the  ascending  colon,  which  has  to  force  its 
way  over  the  kidney  in  its  descent,  thus  separating  the  latter  organ 
from  the  spinal  column.  According  to  this  view  enteroptosis 
may  also  be  congenital  or  acquired  : (i)  The  congenital  entero- 
ptosis is  the  persistence  of  the  fetal  situation  of  all  or  of  a part  of 
the  abdominal  viscera;  (2)  acquired  enteroptosis  is  the  gradual 
retrograde  development  from  the  normal  to  the  congenital  or  fetal 
position. 

The  development  of  icterus  in  cases  of  right-sided  nephroptosis 
and  the  frequent  occurrence  of  gall-stones  in  women  shortly  after 
labor  are  explained  by  the  tension  of  the  hepatoduodenal  ligament 
and  by  the  altered  course  of  the  duodenum  caused  thereby  during 
enteroptosis. 

The  author  has  tested  Rosengart’s  theory  by  the  dissection  of 
fourteen  cadavers  of  infants — five  born  before  term  (miscarriages) 
and  nine  born  at  full  term.  Some  of  the  dissections  were  carried  on 
by  the  associate  professor  of  anatomy  at  the  University  of  Maryland, 
Dr.  J.  Holmes  Smith.  We  were  enabled  to  confirm  the  positions 
assigned  by  Rosengart  to  the  stomach,  liver,  and  kidney  of  the 
neonatus,  but  all  except  two  of  the  infants  had  a transverse  colon 
about  one  inch  above  the  umbilicus.  Rosengart  asserts  that  the 
ascending  and  transverse  colons  were  merged  into  one  straight 
line,  ascending  diagonally  from  the  cecum  in  the  right  lower 
abdomen  directly  across  to  the  splenic  flexure,  so  that  there  was 


UPWARD  DISPLACEMENTS. 


707 


really  no  transverse  colon  in  the  fetus.  Of  the  five  full-term 
infants  we  dissected,  three  had  a distinct  transverse  colon  and 
two  were  as  Rosengart  describes  (/.  c.,  p.  221). 

Peritonitis  of  the  female  sexual  organs,  and  especially  of  their 
appendages,  comes  under  consideration  in  connection  with  dis- 
location of  the  transverse  colon  and  of  the  stomach.  In  almost 
all  adults  partial  states  of  dislocation  of  the  viscera,  and  especially 
of  the  intestines,  occur  so  frequently  that  more  persons  have  this 
displacement  than  a normal  location  of  the  intestines  (Virchow, 
/.  c).  The  French  authors  are  justified  in  assuming  the  great  fre- 
quency of  these  dislocations.  Undoubtedly,  the  majority  of  all 
civilized  peoples  have  a certain  deviation  in  the  location  of  their 
intestines,  or,  in  other  words,  some  slight  degree  of  enteroptosis. 
While  it  is  undoubtedly  true  that  the  majority  of  these  dislocations 
are  due  to  sinking,  nevertheless  the  contrary  is  also  found.  There 
are  also  dislocations  that  move  upward,  in  which,  for  instance,  the 
splenic  flexure  (flexura  linealis)  comes  to  a position  above  the  spleen 
immediately  next  to  the  diaphragm ; and  others  in  which  the 
hepatic  flexure  moves  upward  far  under  the  liver.  This  upward 
distortion  of  the  intestines  should  also  receive  careful  consideration. 
It  is  evident,  however,  that  every  decided  change  in  situation  of  this 
sort — especially  if  it  is  at  the  same  time  accompanied  by  kinking, 
or  if  considerable  deviation  in  the  direction  of  the  intestines  occurs 
— must  bring  about  an  interference  with  the  passage  of  the  con- 
tents of  the  intestines;  and,  therefore,  nothing  is  more  frequent 
than  to  find,  at  the  necropsy,  collections  of  fecal  matter  just  at 
these  angles  and  flexures,  or  that  accumulations  of  gases  occur, 
while  adjacent  parts  of  the  intestines  are  contracted.  Thus  we  get 
a picture  in  which  spastically  contracted  parts  of  the  intestines 
alternate  with  much  dilated  portions.  The  colon  is  the  main  seat 
of  this  difficulty,  and  the  dislocation  occurring  most  frequently 
is  a lowering  of  the  transverse  colon,  which  often  sinks  under  the 
navel,  and  sometimes  even  to  the  true  pelvis,  and  then  forms  a 
V-shaped  loop,  or  one  with  two  parallel  legs.  The  next  most 
frequent  point  is  the  sigmoid  flexure,  which  may  show  all  the  pos- 
sible varieties  of  descents  and  displacement  toward  the  right.  The 
two  large  flexures  in  the  upper  part  of  the  abdomen — the  hepatic 
and  the  splenic — are  third  in  the  order  of  frequency  of  disloca- 
tions. The  cecum  may  also  be  drawn  into  similar  displacements, 
and  may  sometimes  move  under  the  liver,  and  at  other  times  sink 
down  into  the  true  pelvis.  These  states  are  relatively  frequent, 


708 


ENTEROPTOSIS — GASTROPTOSIS. 


although  little  attention  has  been  given  to  these  very  chronic 
conditions,  because  in  life  it  is  not  known  to  what  extent  certain 
symptoms  are  connected  with  them,  and,  as  a rule,  no  one  dies 
from  these  displacements. 

In  a treatise  by  Virchow  (“  Virchow’s  Archiv,”  Bd.  v)  it  was 
distinctly  proved  that  anomalous  adhesions  frequently  occur  simul- 
taneously with  these  states ; for  instance,  growing  together  of 
the  intestines  with  each  other — that  is,  of  the  various  curves  and 
loops  among  themselves — and  at  other  times  with  the  adjacent 
organs.  The  hepatic  flexure  of  the  colon  to  a great  extent  be- 
comes connected  with  the  gall-bladder  and  the  whole  apparatus  of 
the  evacuating  gall-passages  (see  our  illustrations  of  similar  adhe- 
sions, plate  XIV)  ; and,  on  the  other  hand,  the  splenic  flexure  comes 
into  close  connection  with  the  spleen  and  the  diaphragm,  and 
the  iliac  flexure  with  the  sexual  organs,  especially  in  women.  These 
reciprocal  relations  undoubtedly  produce  pulling  of  the  various 
parts  among  one  another. 

The  relation  of  partial  peritonitis  to  visceral  dislocations  is  more 
difficult  to  understand,  and  in  this  respect  two  conditions  are  to  be 
distinguished — namely,  a primary  one,  in  which  peritonitis  occurs 
earlier,  and  a secondary  one,  in  which,  conversely,  the  peritonitis  is 
caused  by  the  dislocation  and  by  the  other  processes  going  on 
within  the  adherent  part  of  the  intestines. 

Concerning  the  first,  we  have  a clear  example  in  the  recognized 
cases  of  circumscribed  peritonitis,  which  are  caused  by  processes 
starting  from  the  gall-bladder  (perihepatitis,  peritonitis  cystica), 
when  adhesions  are  formed  within  the  environment  of  the  gall- 
passages  ; this  is  followed  by  a shifting  of  the  parts  among  one 
another,  since  the  adhesive  masses  gradually  contract  and  the 
retraction  proceeds  further  and  further.  On  the  other  hand, 
secondary  peritonitis  is  much  more  difficult  to  prove  in  cases  in 
which  one  is  confronted  with  the  completed  process ; one  can  only 
recognize  it  when  fresh  processes  still  exist.  These  are  found 
chiefly  in  those  cases  when  inflammation  of  the  mucous  mem- 
branes, extending  to  the  peritoneum,  causes  a bending  or  kinking 
of  the  intestine. 

Virchow  was  the  first  to  draw  attention  to  the  facts  in  studies  on 
dislocations  with  so-called  diphtheric  dysentery,  which  may  appear 
distributed  in  a variable  manner,  so  that  the  foci  of  inflammation 
are  separated  by  long  stretches  of  normal  mucous  membrane. 
Apparently  normal  sections  are  succeeded  by  new  areas  of  very 


PERITONITIS  AND  COLITIS  AS  CAUSES.  7O9 

severe  disease,  so  that  one  may  distinguish  a sort  of  interrupted 
localization.  He  suggested  that  the  anomalous  flexure,  just  as  the 
normal,  is  in  itself  a motive  for  localization,  in  that  it  brings  with 
it  a retardation  in  the  passage  of  the  contents  of  the  intestines, 
which  contain  injurious  substances  that  react  upon  the  mucous 
membrane,  and  from  which  the  irritative  process  is  developed.  It 
is  exactly  the  same  thing  that  we  see  in  stenoses,  where  further 
disturbances  arise  above  the  obstruction,  or  with  incarcerated 
herniae,  where  the  inflammation  develops  in  the  part  of  the  intestine 
above  the  incarceration,  and  sooner  or  later  extends  to  the 
peritoneum. 

These  consequences  (secondary  peritonitis)  of  partial  enteropto- 
ses  due  to  acute  inflammations  are  easily  recognized  (“Arch.  f. 
pathol.  Anat.  u.  Physiol.,”  1871,  lii,  34). 

Enteroptosis  is  not  an  anatomical  process  connected  with  con- 
stant clinical  symptoms.  On  the  contrary,  the  symptoms  will 
probably  be  manifold,  according  to  the  special  pathological  circum- 
stances occurring  in  various  cases.  Accordingly,  the  disease  in 
each  case  will,  to  some  degree,  come  under  different  categories, 
and  one  may  not  bring  diphtheric  or  simple  colitis,  developed 
in  anomalous  flexures,  into  the  same  category  as  dislocation 
pure  and  simple ; these  are  two  very  different  things  (Virchow). 
I,  therefore,  do  not  consider  enteroptosis  an  entity,  but  prefer 
to  divide  it  into  several  groups  of  diseases  when  it  is  regarded 
symptomatologically  and  therapeutically.  We  are  dealing  here 
with  very  common  deviations,  and,  if  we  could  count  the  cases, 
they  would  be  found  to  be  more  frequent  than  the  normal  state  ; 
the  less  complicated  dislocations  only  from  time  to  time  become 
the  origin  of  severer  symptoms. 

Leshaft  has  shown  that  the  size  and  fullness  of  the  abdominal 
organs,  as  well  as  the  condition  of  the  abdominal  integument,  are 
important  for  the  reciprocal  conduct  and  relation  of  the  intra- 
abdominal organs. 

Every  abnormal  fullness  or  increase  in  size  of  one  of  these 
organs,  as  well  as  a decrease  in  the  power  of  resistance  within  the 
compass  of  the  abdominal  integuments,  will  produce  a change  in 
location — a sort  of  ptosis,  in  the  sense  of  Glenard.  It  has  been 
proved  that  a descent  of  the  transverse  colon,  especially  the  right 
flexure,  carries  with  it  a lowering  of  the  stomach  and  a descent  of 
the  right  kidney.  It  is  evident  that  the  transverse  colon  does 
not  descend  spontaneously  without  pathological  causes,  so  that 


7io 


ENTER0PT0SIS GASTROPTOSIS. 


there  can  not  well  be  a primary  enteroptosis.  It  is  caused  by 
etiological  factors,  such  as  abnormal  adhesions,  change  of  con- 
tents (coprostasis),  anomalous  flexures  (Virchow),  tumors,  perpetua- 
tion of,  or  reversion  to,  a fetal  condition,  etc.,  by  which  the  trans- 
verse colon  is  pulled  down,  and  with  it,  secondarily,  the  stomach 
and  small  intestine,  and  eventually  the  kidney,  especially  on  the 
right  side.  Therefore  most  enteroptoses  are  of  secondary  nature. 

Dislocation  of  the  Kidneys. — In  1887  Litten  first  emphasized 
that  “ in  the  anomalies  of  location  of  the  kidney  one  must  sharply 
distinguish  dislocation  and  movability.”  Although  both  irregu- 
larities often  occur  together  and  simultaneously,  there  is  no 
organic  necessity  for  the  same ; rather,  both  processes  may  ap- 
pear entirely  independent  of  each  other,  although  in  many  cases 
one  finds  a dislocated  and  a movable  kidney  in  the  same  individual. 

Renal  displacements  may  be  (1)  congenital  or  (2)  acquired.  Con- 
genital displacement  occurs  more  frequently  with  the  left  kidney, 
and  oftener  in  males  than  in  females.  (The  ratio  of  Stern  is  20  : 9.) 
It  rarely  occurs  in  both  kidneys,  except  in  those  cases  in  which 
they  have  grown  together.  These  kidneys  are  found  in  the  pelvis 
or  above  the  promontory  of  the  sacrum,  and  are  often  associated 
with  intestinal  and  genito-urinary  abnormalities ; but  as  the  con- 
dition gives  rise  to  few  symptoms,  it  has  more  of  a pathological 
than  a clinical  interest.  The  diagnosis  is  difficult  unless  the  mass 
can  be  palpated  from  the  rectum  or  vagina,  or  unless  fluid  can  be 
aspirated  from  it,  giving  the  reactions  of  urine.  The  acquired 
renal  displacement  is  (1)  due  to  tumors  in  the  neighborhood  of 
the  organ,  or  (2)  due  to  abnormal  movability,  assigned  to  various 
causes  already  mentioned.  In  both  congenital  and  acquired  dis- 
placements the  abnormally  situated  kidney  may  be  fixed  or  mova- 
ble. Congenital  displacements  are,  as  a rule,  fixed ; the  acquired 
show  a variable  movability.  A movable  kidney  may  be  ( a ) in  a 
normal  position  or  ( b ) dislocated ; a dislocated  kidney  may  be  ( a ) 
movable  or  ( b ) fixed.  The  so-called  floating  kidney  (Wander- 
niere)  belongs  to  the  second  type,  variety  a;  it  is  a dislocated, 
movable  kidney. 

According  to  Kuttner,  Litten,  and  Ewald,  four  distinct  phases  or 
degrees  of  nephroptosis  may  be  differentiated  by  palpation  : (1)  A 
respiratory  movability  without  dislocation.  (2)  Respiratory  mov- 
ability with  slight  anterior  dislocation — one-third  to  two-thirds  of 
the  kidney  can  be  palpated  ; this  is  termed  a “ dislocation  of  the 
first  degree.”  (3)  Respiratory  movability  with  close  approximation 


MOVABI LITY  AND  DISLOCATION. 


7 ii 


to  the  anterior  abdominal  wall.  The  kidney  is  palpable  in  its 
entirety,  and  can  be  easily  moved  about;  this  is  termed  a “ disloca- 
tion of  the  second  degree.”  (4)  The  dislocated  kidney  is  firmly 
adherent  in  its  abnormal  position. 

Litten  distinguishes  the  following  relations  concerning  the  loca- 
tion and  movability  of  the  kidney  : First,  a simple  dislocation  of  the 
same;  this  is  more  frequently  congenital  than  acquired.  The  con- 
genitally dislocated  kidney  is  found  more  frequently  on  the  left 
than  on  the  right,  and  with  approximately  equal  frequency  in  men 
and  women.  Often  both  organs  are  dislocated.  Not  taking  into 
account  the  most  frequent  form  of  dislocation, — the  so-called 
horseshoe  kidney,  in  which  both  organs  are  united  into  one, — the 
dislocated  kidney  is  found  either  close  under  the  bifurcation  of  the 
aorta,  or  above  the  promontory  of  the  sacrum,  or,  finally,  above  the 
sacro-iliac  synchondrosis.  With  the  change  in  location  there  is 
almost  always  connected  an  anomaly  of  the  origin  or  course  of  the 
renal  artery,  while  the  suprarenal  capsule  more  frequently  remains 
in  its  place  and  does  not  follow  the  kidney  to  which  it  belongs. 
Congenitally  dislocated  kidneys  are  almost  always  fixed  in  the 
place  of  their  dislocation.  An  exception  to  this  is  the  movable 
horseshoe  kidney. 

Acquired  dislocations  of  the  kidneys  are  chiefly  due  to  patho- 
logical enlargements  of  neighboring  organs  (spleen,  liver,  pan- 
creas, suprarenal  capsule),  and  are  found  higher  or  lower  than  the 
normal  and  nearer  to  or  further  from  the  vertebral  column.  The 
pressure  of  articles  of  clothing  (such  as  corsets,  belts,  girdles,  etc.) 
seems  to  have  considerable  influence,  by  which  the  liver,  and  with 
it  the  kidney,  is  pushed  down.  Consequently,  this  anomaly  of 
location  is  found  less  frequently  left  than  right — more  frequently 
in  women  than  in  men.  By  the  sinking  of  the  liver — e.  g .,  in  con- 
sequence of  hydatid  cysts — the  kidneys  may  be  completely  turned 
around,  as  a result  of  which  one  may  feel  the  inner  edge  with  the 
hilus  upward,  the  convex  edge  downward,  or  pointing  in  some 
other  abnormal  direction.  Most  frequently  in  this  form  of  disloca- 
tion one  finds  the  kidney  pushed  downward  and  inward : i.  e., 
toward  the  median  line.  This  form  of  dislocation  of  the  kidney, 
acquired  late  in  life,  may  become  movable;  it  is  almost  always 
replaceable  if  it  has  not  become  fixed  in  its  new  location  by 
secondary  inflammation. 

While  one  might  describe  the  above-mentioned  forms  as  dis- 
location of  the  kidney  with  and  without  movability,  we  now 


712 


ENTEROPTOSIS GASTROPTOSIS. 


come  to  the  forms  in  which  the  movability  plays  the  main  role, — 
dislocation  of  the  secondary  kind, — movable  kidneys  with  and 
without  dislocation.  Here  we  have  to  distinguish  two  main 
classes:  (i)  the  wandering  or  floating  kidney;  (2)  the  movable 
kidney. 

The  floating  kidney  is  distinguished  by  the  mesonephron, — a 
mesenteric  fold  fastened  to  the  kidney, — which  generally  consists 
of  two  plates,  between  which  the  organ  is  held  and  with  which  it 
is  surrounded.  The  characteristic  of  this  form  is  not  the  abnormal 
position,  but  the  ability  to  change  one  abnormal  position  with 
others,  to  reach  extreme  positions,  and  even  to  reach  the  normal 
position  again,  of  itself.  The  presence  of  this  anomaly  is  always 
to  be  traced  back  to  a congenital  disposition  of  the  peritoneum, 
with  consequent  stretching  of  the  renal  vessels.  Generally,  one 
finds  at  the  autopsy  in  these  cases  that  all  the  folds,  protrusions  of 
the  peritoneum  and  mesenteries,  are  abnormally  long  and  lax,  and 
the- foramen  of  Winslow  is  very  wide,  corresponding  to  the  laxity 
of  the  lesser  omentum  and  the  duodenal-hepatic  ligament. 

If  one  uses  this  anatomical  arrangement  for  the  classification,  and 
does  not  designate  at  will  every  unusually  mobile  kidney  as  a 
“ floating  ” or  “ wandering  kidney,”  as  is  frequently  done  from  a 
clinical  point  of  view,  it  is  evident  that  every  floating  kidney,  in 
the  sense  adopted  by  Litten,  must  be  congenital.  It  will  hardly  be 
possible,  therefore,  during  life  to  distinguish  these  two  processes 
from  each  other ; on  the  other  hand,  there  will  also  be  cases  in 
which  a very  short  and  tight  mesonephron  will  restrict  the  extent 
of  wandering  of  the  floating  kidney.  A simultaneous  permanent 
dislocation  of  the  kidney  may  be  present,  but  not  necessarily;  it 
happens,  occasionally,  that  a floating  kidney  in  the  course  of  time 
becomes  fixed  and  permanent  in  any  abnormal  location  by  means 
of  perinephritic  processes,  so  that  in  spite  of  its  mesentery  it  is  no 
longer  movable.  Litten  has  reported  a considerable  dislocation  in 
a wandering  horseshoe  kidney,  where  one  portion  of  the  organ  lay 
in  the  right  inguinal  region,  while  the  opposite  part  lay  upon  the 
horizontal  ramus  of  the  right  os  pubis.  The  organ  could  be 
pushed  about  within  the  widest  limits,  and  it  also  moved  spon- 
taneously, causing  unpleasant  sensations  to  the  patient.  In  this 
intraperitoneal  position  of  the  kidney  the  organ  seems  to  lie  imme- 
diately under  the  abdominal  integuments,  where  one  can  not  only 
palpate  it,  but  can  sometimes  also  recognize  its  contour  distinctly 
through  the  abdominal  integuments.  Percussion  over  the  organ 


ETIOLOGICAL  FACTORS. 


713 


produces  in  these  cases  a distinct  dullness,  not  a tympanitic  sound, 
as  in  the  case  with  the  kidney  situated  extraperitoneally. 

The  movable  kidney  is  distinguished  from  the  normal  solely  by 
an  excessive  movability,  which  is  revealed  to  a greater  or  less  de- 
gree (not  taking  into  account  the  normal  respiratory  movability)  in 
changes  in  the  position  of  the  body.  Often  this  anomaly  is  acci- 
dentally recognized  in  manipulations  instituted  for  the  examina- 
tion of  the  abdomen.  A dislocation  of  the  kidney  can  and  often 
does  exist  simultaneously  with  the  above-mentioned  condition,  but 
it  does  not  necessarily  have  to  exist.  We  find  the  right  kidney 
more  frequently  movable  than  the  left  (the  proportion  being  15 
to  1),  and  the  anomaly  is  more  frequent  in  women  than  in  men  (the 
proportion  being  84  to  16).  The  degree  of  movability  seems  to  be 
chiefly  dependent  upon  the  varying  laxity  of  the  part  of  the  peri- 
toneum descending  in  front  of  the  kidney,  as  well  as  upon  the 
abundance  or  absence  of  the  perinephritic  or  subperitoneal  adipose 
tissue  in  the  region  of  the  loins,  and  the  greater  or  lesser  power  of 
resistance  of  the  intra-abdominal  organs,  including  the  abdominal 
integuments. 

One  can  often  feel  the  kidney  so  distinctly  that  it  may  be 
palpated  with  anatomical  exactness,  although  it  lies  extra-peri- 
toneally,  separated  from  the  anterior  abdominal  wall  by  intestinal 
loops;  consequently  it  gives  forth  a decided  tympanitic  sound, 
although  one  can  press  it  very  close  to  the  abdominal  wall.  The 
degree  of  movability  is  just  as  variable  as  the  degree  of  dislocation  ; 
in  most  cases  we  find  only  slight  dislocations  from  the  normal  posi- 
tion, downward  and  inward.  In  by  far  the  greater  number  of  cases 
this  condition  is  acquired,  especially  in  the  years  between  twenty 
and  forty. 

Etiologically , the  following  factors  seem  to  have  the  greatest 
influence:  The  disappearance  of  the  fat  in  the  adipose  capsule  in 
which  the  kidney  is  held — through  this  the  kidney  becomes  mov- 
able in  this  capsule;  the  disappearance  of  the  perinephritic  adipose 
tissue,  through  which  the  kidney,  and  also  its  fat  capsule,  are  moved 
out  of  place;  further,  the  laxity  of  the  peritoneum,  the  increase  in 
the  weight  of  the  liver,  together  with  the  respiratory  displacement 
of  the  same,  prolapse  of  the  uterus  and  of  the  vagina,  neoplasms 
and  retroflexions  of  the  uterus,  herniae,  weakness  and  laxity  of  the 
abdominal  walls,  and,  above  all,  the  much-discussed  enteroptosis. 
Also  heavy  lifting,  coughing,  pressing,  repeated  pregnancies,  vom- 
iting, as  well  as  traumatism  and  violent  agitation,  are  given  as 


ENTEROPTOSIS  — GASTROPTOSIS. 


7H 

causes.  One  of  the  most  frequent  causes  for  the  movability  of  the 
right  kidney  seems  to  be  lacing  with  corsets,  belts,  and  girdles. 
Thus,  von  Fischer-Benzon,  in  his  dissertation  from  the  pathological 
institute  at  Kiel,  states  that  in  twenty-one  cases  of  movable  kidney 
there  was  found  in  eleven  cases  a furrow  in  the  liver  due  to  lacing. 

By  lacing  a decided  pressure  is  exerted  upon  the  lower  part  of 
the  thorax,  by  which  this  is  greatly  narrowed  and  the  organs  lying 
within  it  compressed.  The  liver,  being  the  largest  and  least  com- 
pressible of  these  organs,  will  suffer  especially.  The  liver,  and  the 
kidney  closely  connected  with  it,  are  pushed  down,  and  the  latter 
must  participate  in  the  respiratory  excursions  of  the  liver. 

The  more  frequent  displacement  of  the  right  kidney  is  partly 
explained  by  the  anatomic  arrangement  of  its  blood  supply.  The 
left  kidney  has  a shorter  renal  artery  and  a tighter  attachment  to 
the  suprarenal  body,  by  means  of  the  suprarenal  vein,  which  on 
the  left  side  opens  into  the  renal  vein. 

H.  Schmid  (Penzoldt  and  Stintzing’s  “ Handbuch  d.  Therapie,” 
Bd.  vi,  S.  345)  regards  the  renal  vessels  as  the  most  important 
attachments  of  the  kidney ; if  the  vessels  are  abnormally  long,  an 
essential  support  is  lost.  L.  Knapp  (/.  cl)  looks  upon  uterine 
displacements  and  consequent  dragging  upon  the  ureters  as  a 
frequent  cause. 

Since  the  respiratory  movements  of  the  diaphragm  are  com- 
municated to  the  kidney,  the  respiratory  movability  of  the  kidney 
may  be  regarded  as  physiological.  The  author,  following  the 
observation  of  James  Israel,  has  convinced  himself  of  this  normal 
movability  at  operations. 

Method  of  Palpating  the  Kidneys. — The  chances  of  feeling  the 
respiratory  movability  of  the  right  kidney  will  vary  according  to 
the  relaxation  and  the  degree  of  resistance  of  the  abdominal 
integuments,  the  control  and  experience  of  the  patient  in  breath- 
ing, and  according  to  the  manual  dexterity  of  the  examiner.  It 
is  especially  important  that  the  patient  inspire  deeply ; this  can 
be  learned  easily  enough  by  practice.  The  knees  and  thighs 
of  the  patient  must  be  flexed.  The  examiner  himself  must  not 
cause  any  pain  or  tension  of  the  abdominal  integuments  by  his 
manipulations.  It  will  then  be  possible  in  many  cases,  by  means 
of  the  bimanual  method  of  examination,  to  feel  the  kidneys,  espe- 
cially the  right  one,  as  it  is  more  easily  palpable.  It  would,  how- 
ever, be  entirely  false  to  believe  that  one  could  prove  the  respira- 
tory movability  of  the  kidneys  in  females  only,  and  especially  in 


PALPATION  OF  KIDNEYS. 


715 


multipart.  On  the  contrary,  it  may  be  shown  with  the  greatest 
distinctness  in  men  and  girls,  and  even  in  small  children.  In 
bimanual  examination,  in  order  to  feel  the  right  kidney  the  left 
hand  is  placed  immediately  in  the  rear,  under  the  edge  of  the  ribs 
on  the  right  side,  while  the  tips  of  the  fingers  of  the  right  hand, 
similarly  placed  together,  take  the  corresponding  position  at  the 
lower  arch  of  the  ribs  on  the  same  side ; on  gradual  downward 
pressure  one  feels  a larger  or  smaller  part  of  the  organ  between  the 
fingers  during  deep  inspiration.  The  deeper  the  inspiration,  the 
greater  the  portion  of  the  kidney  that  becomes  palpable,  until  with 
forced  inhalation  one  may  sometimes  feel  the  whole  organ  pressed 
out  under  the  arch  of  the  ribs,  and  can,  with  the  greatest  distinct- 
ness, examine  it  by  palpation  between  both  hands.  If  the  fingers 
of  both  hands  are  pressed  together,  the  kidney  escapes  from  the 
hands  (this  is  a characteristic  sign),  and  the  person  examined  feels  a 
slightly  unpleasant  sensation,  and  sometimes  a decided  sensation 
of  pressure  or  pain,  or  a distinct  jerk.  The  difficulties  in  the  way 
of  kidney  palpation  have,  in  the  author’s  experience,  been  very 
adipose  abdominal  walls,  tightly  contracted  recti  muscles,  fecal 
accumulations  in  the  colon,  and,  rarely,  neoplasms  of  the  gall- 
bladder and  colon,  hydatids  of  the  liver,  and  causes  enlarging  or 
lowering  the  liver,  or  separating  a portion  of  the  lower  edge  by 
a furrow  due  to  compression. 

With  this  method  of  examination  one  may  get  a precise 
conception  of  the  size,  consistency,  and  thickness  of  the  organ ; 
possibly  of  neoplastic  formations,  lobulations,  irregularities,  even 
granulations  and  processes  of  shriveling,  and  especially  of  increase 
in  consistency,  size,  and  diameter.  The  looser  the  abdominal  in- 
teguments, and  the  more  completely  the  condition  of  enteroptosis 
is  developed,  the  more  favorable  are  the  conditions  for  palpation. 
If  the  kidney  can  not  be  palpated  when  the  patient  is  in  the  dorsal 
position,  I have  frequently  succeeded  in  palpating  it  by  placing 
the  patient  on  her  hands  and  knees  in  bed.  The  examiner  stands 
on  the  left  side  of  the  bed  and  patient,  facing  the  head.  Both 
arms  are  passed  around  the  patient’s  body ; the  right  hand  is  in- 
serted beneath  the  lower  edge  of  the  liver  while  the  left  seeks  to 
meet  it  by  pressure  from  a point  about  two  inches  above  the 
umbilicus. 

Gastroptosis. — Diseases  of  the  stomach  are  frequently  con- 
nected with  dislocation  and  movability  of  the  kidney.  Ewald  and 
others  are  of  the  opinion,  supported  by  observation  of  numerous 


ENTEROPTOSIS GASTROPTOSIS. 


7l6 

successive  cases,  that  the  frequency  of  gastrectasia  with  dislocation 
of  the  right  kidney  is  due  to  an  etiological  connection.  The 
view  taken  by  Quincke,  Nothnagel,  and  Leube  is  that  both  patho- 
logical processes  occur,  indeed,  very  often  side  by  side,  without  any 
causal  connection  necessarily  existing  between  them.  I have  not 
seen  an  undoubted  case  of  dilation  of  the  stomach  due  to  obstruction 
of  the  pylorus  or  duodenum  by  floating  kidney.  I have  observed 
gastroptosis  and  nephroptosis  occurring  together  in  numerous 
cases — the  combination  being  due  to  the  same  cause.  The  changes 
of  position  (after  descent)  of  the  stomach  in  consequence  of  so- 
called  enteroptosis  and  dislocation  of  the  right  kidney  are  not  the 
classic  gastrectasias  that  develop  in  consequence  of  mechanical 
obstructions  at  the  pylorus  (new  formations,  cicatrices  of  ulcers, 
distortions  in  consequence  of  adhesions,  compression,  obliteration, 
kinking,  etc.,  page  231  of  the  “Proceedings  of  the  German  Con- 
gress for  Internal  Medicine,”  1887),  but  consist  in  the  insufficiency 
of  the  pylorus,  with  deep  location  and  dilation  of  the  stomach, 
because  the  pylorus  and  the  duodenum  frequently  retain  a normal 
position.  If  one  does  not  take  into  account  the  gastrectasias 
resulting  from  mechanical  causes,  there  still  remains  a very  large 
number  of  functional  disturbances  of  the  stomach,  which  lead, 
further,  to  insufficiency  of  the  musculature  and  to  dilation  and 
low  position  of  the  organ.  To  this  class  are  assigned : 

1.  Disease  of  the  musculature  of  the  stomach  in  consequence  of 
protracted  chronic  gastritis. 

2.  Excessive  exertion  of  the  stomach  in  consequence  of  exces- 
sive amounts  of  healthy  food  or  unsuitable  indigestible  food. 

3.  Abnormally  slow  peristalsis  with  retention  of  food,  as  well 
as  the  abnormal  decomposition  of  the  retained  ingesta,  with  exces- 
sive formation  of  gases. 

As  a result  of  these  various  chronic  pathological  conditions  of 
the  stomach,  each  of  which  singly  forms  only  a link  in  the  whole 
chain,  a dilation  of  the  stomach,  with  attenuation  of  the  walls, 
finally  develops,  and  later  a sinking  down  of  the  organ  and  descent 
of  the  right  kidney,  with  abnormal  movability.  The  function  of 
the  stomach  is  seriously  injured  in  many  directions,  especially  the 
motor  power,  which  under  some  circumstances  ceases  entirely. 

In  such  individuals  200  c.c.  of  liquid  food  are  often  found  in  the 
stomach  from  seven  to  eight  hours  after  ingestion.  Such  con- 
ditions (called  by  the  French  “ dyspepsie  des  liquids  ”)  concern 
only  liquid  food,  while  solid  foods  are  digested,  though  much 


CAUSES  OF  ENTEKOPTOSIS. 


717 


more  slowly  than  normally.  It  was  thus  possible  to  effect 
a nearly  normal  digestion  of  discs  of  albumin  placed  in  the 
gastric  juice  pumped  out  of  the  stomach.  These  observations 
are  more  intelligible  in  the  light  of  von  Mering’s  experiments 
(see  part  first),  according  to  which  it  is  certain  that  no  ab- 
sorption of  water  takes  place  from  the  stomach,  even  normally; 
and  for  the  resorption  of  substances  that  can  be  taken  up  by  the 
mucosa,  a return  secretion  of  liquid  takes  place  from  the  mucosa 
into  the  stomach.  So  that  it  sometimes  happens  that  after  six  or 
eight  hours  more  liquid  is  drawn  out  of  the  stomach  than  was  in- 
gested. The  digestive  power  varies  in  these  cases  with  the  state  of 
HC1;  it  may  be  fairly  good,  but  it  may  be  entirely  absent.  There 
are  undoubtedly  cases  of  gastroptosis  in  which  the  dislocated 
stomach  functions  normally. 

The  displacements  of  the  intestines,  which  arise  through  circum- 
scribed peritonitis,  through  obstruction  of  the  feces,  etc.,  were  de- 
scribed by  Virchow  as  early  as  1853.  Glenard  and  Ewald  have 
made  reference  to  the  entirely  uncomplicated,  one  might  say  the 
purely  gastric  and  intestinal,  cases. 

The  suggestion  of  Landau,  not  to  be  content  with  the  diagnosis 
of  the  movable  kidney,  floating  liver,  and  kinking  of  the  transverse 
colon,  but  to  seek  the  etiological  diagnosis,  in  order  not  to  come 
to  the  incorrect  conclusion  that  we  have  to  do  with  independent 
diseases,  would  be  valuable  if  it  were  easy  of  execution.  In  the 
author’s  opinion,  the  etiological  diagnosis  is  difficult,  sometimes 
impossible.  Enteroptoses,  etc.,  are  secondary  states,  and  should, 
for  diagnosis  and  treatment,  be  considered  in  the  same  light  as 
roseola  occurring  with  typhus  or  syphilis,  in  which  one  is  cer- 
tainly not  content  to  diagnose  roseola  simply,  but  adds  typhus  or 
syphilis  with  roseola. 

Causes. — The  diseases  that  cause  a sinking  of  one  or  more  of 
the  abdominal  organs  are  all  those  which  absolutely  or  relatively 
increase  the  capacity  of  the  abdomen,  and  thus  allow  the  large  in- 
testine, fastened  by  the  relatively  long  mesocolon,  to  sink,  accord- 
ing to  its  weight.  The  simplest  or  first  degree,  for  instance,  may 
be  said  to  exist  when  we  meet  with  a light  inguinal,  femoral,  or 
umbilical  hernia.  In  this  case  all  the  intestines  not  in  the  hernial 
sac  may  sink,  through  pulling  and  dragging.  Since  the  portions 
of  the  intestines  which  were  formerly  in  the  peritoneal  cavity  have 
come  out,  the  capacity  of  the  abdomen  has  been  relatively  in- 
creased. 


7i8 


ENTEROPTOSIS — GASTROPTOSIS. 


It  is  true,  splanchnoptosis  is  not  a necessary  consequence  of 
large  ruptures.  When  the  elasticity  and  contracting  power  of  the 
abdominal  integuments  are  very  great,  they  may  counteract  the 
increase  in  volume  by  tonic  contractions.  A number  of  cases  are 
reported  in  which  almost  all  the  intestines  lay  in  ruptures;  and  in 
spite  of  this,  the  kidney,  liver,  and  uterus  were  approximately  in 
normal  positions.  The  abdominal  integuments  were  contracted 
tightly  inward  and  were  concave. 

Of  far  greater  importance  for  the  origin  of  all  kinds  of  entero- 
ptoses  is  a second  great  category  of  diseases — namely,  all  wasting 
diseases , which  produce  a quick  consumption  of  the  fat  of  the  body, 
and  also  disturbances  in  the  nutrition  of  the  abdominal  integu- 
ments. Thus,  after  typhoid  fever,  scarlet  fever,  and  other  infectious 
diseases,  splanchnoptoses  of  all  kinds,  such  as  dislocation  of  the 
kidneys  and  of  the  liver,  etc.,  have  been  recognized.  It  is  evident 
that  the  transverse  colon  must  be  lowered  also  when  the  liver  and 
kidney  can  be  felt  to  have  descended,  for  the  transverse  colon,  lying 
under  these  organs,  and  connected  with  them  directly  and  indi- 
rectly, can  not  retain  its  position  under  these  conditions.  To  prove 
the  descent  of  the  transverse  colon  in  such  cases,  the  method  of 
the  injection  of  air  into  the  stomach  and  into  the  colon  alternately 
(Ewald)  is  not  always  necessary,  nor  the  very  doubtful  direct 
palpation  of  the  transverse  colon,  as  given  by  Glenard. 

Chronic  diseases,  such  as  phthisis,  produce  exactly  the  same 
effect  as  acute  diseases ; and  Landau  holds  that  primary  nervous 
dyspepsia,  primary  chronic  gastritis,  duodenitis,  etc.,  are  fre- 
quently not  the  result  of  enteroptosis,  but,  by  means  of  the 
disappearance  of  fat  and  weakening  of  the  abdominal  integuments, 
causes  of  it.  Individuals  may  be  examined  at  one  period  of  indis- 
position and  no  sinking  of  the  liver  and  kidney  can  be  demon- 
strated, but  if  they  should  acquire  an  ulcer  of  the  stomach  or 
nervous  dyspepsia,  with  disturbances  of  nutrition,  we  may  be  able 
to  show  prolapse  of  the  liver  or  kidney  in  the  later  course  of  the 
disease. 

Among  the  patients  observed  by  us — sufferers  from  disturbances 
of  nutrition,  nervous  dyspepsia,  emaciation,  etc. — in  which  the 
splanchnoptoses  were  demonstrated,  there  were  a number  of  cases 
in  which  the  disturbances  of  nutrition  caused  the  ptoses,  and  not 
the  reverse.  In  five  cases  the  patients  had  been  closely  examined 
repeatedly  before,  and  signs  of  enteroptosis  were  discoverable ; in 
later  years  these  had  become  very  evident. 


STENOSING  OF  INTESTINES. 


7 1 9 


Relaxation  of  the  abdominal  muscles , with  or  without  pendulous 
abdomen,  is  a frequent  cause  of  splanchnoptosis.  Sinking  of  the 
kidneys  and  liver  develops  in  women  from  whom  large  ovarian 
tumors  or  myomata^  have  been  removed  by  laparotomy.  Other 
cases  of  pendulous  abdomen  are  acquired  by  repeated  and  rapidly 
consecutive  births , and  by  unsuitable  treatment  during  and  after 
confinement. 

Similarly,  splanchnoptoses  will  appear  in  individuals  who  suffer 
from  ascites , and  who  have  been  punctured  repeatedly,  and  in  whom 
the  abdominal  muscles  have  finally  become  paretic  on  account 
of  abnormal  fullness  and  distention.  The  typical  form  of  pendu- 
lous abdomen  does  not  always  arise  in  these  cases.  If  the  support 
of  the  abdominal  viscera,  formed  by  the  abdominal  integuments, 
becomes  insufficient,  the  intestines  follow  the  law  of  gravitation 
and  descend  the  length  of  their  mesenteries,  the  peritoneal  folds  of 
the  liver  and  kidney  relax  also,  and  these  viscera  descend,  because 
one  of  their  main  supports — namely,  the  intestinal  mass — has  been 
withdrawn.  That  which  is  principally  and  etiologically  of  prime 
importance  in  these  particular  cases,  therefore,  is  not  the  sinking  of 
the  transverse  colon,  but  disease  of  the  abdominal  integuments. 

There  are  five  places  especially  at  which  stenosing  phenomena 
may  appear  through  temporary  kinking  : 

1.  At  the  pyloric  part  of  the  stomach,  or  where  the  duodenum 
passes  over  from  the  superior  horizontal  part  into  the  vertical 
portion,  which  is  tightly  joined  to  the  spinal  column. 

2.  At  the  entrance  of  the  jejunum  into  the  duodenum,  at  the 
duodenojejunal  flexure  (E.  C.  Perry  and  L.  E.  Shaw,  “ Diseases  of 
the  Duodenum,”  “ Guy’s  Hospital  Reports,”  1893,  p.  171). 

3.  At  the  transition  of  the  small  intestine  into  the  fixed  portion 
of  the  cecum. 

4.  At  the  transition  of  the  transverse  colon  into  the  descending 
colon,  which  is  comparatively  tightly  fixed  at  the  posterior  lateral 
abdominal  wall,  and  is  further  attached  high  up  into  the  left 
hypochondrium  by  the  phrenocolic  ligament  (Phoebus).  The  left 
flexure  of  the  colon  normally  forms  a right  angle,  which,  however, 
becomes  an  acute  angle  in  patients  with  pendulous  abdomen. 

5.  In  some  cases,  when  the  hepatic  flexure  of  the  colon  has  not 
sunk,  stenoses  may  develop  in  it  at  a corresponding  place,  as  de- 
scribed in  No.  4 (Landau,  on  “ Pendulous  Abdomen,”  p.  82,  et  seq.). 

The  floating  kidney  is  to  be  put  semiotically  on  a level  with 
enteroptosis  ; it  is  not  a disease  sui generis. 


720 


ENTEROPTOSIS GASTROPTOSIS. 


The  dangerous  sequences  of  floating  kidney  are  hydronephrosis, 
intermittent  hydronephrosis,  and  incarceration  of  the  kidney  (first 
described  by  Dittl).  This  dangerous  condition  is  largely  ascrib- 
able  to  compression  of  the  renal  veins. 

Diagnosis. — Movable  kidney  may  be  undoubtedly  recognized 
in  all  cases  where  we  can  firmly  grasp  it  between  the  fingers,  and 
can  thus  determine  exactly  its  entire  configuration.  Secondly,  the 
diagnosis  is  comparatively  simple  in  those  cases  when  we  may 
not  determine  the  configuration,  it  is  true,  but  when  we  discern  only 
a smooth,  movable  body,  often  movable  only  within  narrow  limits, 
if  we  are  aided  by  the  instructions  of  the  patient,  that  after  bodily 
exertion,  this  body  was  suddenly  felt.  But  there  are  cases  where 
this  information  of  the  patient  is  lacking,  where  we  can  not  make 
the  diagnosis  by  palpation  with  certainty,  and  here  mistakes  are 
possible.  An  error  which  has  occurred  repeatedly,  according  to 
our  experience,  is  to  mistake  a small  lower  part  of  the  liver,  sepa- 
rated from  it  by  a strong  furrow  due  to  compression,  which  part,  on 
account  of  the  depth  of  the  furrow,  seems  to  be  movable,  for  a 
floating  kidney.  Guttmann  has  seen  such  cases  repeatedly  in 
autopsies,  which  during  life  were  regarded  as  movable  livers.  Osier 
(“  Lectures  on  the  Diagnosis  of  Abdominal  Tumors,”  p.  97)  gives 
an  illustration  of  a tongue-shaped  prolongation  of  the  anterior  mar- 
gin of  the  right  lobe,  with  the  gall-bladder  projecting  below  it. 

By  means  of  the  bimanual  examination,  which  has  been  described 
in  detail,  we  are,  at  least  in  a large  number  of  cases,  able  to  feel  the 
lower  end  of  the  right  kidney  during  inspiration.  And  since  abnor- 
mal (extreme)  movability  occurs  most  frequently  with  the  right  kid- 
ney (in  more  than  eighty  per  cent,  of  the  cases),  therefore,  by  finding 
the  right  lower  edge  of  the  kidney  in  bimanual  palpation,  the  error 
of  mistaking  a portion  of  the  liver  (separated  from  it  by  a furrow) 
for  the  kidney  should  be  avoidable. 

Proving  by  means  of  percussion  that  the  kidney  is  not  in  the 
proper  place  is  very  unsatisfactory.  It  seems,  indeed,  in  some  cases, 
that  the  dullness  is  less  on  that  side  where  the  kidney  is  wanting, 
than  on  the  opposite  side,  where  the  kidney  is  present.  But  in 
most  cases  of  movable  kidney  there  was  no  difference  in  the  reso- 
nance in  the  region  of  the  loins  on  either  side.  We  therefore 
attach  no  value  to  the  results  of  percussion  in  the  diagnosis  of 
dislocated  kidney,  and  the  same  opinion  of  the  use  of  percussion 
holds  good  in  diseases  of  the  kidney  in  general.  Only  in  isolated 
circumstances  it  may  aid  the  other  methods  of  examination, — e.g., 


FREQUENCY  OF  NEPHROPTOSIS. 


72  I 

in  cases  of  great  swelling  of  the  kidneys, — but  in  most  cases  per- 
cussion of  the  kidneys  is  entirely  worthless,  and  hence  I do  not 
consider  it  a diagnostic  method. 

Frequency  of  Dislocated  Kidney. — The  statements  of  various  clin- 
icians concerning  the  frequency  of  floating  kidney  vary  consider- 
ably. Lindner  stated  that  it  was  the  most  frequent  abnormality  of 
the  female  body,  and  that  one  woman  in  five  to  seven  was  afflicted 
with  the  trouble.  Edebohls  gives  18  per  cent.,  Mathieu  27.1  per 
cent.,  Fischer-Benzon  17  to  22  per  cent.,  John  Schmitt  10  per 
cent.  (New  York,  “ Medic.  Monatsschrift,”  March,  1891).  Ludwig 
Knapp  (“  Wanderniere  bei  Frauen,”  Berlin,  1896)  gives  5 per 
cent.  Einhorn  gives  1.8 1 per  cent,  for  men  and  20  per  cent,  for 
women  (“  New  York  Med.  Record,”  Aug.,  1898). 

As  far  as  our  clinical  material  permits  us  to  judge  (260  examina- 
tions of  females  from  hospital  and  private  practice),  the  rate  for 
our  Baltimore  cases  is  six  per  cent.  The  right  kidney  is  dislocated 
more  frequently  than  the  left,  the  proportion  being  15  to  I,  and 
bilateral  dislocation  was  found  only  once.  This  rate  includes  only 
strictly  dislocated  kidneys,  not  palpable,  nor  even  movable,  kid- 
neys. Twelve  cases  in  which  the  organ  could  be  moved  up  and 
down  within  a space  of  from  1 to  1 y2  inches  approximately  were 
not  included  ; they  were  found  in  females  giving  no  signs  or  symp- 
toms of  abdominal  disease,  being  in  the  hospital  for  acute  pul- 
monary diseases,  injuries,  and  throat  inflammations. 

A fundamental  requisite  in  describing  these  conditions  is  to 
distinguish  precisely  between  (1)  palpable,  (2)  movable,  and  (3) 
dislocated  kidneys.  The  last  may  be  ( a ) movable — i.  e.,  the  so- 
called  floating  kidney — or  ( b ) immovable : i.  e.y  anchored  down 
in  its  abnormal  position.  (See  classification  on  p.  710.)  Unless 
unusually  adipose  abdominal  walls  or  firmly  contracted  recti 
muscles  interpose  between  the  palpating  fingers  and  the  kidney, 
the  latter  should  always  be  palpable : i.  e.}  one  should  be  able 
to  feel  the  kidney  in  about  fifty  per  cent,  of  all  cases.  Fur- 
thermore, these  palpable  kidneys  should,  even  in  the  majority 
of  cases,  be  made  out  as  mobile,  for  these  organs,  especially 
the.  right  one,  are  normally  mobile  to  a slight  degree.  James 
Israel  has  observed  the  respiratory  movements  of  the  kidney  in  a 
case  in  which  the  lumbar  regions  had  been  opened.  In  animals 
(dogs)  the  author  has  never  observed  a movable  kidney  under 
normal  conditions;  this  is  accounted  for  by  the  horizontal  position 
of  the  body.  But  in  human  beings  the  right  kidney  was  slightly 


722 


ENTEROPTOSIS GASTROPTOSIS. 


movable  in  fifty  per  cent,  of  our  cases.  Palpable  and  movable  kid- 
neys, as  a rule,  give  no  symptoms — only  the  various  types  of  dis- 
located kidneys  are  clinically  important.  Occasionally,  the  kidneys 
can  not  be  palpated  in  highly  nervous  individuals,  because  of  con- 
traction of  the  recti ; if  it  is  absolutely  necessary  to  locate  the 
kidneys  in  these  cases,  they  should  be  examined  in  a warm  bath 
or  under  narcosis. 

Dislocated  kidneys  are  such  as  can  be  moved  out  of  their  nor- 
mal position  more — i.  e .,  further — than  any  distance  ascribable  to 
the  normal  respiratory  movability,  and  that  can  exchange  one 
abnormal  position  with  another  or  with  the  normal,  and  that  give 
rise  to  abnormal  symptoms,  as  a rule.  A kidney  that  is  movable 
in  its  adipose  imbedding  from  one  to  two  inches  is  not  yet  dislo- 
cated, and  symptoms  due  to  torsion  of  the  ureters  and  vessels  do 
not  arise  until  the  mobility  exceeds  that  limit.  Great  accuracy  and 
precision  are  needed  in  the  use  of  the  terms  palpable,  movable,  dis- 
located, and  floating  kidney,  and  there  must  be  some  consensus  or 
agreement  concerning  the  clinical  meaning  of  these  words,  and 
some  limit  to  their  significance,  before  statistics  can  have  any  value. 
Up  to  the  present,  this  matter  is  in  a state  of  confusion.  The 
degrees  of  dislocation  schematically  given  on  page  710  may  aid  us 
in  reaching  an  understanding. 

Ewald’s  assertion  of  the  extraordinary  frequency  of  movable 
kidney  is  the  more  astonishing  because  in  autopsies  one  does  not 
often  find  movable  kidneys.  Guttmann,  in  reporting  his  experience, 
resting  upon  about  8000  autopsies  at  Berlin,  which  for  the  most 
part  he  himself  noted  down,  stated  that  in  these  autopsies  the  float- 
ing kidney  was  not  frequent.  His  experience  agrees  with  that  of 
the  pathological  institute  of  the  Charite,  Berlin.  Landau,  in  his 
monograph  on  the  floating  kidney,  states  that  in  the  Charite  float- 
ing kidneys  were  found  very  rarely  at  autopsies.  It  may  be  added, 
however,  that  in  a horizontal  position  the  movable  kidney  sinks 
back  to  its  normal  position,  and  is,  therefore,  liable  to  be  overlooked 
in  the  necropsy ; but  the  movability  must  persist,  and  this  must 
attract  attention  when  the  kidney  is  taken  out.  In  taking  out  the 
kidney  an  experienced  dissector  will  notice  at  once  whether  it  is 
normally  fixed  or  movable,  dislocated,  or  fixed  in  an  abnormal 
position.  The  explanation  given  by  Neumann  of  the  scarcity  of 
floating  kidneys  at  autopsies,  that  the  fatty  envelop,  becoming 
solidified  after  death,  tends  to  fix  the  kidney,  is  unsatisfactory.  In 
the  first  place,  the  fatty  envelop,  if  there  is  any  left,  is  not  any  more 


SYMPTOMS  OF  GASTROPTOSIS. 


723 


solid  after  death,  necessarily,  than  before,  because  rigor  mortis  does 
not  affect  the  solidity  of  fat;  this  is  influenced  only  by  the  tempera- 
ture of  the  cadaver.  But  Oppolzer,  Ebstein,  and  others  assign  loss 
of  the  fatty  imbedding  as  a cause  of  floating  kidney,  and  any  one 
who  has  observed  a nephrorrhaphy  can  assure  himself  of  the  scarcity 
of  fat  about  such  dislocated  organs.  Besides,  it  requires  a power- 
ful effort  of  the  imagination  to  conceive  of  replacement  of  a kidney 
(dislocation  of  the  second  degree)  that  may  be  as  far  as  ten  inches 
away  from  its  normal  position  by  solidification  of  a supposed  fatty 
envelop. 

Reversal  of  the  Location  of  the  Viscera  {Situs  viscerum  inversus ). — 

In  this  state  the  stomach  lies  normally  on  the  right  side,  the  heart 
on  the  right  side,  the  liver  on  the  left.  The  site  of  all  the  viscera 
is  exactly  reversed  ; there  is  a situs  inversus , however,  in  which  the 
heart  is  found  in  the  normal  position  at  the  same  time;  the 
location  of  all  other  organs  is  reversed. 

Vertical  position  of  the  stomach  is  an  anomaly  frequently  associated 
with  atony,  and  is  attributed  to  tight  lacing.  It  becomes  important 
clinically  only  when  the  motor  function  is  interfered  with,  in  which 
case  the  treatment  is  the  same  as  that  for  motor  insufficiency.  The 
diagnosis  of  vertical  stomach  should  present  no  difficulties  when 
the  methods  stated  on  pages  98  to  112  are  employed. 

Symptoms  of  Gastroptosis. — The  symptoms  are  brought  on 
by  the  gastric  and  intestinal  atony,  by  the  mechanical  disturbances 
caused  by  the  descent  of  the  organ,  and  neurasthenia.  We  have 
observed  a number  of  cases  of  gastroptosis  that  presented  no  diges- 
tive symptoms  whatever.  The  dyspeptic  symptoms  that  are  most 
common  are  : pressure,  fullness,  distention,  and  pain  (gastralgia), 
coming  on  at  irregular  intervals,  and  independently  of  the  digestive 
act  or  of  the  quality  and  quantity  of  the  food.  A sensation  of  heat 
or  burning  at  or  below  the  umbilicus  is  at  times  described.  Eruc- 
tations, nausea,  vomiting,  and  pyrosis  may  be  complained  of. 
Chronic  constipation  is  a typical  accompaniment ; flatulence  and 
occasional  attacks  of  diarrhea  alternate  with  constipation. 

When  there  is  an  evident  coloptosis,  a very  stubborn  membran- 
ous dysentery  is,  as  a rule,  present ; being,  no  doubt,  caused  by 
abnormal  kinking  and  stenosing  flexures  in  the  course  of  the  large 
intestine. 

The  quantity  of  the  urine  may  be  very  variable,  and  depends 
upon  the  permeability  of  the  ureters.  Absolute  obliteration  of  the 
ureter  by  kinking  may  produce  oliguria  or  anuria,  which  may  be 


724 


ENTEROPTOSIS GASTROPTOSIS. 


followed  by  profuse  urination  when  the  ureter  becomes  straight- 
ened. 

Cirailatory  Symptoms. — A low  blood  pressure  in  the  systemic 
vessels  is  characteristic  of  this  disease.  Disturbances  in  the 
rhythm  and  rate  of  the  heart-beat  are  common.  Tachycardia 
after  evacuation  of  the  bowels  I have  also  observed  frequently. 

Nervous  Symptoms. — The  typical  clinical  picture  of  aggravated 
neurasthenia  is  frequently  associated  with  these  cases.  The  mani- 
fold pains  complained  of  during  bodily  exertion  are  referable  to 
drawing  and  tugging  upon  the  nervous  apparatus  supplying  the 
dislocated  organs.  Intense  lumbago  is  a most  frequent  sign. 

The  spleen  has  been  very  rarely  found  dislocated  in  splanchno- 
ptosis, Glenard  having  observed  splenoptosis  only  twice  in  148  cases. 

Hepatoptosis  can  be  recognized  by  a lowering  of  the  area  of 
hepatic  dullness.  There  are  several  degrees  of  liver  displace- 
ment : (1)  A portion  of  the  liver  projects  beyond  the  arch  of  the  ribs 
into  the  abdomen,  and  the  upper  border  is  correspondingly  lower. 
(2)  The  lower  portion,  from  y2  to  of  the  liver  projects  into  the 
abdomen  ; the  liver  dullness  above  the  edge  of  the  ribs  is  reduced 
to  a narrow  zone  or  is  entirely  absent.  (3)  The  entire  liver  is 
located  within  the  lower  abdomen. 

Coloptosis. — Descent,  displacement, with  consequent  local  sten- 
osis, and  dilation  of  portions  of  the  colon  can  be  recognized  by 
distending  the  colon  with  air  or  water.  The  air  is  usually  forced 
in  through  a long  colon  tube  (Langdon)  by  means  of  a double-bulb 
pump,  or  from  600  c.c.  to  one  liter  of  warm  water  are  gradually 
allowed  to  run  in  under  gentle  pressure.  Normally,  a distended 
area  is  palpable,  and  even  visible,  two  or  three  inches  above  the 
umbilicus;  the  ascending  and  descending  colon  can  be  recognized 
as  two  arching  elongated  prominences  about  three  inches  to  each 
side  of  the  umbilicus.  When  the  colon  is  prolapsed,  the  transverse 
portion  is  found  touching  at  the  symphysis  pubis,  or  even  within 
the  pelvis.  I have  occasionally  observed  that  a prolapse  of  the 
colon  was  recognizable  by  the  distention  that  had  occurred  through 
gaseous  fermentation,  and  that  artificial  distention  was  unneces- 
sary. When  a prolapsed  colon  is  distended  with  warm  water,  it 
changes  its  position  with  the  attitude  of  the  patient.  Thus,  a 
colon  that  rests  on  the  symphysis  will  rise  to  its  normal  location 
when  the  pelvis  is  elevated  and  the  thorax  depressed.  If  this  does 
not  occur,  the  colon  is  adherent  in  its  normal  location. 

Idiopathic  dilation  of  the  colon  may  give  rise  to  symptoms  that 


COURSE  OF  GASTROPTOSIS. 


725 


may  cause  confusion  in  differentiating  the  location  of  stomach  and 
colon.  Reginald  H.  Fitz  called  attention  to  the  similarity  in  the 
clinical  histories  of  chronic  phantom  tumor  and  that  of  idiopathic 
dilation  of  the  colon  (“Am.  Jour.  Med.  Sciences,”  Aug.,  1899,  p. 
134).  The  methods  given  will  suffice  to  determine  the  location 
and  capacity  of  the  colon  as  well  as  that  of  the  stomach. 

Electrodiaphany  is  an  available  method  of  diagnosing  the  course 
and  location  of  the  colon.  The  author  has  frequently  used  it  for 
that  purpose  (see  pp.  104  to  112).  The  results  and  conclusions 
derived  therefrom  are  subject  to  the  same  limitations  as  when  the 
electrodiaphane  is  used  within  the  stomach. 

Gastroptosis  can  occasionally  be  recognized  by  inspection ; the 
methods  described  in  chapter  xi,  pages  98-104,  if  systematically 
carried  out,  can  leave  no  possible  doubt  regarding  the  existence  of 
this  dislocation.  The  differentiation  between  prolapse  and  dila- 
tion is  facilitated  by  electrodiaphany.  If  the  stomach  is  dilated,  not 
prolapsed,  the  transillumination  area  will  exhibit  respiratory  mov- 
ability.  Ewald,  Litten,  and  Bartels  assert  that  dilation  of  the 
stomach  frequently  occurs,  with  nephroptosis  or  hepatoptosis ; this 
is  not  confirmed  by  Boas.  Myasthenia,  with  overretention  and 
stasis  of  ingesta,  is  frequently  observed,  though  not  in  all  cases  of 
prolapse  of  the  stomach.  The  typical  clinical  picture  of  classical 
dilation  may  occur  in  connection  with  gastroptosis.  By  insuffla- 
tion and  coating  of  the  stomach  with  subnitrate  of  bismuth  by 
means  of  the  intragastric  powder-blower  the  size  and  location  of 
the  organ  can  be  demonstrated  by  means  of  the  Rontgen  rays. 

Analysis  of  the  gastric  contents  in  gastroptosis,  though  yielding 
few  practical  aids  to  diagnosis,  is  useful  in  selecting  a proper  diet. 
The  results  of  such  chemical  analyses  are  variable. 

The  course  of  gastroptosis  is  protracted  and  generally  chronic. 
Great  feebleness,  abnormal  sensations  of  pain  and  compression, 
or  of  cold  and  hot  aurae,  indisposition  to  exertion,  and  faintness  are 
among  the  most  common  symptoms  in  this  most  variable  clinical 
picture.  Severe  disturbances  of  nutrition  and  anemia  unfailingly 
appear  as  the  digestive  distress  continues. 

The  points  of  differentiation  between  falling  of  the  stomach  and 
dilation  and  atony  have  been  considered  in  the  chapters  on  these 
diseases.  The  differential  diagnosis  between  the  symptoms  of 
gastroptosis  and  nervous  dyspepsia  is  difficult,  sometimes  requiring 
all  the  ingenuity  of  an  experienced  diagnostician.  This  is  prin- 
cipally because  the  symptoms  of  both  states  are  occasionally 
48 


726 


ENTEROPTOSIS GASTROPTOSIS. 


identical,  and  because  gastroptosis  is  often  associated  with  nervous 
dyspepsia.  The  state  of  the  peristalsis  is  normal  in  nervous  dys- 
pepsia, but  in  gastroptosis  there  is,  as  a rule,  a myasthenia,  with 
overretention  of  ingesta. 

Treatment  of  Gastroptosis. — Prophylaxis. — The  frequency  of 
gastroptosis  and  enteroptosis  in  women  demands  that  the  physician 
should  emphatically  oppose  tight  lacing,  or  any  garment  that  con- 
stricts the  waist.  The  dresses  should  be  so  constructed  as  to  be 
supported  from  the  shoulders.  We  have  already  spoken  of  this 
under  the  heading  of  acute  gastritis.  If  possible,  the  modifications 
in  dress  should  be  made  in  accordance  with  the  rules  of  fashion. 
It  will  do  no  good  to  oppose  the  unrestricted  domination  of  this 
tyrant  of  the  female  sex,  without  clear  indications  of  the  benefit  to  be 
derived.  We  have  already  emphasized  the  fact  that  a properly  con- 
structed corset  does  not  necessarily  work  harm,  but  may  eventually 
be  useful,  by  the  support  it  gives  to  the  back  and  breasts.  The 
dresses  should,  however,  be  supported  from  the  shoulders.  It  is 
necessary  to  do  this  before  the  enteroptosis  is  developed. 

The  relaxation  of  the  abdominal  muscles  must  be  prevented  by 
using  well-applied  bandages  after  confinements,  worn  for  several 
months.  The  bowels  must  be  kept  regular.  Massage,  electricity, 
and  cold-water  applications  may  contribute  to  a vigorous  abdom- 
inal musculature,  but  the  most  effective  method  of  strengthening 
the  abdominal  muscles  is  by  abdominal  gymnastic  exercise.  (See 
Illoway,  “ Constipation.”) 

We  will  briefly  describe  two  of  the  most  practical  methods  of 
training  the  abdominal  muscles  : 

No.  i. — The  patient  places  himself  on  a couch  or  on  a blanket 
spread  on  the  floor,  clothed  simply  in  his  underwear;  the  hands 
are  placed  at  the  sides.  The  exercise  begins  by  slowly  raising  the 
limbs  from  the  couch  to  a vertical  position  in  the  air,  keeping  them 
there  for  thirty  seconds,  then  very  slowly  letting  them  return  to 
the  horizontal  position  of  rest.  The  secret  of  this  manoeuver  is  its 
slow  execution.  With  one  hand  on  the  abdominal  muscles,  the 
patient  may  feel  the  tightening  and  rigidity  that  occur  in  the  act 
of  raising  the  limbs.  This  exercise  should  be  repeated  ten  times. 

No.  2. — The  second  exercise  should  be  carried  out  in  the  follow- 
ing manner  : The  patient  places  himself  flat  on  a blanket  on  the 
floor,  with  his  feet  inserted  under  a bureau  or  under  a piece  of 
heavy  furniture  of  any  kind  ; both  hands  are  placed  at  the  sides. 
The  patient  now  must  slowly  bring  the  trunk  of  his  body  into  an 


TREATMENT  OF  GASTROPTOSIS.  727 

erect  position,  and  when  this  has  been  reached,  the  trunk  is  just  as 
slowly  replaced  in  a prone  position  on  the  floor. 

Both  of  these  exercises  are  quite  similar;  in  No.  i it  is  the  trunk 
which  is  fixed  and  the  lower  limbs  are  slowly  moved  up  and  down, 
and  in  No.  2 the  lower  limbs  are  fixed  and  the  trunk  is  moved  up 
and  down.  These  exercises  should  be  carried  out  systematically 
and  methodically  ten  times  every  morning  and  evening.  Sandow’s 
book  on  training  will  instruct  those  desiring  information  on  this 
very  useful  subject. 

Rapid  emaciation  must  be  avoided.  Physicians  are  nowadays 
frequently  consulted  by  thin  people  desiring  to  get  fat,  and  by  fat 
people  desiring  to  become  thin,  in  the  most  convenient  manner. 
Rapid  falling-off  and  loss  of  fat,  when  undertaken  as  a cure  for 
obesity,  is  a hazardous  undertaking.  The  fat  is  lost  not  only  from 
the  trunk  and  extremities,  but  the  internal  organs  are  deprived  of 
their  normal  incasing  and  imbedding  of  fat,  which  constitutes  their 
support,  so  that  treatments  tending  to  reduce  the  weight  of  the 
body  should  be  conducted  only  under  careful  supervision. 

The  Mechanical  Treatment. — The  mechanical  treatment  consists  in 
applying  a properly  selected  and  adapted  abdominal  bandage. 
There  is  no  one  particular  bandage  that  will  suit  all  cases.  The 
bandages  should  have  their  main  support  and  resting-places  upon 
the  crests  of  the  ilium,  symphysis  pubis,  and  spinal  column.  From 
here  the  strength  of  the  bandage  is  secured  by  broad  pieces  of 
metal  or  whalebone  inserted  into  the  linen,  leather,  or  rubber  parts 
of  the  bandage.  These  bandages  must  be  measured  to  the  nude 
figure,  must  fit  perfectly,  and  should  be  worn  day  and  night.  Boas 
recommends  the  bandage  of  Landau  and  Bardenheuer.  Prolonged 
rest  in  a horizontal  position  on  the  back  favors  restitution  of  the 
abdominal  viscera  to  their  normal  position.  In  cases  of  great 
weakness,  therefore,  with  emaciation,  the  Weir  Mitchell  rest  cure 
is  one  of  the  most  effective  means  of  treatment. 

Constipation  is  best  combated  by  proper  diet.  The  author  recom- 
mends compotes  of  fruit,  such  as  figs,  prunes,  apples,  pears,  plums, 
and  sweet  grapes.  Buttermilk,  kefyr,  and  good  cider  favor  normal 
evacuation.  Sugar  of  milk,  y2  of  an  ounce  three  times  daily, 
is  also  helpful.  The  injection  of  eight  ounces  of  olive  oil  high 
up  into  the  colon  is  an  excellent  treatment  for  this  symptom 
(Fleiner).  As  gastroptosis  predisposes  to  dilation,  it  may  occur 
that  the  foods  are  retained  an  abnormally  long  time  within  the 
stomach.  In  these  cases  lavage  will  be  indispensable. 


728 


ENTEROPTOSIS GASTROPTOSIS. 


When  the  symptoms  of  atony  and  motor  insufficiency  are  pro- 
nounced, local  intragastric  douches  with  alternating  cold  and  warm 
water  are  very  effective  in  restoring  partial  tonicity  to  the  muscular 
walls.  Turck’s  gastric  resuscitator  is  available  for  this  purpose. 
The  temperature  of  the  water  should  be  changed  every  two  or 
three  minutes  by  alternately  connecting  the  stomach-tube  with 
hot  and  cold  reservoir-bottles,  elevated  to  about  the  level  of  the 
patient’s  head.  The  tube  is  of  the  return  or  double-current  type, 
and  the  water  does  not  come  in  contact  with  the  mucosa,  but  flows 
through  a rubber  bag  which  distends  the  stomach  moderately. 
(See  Gillespie,  “ Modern  Gastric  Methods,”  p.  164.)  Treating  the 
abdominal  muscles  by  massage  and  the  faradic  current  is  of  some 
utility  in  patients  that  are  too  feeble  to  undergo  the  abdominal  gym- 
nastic training.  These  means  of  treatment  may  be  applied  also  in 
those  cases  that  have  not  the  will-power  to  persist  in  such  abdominal 
gymnastics;  but  electricity  and  massage  can  not  effect  the  per- 
manent improvement  that  results  from  abdominal  gymnastics. 

Floating  kidneys,  according  to  Bachmeier  (“  Wien.  med.  Presse,” 
1891,  Nos.  19  and  20),  may  be  replaced  best  in  the  following 
manner : The  patient  occupies  the  dorsal  position  in  bed,  the 
physician  taking  a chair  facing  the  head  end  of  the  bed ; both 
hands  are  placed  on  the  right  side  of  the  patient,  under  the  anterior 
arch  of  the  ribs ; if  possible,  the  kidney  is  grasped  with  the  fingers 
of  the  right  hand ; the  hands  are  then  pressed  gently  and  firmly 
toward  the  posterior  and  superior  parts  of  the  abdomen.  While 
this  pressure  i^  exerted,  the  finger-tips  must  make  constant  shaking 
and  trembling  motions.  The  author  prefers  placing  the  patient  in 
a recumbent  dorsal  position  with  the  pelvis  very  much  elevated  and 
the  chest  and  head  low;  for  example,  the  patient  may  sit  upon  the 
high  part  or  head-rest  of  a sofa,  and  let  the  body  sink  slowly  down 
backward  upon  the  couch ; the  dislocated  kidney  will  then  of 
itself  resume  its  normal  location, — provided  it  is  not  adherent, — 
particularly  if  the  manipulations  just  described  are  carried  on  at 
the  same  time. 

Diet. — In  enteroptosis  and  gastroptosis  the  diet  should  be  as 
nourishing  as  possible,  and  adapted  to  the  state  of  motility  and 
secretion.  If  the  condition  of  the  digestive  organs  will  permit, 
attempts  should  be  made  at  increasing  the  adipose  tissue.  Distinct 
diseases  of  the  gastric  mucosa  contraindicate  a large  food-supply. 
Experience  has  taught  us  that  one  of  the  best  treatments  for  float- 
ing kidney  is  that  which  causes  an  increased  deposition  of  fat. 


MEDICINAL  TREATMENT. 


729 

Fat  is  best  introduced  in  diet  in  the  form  of  fresh  butter,  rich 
gravies,  and  cream.  For  further  particulars  of  nourishing  diet  we 
refer  to  the  section  on  Dietetics.  In  the  author’s  sanatorium  for 
digestive  diseases  the  schedule  on  pages  249  and  250  has  been 
found  useful  in  nephroptosis.  In  a number  of  cases  where  fats  in 
the  diet  gave  digestive  distress,  I succeeded  in  increasing  the  body 
weight  by  hypodermic  injections  of  sterile  olive  oil. 

Medicinal  Treatment. — The'  use  of  medicines  is  sometimes  una- 
voidable for  the  treatment  of  constipation.  My  favorite  remedy 
for  this,  when  it  becomes  necessary,  is  the  fluid  extract  and  the 
active  syrup  of  cascara  sagrada  (Clinton  Pharm.  Co.),  or  large  colon 
irrigations  with  warm  water,  which  will  also  benefit  the  mem- 
branous colitis.  When  patients  can  take  it,  the  time-honored 
castor  oil  is  a good  and  harmless  remedy,  but  must  not  be  given 
when  there  is  gastric  stagnation.  Of  other  laxative  remedies,  I 
favor  aloes,  strychnin,  rhubarb,  magnesia,  senna,  and  podophyllin. 
Jalap  and  scammony  do  not  act  well,  nor  do  the  very  drastic  pur- 
gative waters,  such  as  the  Hunyadi  Janos  and  Rubinat-Condal.  In 
such  rare  cases  as  could  tolerate  water-drinking  I have  seen  more 
favorable  results  follow  the  persistent  use  of  Bedford  Magnesia 
Springs  water,  which  is  rather  mild  in  its  purgative  qualities.  On 
the  whole,  I have  observed  no  permanent  improvement  under  the 
use  of  any  mineral  waters. 

Glenard  recommended  magnesium  and  sodium  sulphate  to  com- 
bat the  effects  of  autointoxication ; but  Boas,  after  a prolonged 
trial  of  these  remedies,  asserts  that  he  has  observed  detrimental 
results  from  them.  The  author’s  formula  for  combating  auto- 
intoxication in  gastroptosis  is  the  following : 

R.  Betanaphthol  bismuth, 4.0 

Resorcin  resublim.,  4.0 

Strychnin,  sulphatis, 0.02 

In  anacidity  (achylia)  dilute  HC1,  gvj,  should  be  added 

Elix.  gentianse, 1 80.0 

Sig. — One  tablespoonful  three  times  daily. 

In  addition  to  these,  the  salicylate  of  bismuth,  salicylic  acid, 
chloroform  water,  and  betanaphthol  have  been  recommended. 
They  are  made  more  efficacious  if  combined  with  strychnin  and  an 
adapted  diet. 

It  is  conceivable  that  methods  of  surgical  procedure  for  replac- 
ing a prolapsed  stomach,  by  attaching  it  partly  to  the  diaphragm, 
ensiform  cartilage,  and  perhaps  to  the  retroperitoneal  fascia,  in 


■ Z) 

3J 

gr-  A 

fgvj.  M. 


730 


ENTEROPTOSIS GASTROPTOSIS. 


such  a manner  as  to  avoid  kinking  or  stenosis  (gastropexy),  may 
prove  practicable.  This  operation  has  been  recently  described  in 
the  following  publications:  Duret,  see  “ Rev.  de  Chir.,”  1896,  xvi, 
p.421  ; also  Davis,  “ Western  Med.  Rev.,”  Oct.,  1897,  W.  W.  Keen, 
“ Cartwright  Lectures,”  “ Phil.  Med.  Jour.,”  vol.  1,  p.  935. 

LITERATURE  ON  GASTROPTOSIS  AND  ENTEROPTOSIS. 

1.  Aaron,  C.  D.,  “ Gastroptosis,”  “Jour.  Amer.  Med.  Assoc.,”  1897,  xxiv. 

2.  Adler,  H.,  “Gastroptosis:  A Clinical  Study,”  “Maryland  Med.  Jour.,” 
Baltimore,  1898,  xxxix. 

3.  Arendt,  “ Ueber  Mastcuren  und  ihre  Anwendung  bei  chronischen  Krank- 
heiten  der  weiblichen  Sexualorgane,”  “ Therap.  Monatshefte,”  1892,  Heft  1,  S.  9. 

4.  v.  Bachmaier,  “ Die  Wanderniere  und  deren  manuelle  Behandlung,  nach 
Thure  Brandt,”  “Wiener  med.  Presse,”  1892,  Nr.  19  u.  20. 

5.  Bial,  M.,  “Ueber  die  Beziehung  der  Gastroptose  zu  nervosen  Magen- 
leiden,”  “ Berl.  klin.  Wochenschr.,”  1897,  xxiv. 

6.  Bial,  M.,  “ Gastroptose,”  “ Verhandl.  d.  Cong.  f.  innere  Med.,”  Wies- 
baden, 1897,  xv. 

7.  Boas,  “ Ueber  die  Bestimmung  der  Lage  und  Grenzen  des  Magens 
durch  Sondenpalpation,”  “ Centralbl.  f.  klin.  Med.,”  1896. 

8.  Bourget,  “Ueber  den  klinischen  Werth  des  Chemismus  des  Magens,” 
“Therap.  Monatshefte,”  1895. 

9.  Chapotot,  “ L’Estomac  et  le  Corset,”  Paris,  1891. 

10.  Cheron,  “ De  l’Enteroptose,”  “Union  Med.,”  20.  Dec.,  1888. 

11.  Cuilleret,  “Etude  Clinique  sur  l’Enteroptose  ou  Maladie  de  Glenard,” 
“ Gazette  des  Hopit.,”  1888,  et  No.  105,  1889. 

12.  Czerny,  “ Zur  Prophylaxis  des  Hangebauches  der  Frauen,”  “ Centralbl. 
f.  Gynakologie,”  1886. 

13.  Dehio,  “ Zur  physikalischen  Diagnostik  der  mechanischen  Insufficienz 
des  Magens,”  VII.  Congress,  f.  innere  Medicin,  1888. 

14.  Dujardin-Beaumetz,  “ Neurasthenie  Gastrique  et  leur  Traitement,” 
“ Lemons  de  l’Hopital  Cochin,”  in  the  “ Therapeut.  Gaz.,”  15  Jan.,  1890. 

15.  Edinger,  “ Wanderniere,”  “ Eulenberg’s  Real-Encyklop.,”  2.  Aufl.,xxi. 

16.  Einhorn,  M.,  “Die  Gastrodiaphanie,”  “ New  Yorker  med.  Wochenschr.,” 
1889* 

17.  Ewald,  “Ueber  Enteroptose  und  Wanderniere,”  “Berl.  klin.  Woch- 
enschr.,” 1890. 

18.  Fereol,  “ De  l’Enteroptose,”  “ Bulletin  de  la  Societe  Med.  des  Hopitaux,” 
5 Janv.,  1887,  et  i2Novembre,  1888. 

19.  v.  Fischer-Benzon,  “Ein  Beitrag  zur  Anatomie  und  Aetiologie  der  be- 
weglichen  Niere,”  Inaug.-Dissert.,  Kiel,  1887. 

20.  Fleiner,  “Ueber  die  Behandlung  der  Constipation  und  einiger  Dick- 
darm-Affectionen  mit  grossen  Oelklystieren,”  “ Berl.  klin. Wochenschr.,”  1893. 

21.  Fleiner,  “Ueber  die  Beziehungen  der  Form-  und  Lageveranderungen  des 
Magens  und  des  Dickdarms  zu  Functionsstorungen  und  Erkrankungen  dieser 
Organe,”  “ Miinch.  med.  Wochenschr.,”  1895. 

22.  Fromont,  “ Anatqmie  de  la  Portion  Abdominale  de  l’lntestin,”  These  de 
Lille,  1890. 

23.  Gegenbaur,  “ Lehrbuch  der  Anatomie  des  Menschen.” 


LITERATURE  ON  GASTROPTOSIS  AND  ENTEROPTOSIS. 


731 


24.  Glenard,  “Application  de  la  Methode  Naturelle  al’Analyse  de  la  Dys- 
pepsie  Nerveuse,”  “ Lyon  Med.,”  1885  ; “ Enteroptose  et  Neurasthenic,”  Soc. 
Medic,  des  Hop.  de  Paris,  1886;  “ Expos6  Sommaire  du  Traitement  de  l’Ent6- 
roptose,”  “ Lyon  Med.,”  1887,  etc. 

25.  Glenard,  “ De  l’Enteroptose,  conference  facite  a l’hopital  de  Mustapha,” 
Alger-Lyon,  Janv.,  1889,  “ Presse  med.  Belg.,”  Bruxelles,  1889. 

26.  Hahn,  “Operative  Behandlung  der  beweglichen  Niere  durch  Fixation,” 
“ Centralbl.  f.  Chirurgie,”  1881,  No.  29  (Nephrorrhaphy). 

27.  Hasse,  “ Bewegung.  d.  Zwerchfells — Einfluss  derselben  auf  d.  Unter- 
leibsorgane,”  “ Archiv  f.  Anat.  und  Physiol.,”  1886,  S.  185. 

28.  Hertz,  P.,  “ Abnormitaten  in  der  Lage  und  Form  der  Bauchorgane  bei 
dem  erwachsenen  Weibe,”  Berlin,  1894. 

29.  Hilbert,  “ Ueber  palpable  und  bewegliche  Nieren,”  “ Deutsches  Archiv 
f.  klin.  Med.,”  1893,  Bd.  l. 

30.  Huber,  A.,  “ Beitrag  zur  Kenntniss  der  Enteroptose,”  Sonderabdr.  a.  d. 
“ Correspondenzbl.  f.  Schweizer  Aerzte,”  1895,  Nr.  11. 

31.  Hufschmidt,  “ Pathol,  und  Therap.  d.  Enteroptose,”  “ Wien.  klin. 
Wochenschr.,”  1892,  Nr.  52,  including  Literature. 

32.  Israel,  “Ueber  die  Palpation  gesunder  und  kranker  Nieren,”  “ Berl. 
klin.  Wochenschr.,”  1889. 

33.  Kelling,  “ Ein  einfaches  Verfahren  zur  Bestimmung  der  Magengrosse 
mittelst  Luft,”  “ Deutsche  med.  Wochenschr.,”  1892. 

34.  Kelling,  “ Physikalische  Untersuchungen  liber  die  Druckverhaltnisse  in 
der  Bauchhohle,  sowie  liber  die  Vitalcapacitat  des  Magens,”  Leipzig,  1896. 

35.  Keppler,  “ Die  Wanderniere  und  ihre  chirurgische  Behandlung,”  Ber- 
lin, 1879. 

36.  Knapp,  Ludwig,  “ Wanderniere  bei  Frauen,”  Monograph  (Report  from 
Rosthorn’s  Clinic  in  Prague),  Berlin,  1896. 

37.  Konig,  G.,  “ Chemische  Zusammensetzung  der  menschlichen  Nah- 
rungs-  und  Genussmittel,”  Berlin,  1889  und  1893. 

38.  Krez,  L.,  “ Zur  Frage  der  Enteroptose,”  “ Mlinch.  med.  Wochenschr.,” 
No.  35,  1892. 

39.  Kumpf,  “ Ueber  die  Wanderniere  der  Frauen  und  deren  Behandlung,” 
“ Wiener  med.  Blatter,”  1890,  Nr.  14. 

40.  Kussmaul,  “ Die  peristaltische  Unruhe  des  Magens,  nebst  Bemerkungen 
iiber  Tiefstand  und  Erweiterungen  desselben,”  etc.,  “ Volkmann’s  Sammlung 
klin.  Vortrage,”  Nr.  181. 

41.  Kuttner,  “Ueber  palpable  Nieren,”  “Berl.  klin.  Wochenschr.,”  1890. 

42.  Kuttner,  “ Einige  Bemerkungen  zur  elektrischen  Durchleuchtung  des 
Magens,”  “ Berl.  klin.  Wochenschr.,”  1895. 

43.  Kuttner,  L.,  und  Dyer,  “ Ueber  Gastroptose,”  “ Berl.  klin.  Wochenschr.,” 
1897,  XXIV. 

44.  Landau,  “ Die  Wanderniere  der  Frauen,”  Berlin,  1881. 

45.  Leo,  “ Diagnostik  der  Krankheiten  der  Bauchorgane,”  2.  Aufl.,  1895. 

46.  Leube,  “ Specielle  Diagnostik  innerer  Krankheiten,”  1891. 

47.  Lindner,  “Ueber  die  Wanderniere  der  Frauen,”  Neuwied,  1888. 

48.  Litten,  “ Ueber  den  Zusammenhang  der  Magenerkrankungen  mit  Lage- 
veranderungen  der  rechten  Niere,”  “ Verhandl.  des  Congresses  f.  innere 
Medicin,”  vi,  1897;  ferner : Berl.  med.  Gesellschaft,  Sitzung  vom  19.  Marz, 
1890;  “ Berl.  klin.  Wochenschr.,”  1890,  Nr.  15. 


732 


ENTEROPTOSIS GASTROPTOSIS. 


49.  Luschka,  “ Lage  der  Bauchorgane,”  Atlas,  Karlsruhe,  1873. 

50.  Malbranc,  “ Ein  complicirter  Fall  von  Magenerweiterung,”  “ Berl.  klin. 
Wochenschr.,”  1880,  No.  28. 

51.  Martius,  “ Ueber  Grosse,  Lage,  und  Beweglichkeit  des  gesunden  und 
kranken  Magens,”  “ Verhandlungen  der  LX VI.  Naturforscherversammlung,” 
1894. 

52.  Meinert,  E.,  “Ueber  einen  bei  gewohnlicher  Chlorose  des  Entwickelungs- 
alters  auscheinend  konstanten  Befund,”  etc.,  “Volkmann’s  Samml.  klin. 
Vortrage,”  1895,  Nr.  115  u.  116. 

53.  Meinert,  E.,  “ Zur  diagnostischen  Verwerthbarkeit  der  Magendurch- 
leuchtung,”  “ Centralbl.  f.  klin.  Med.,”  1895. 

54.  Meinert,  E.,  “Ueber  normale  und  pathologische  Lage  des  menschlichen 
Magens  und  ihren  Nachweis,”  “Centralbl.  f.  innere  Med.,”  1896. 

55.  Meinert,  E.,  “Zur  Aetiologie  der  Chlorose,”  Wiesbaden,  1894. 

56.  Meltzing,  “ Magendurchleuchtungen,”  “ Zeitschr.  f.  klin.  Med.,”  XXVII. 

57.  Meltzing,  “ Gastroptose  und  Chlorose,”  “ Wiener  med.  Presse,”  1895. 

58.  Moritz,  “ Studien  iiber  die  motorischeThatigkeit  des  Magens,”  “ Zeitschr. 
f.  Biologie,”  xxxii,  Neue  Folge,  xiv. 

59.  Muller-Warneck,  “Ueber  die  widernatiirliche  Beweglichkeit  der  rechten 
Niere,”  “ Berl.  klin.  Wochenschr.,”  1877. 

60.  Munk  und  Uffelmann,  “ Die  Ernahrung  des  gesunden  und  kranken 
Menschen,”  2.  Aufl.,  Wien  und  Leipzig,  1891. 

61.  Oser,  “Die  Ursachen  der  Magenerweiterung,”  “Wiener  Klinik,” 
Januar,  1881. 

62.  Pick,  A.,  “Magen-  und  Darmkrankheit,”  Wien,  1895,  pp.  179-188  (35 
bibliographical  references). 

63.  Pourcelot,  “ De  l’Enteroptose,”  “ Union  Med.,”  20'Dec.,  1888. 

64.  Putnam,  J.  J.,  “ Case  of  Splanchnoptosis  and  Achylia  Gastrica  with  Mel- 
ancholia,” “ Boston  Med.  and  Surg.  Jour.,”  Nov.  17,  1898. 

65.  Reichmann  und  Heryng,  “Ueber  elektrische  Magen-  und  Darmdurch- 
leuchtung,”  “ Therap.  Monatshefte,”  1892,  S.  128. 

66.  Riegel,  “ Die  Erkrankungen  des  Magens,”  Wien,  1896. 

67.  Runeberg,  “ Ueber  die  kiinstliche  Aufblahung  des  Magens  und  des 
Dickdarms  durch  Luft,”  “ Deutsch.  Archiv  f.  klin.  Med.,”  1884,  Bd.  xxxiv. 

68.  Schultz,  E.,  “Wanderniere  und  Magenerweiterung,”  “ Prager  med. 
Wochenschr.,”  14.  Januar,  1885. 

69.  Stiller,  B.,  “Enteroptoseim  Lichte  eines  neuen  Stigma  neurasthenicum,” 
“Archiv  f.  Verdauungskrankh.,”  Bd.  II,  S.  285. 

70.  Sulzer,  M.,  “Ueber  Wanderniere  und  deren  Behandlung  durch  Neph- 
rorrhagie,”  “ Deutsche  Zeitschr.  f.  Chirurgie,”  1891,  Bd.  xxx,  S.  506.  (This 
article  contains  the  complete  literature  on  the  Pathology  and  Treatment  of 
Floating  Kidney  up  to  that  date.) 

71.  Trastour,  “ Les  Desequilibres  du  Ventre,  Enteroptosiques  et  Dilates,” 
“ Semaine  Medic.,”  7 Sept.,  1887. 

72.  Volcker,  “ Die  Schadlichkeit  des  Schniirens,”  Dissert.,  Miinchen,  1893. 

73.  Weil,  “ Handbuch  und  Atlas  der  topographischen  Percussion,”  Leipzig, 
1880. 

74.  Weisker,  Cl.,  “Ueber  den  sog.  intra-abdominellen  Druck,”  “Schmidt’s 
Jahrbiicher  der  gesammten  Medicin,”  Bd.  ccxix,  S.  227. 


NEUROSES  OF  THE  STOMACH. 


733 


CHAPTER  X. 

NEUROSES  OF  THE  STOMACH. 

Gastric  neuroses  may  be  classified  as  follows  : 

I.  Motor. 

II.  Sensory. 

III.  Secretory. 

Under  each  one  of  these  we  may  distinguish — 

(a)  States  of  excitation. 

( b ) States  of  depression  of  nervous  influences. 

I.  Neuroses  of  Motility,  or  Peristalsis. 

(a)  Irritative  states  : 

(1)  Cramp  of  the  cardia,  or  cardiospasm. 

(2)  Cramp  of  the  pylorus,  or  pyloric  spasm. 

(3)  Cramp  of  the  entire  musculature,  or  gastrospasm. 

(4)  The  peristaltic  unrest  of  Kussmaul. 

(5)  Nervous  eructation. 

(6)  Nervous  vomiting. 

(b)  Depressive  states  : 

(1)  Insufficiency  of  the  cardia,  including  rumination  and 

regurgitation. 

(2)  Insufficiency  or  incontinence  of  the  pylorus. 

(3)  Atony  or  insufficiency  of  the  entire  gastric  musculature 

(gastroplegia). 

II.  Sensory  Neuroses. 

(a)  Irritative  states : 

(1)  Hyperesthesia. 

(2)  Gastralgia. 

(3)  Bulimia  and  polyphagia. 

{b)  Depressive  states  : 

(1)  Acoria. 

(2)  Anorexia. 

III.  Neuroses  of  Secretion. 

(a)  Irritative  states  : 

(1)  Hyperchylia,  hyper-  or  superacidity. 

(2)  Supersecretion  or  gastrosuccorrhea,  gastroxynsis. 

(b)  Depressive  states  : 

(1)  Hypochylia  or  subacidity. 

(2)  Achylia  gastrica  and  anacidity. 

Nervous  Dyspepsia. 

Neurasthenia  Gastrica. 


734 


NEUROSES  OF  THE  STOMACH. 


General  Considerations. — All  diseases  of  the  stomach  in  which 
no  pathological  anatomical  change  can  be  demonstrated  in  the 
organ  are  classed  as  neuroses.  Hitherto  we  have  considered  only 
diseases  that  were  based  upon  an  actual  alteration  in  the  structure 
of  the  stomach.  Neuroses,  then,  are  idiopathic  diseases  of  the 
gastric  nerves,  with  absence  of  histological  changes  that  can  be 
demonstrated  in  the  tissues.  The  gastric  nerves  can  be  affected,  it 
is  true,  in  the  course  of  gastritis,  ulcer,  carcinoma,  and  dilation, 
by  the  changes  in  the  deeper  layers  of  the  stomach  brought 
about  by  these  diseases.  A large  portion  of  the  dyspeptic  disturb- 
ances, as  well  as  of  the  anomalies  of  secretion  and  motility,  are 
attributable  to  injurious  influences  exerted  upon  the  nerves  in  the 
course  of  these  diseases.  These  nervous  affections  which  accom- 
pany changes  in  the  gastric  structure  are  known  as  secondary 
symptomatic  nervous  disturbances.  It  is  very  probable  that  ana- 
tomical changes  may  lie  at  the  foundation  of  many  neuroses,  but 
up  to  the  present  time  they  escape  our  microscopical  technic.  For 
instance,  in  more  than  half  the  cases  of  hyperacidity  a proliferation 
of  the  oxyntic  cells,  or  of  the  gland  tubules  as  a whole,  has  been 
ascertained  by  Hayem,  Einhorn,  Cohnheim,  and  myself  (Hem- 
meter,  “ Histologie  d.  Magendriisen  bei  Hyperaciditat,”  “Archiv  f. 
Verdauungskrankh.,”  Bd.  iv,  S.  23).  It  is  more  than  probable,  also, 
that  atrophy  is  present  in  from  one-half  to  two-thirds  of  the  cases 
of  achylia  gastrica.  With  further  progress  and  improvement  of 
our  methods  of  staining  and  hardening  the  number  of  gastric 
neuroses  will  become  more  and  more  reduced. 

The  histological  changes  in  the  mucosa  accompanying  hyper- 
chylia  and  achylia  are  not  caused  by  the  nervous  condition,  but 
constitute  a primary  affection  independent  of  the  neurosis.  This  is 
made  probable  by  the  fact  that  proliferation  of  oxyntic  cells  and 
of  gland  tubules  can  be  found  at  the  autopsy,  in  the  stomachs  of 
individuals  who  have  never  shown  any  symptoms  of  nervous  dis- 
eases or  neurasthenia,  and  also  because  proliferation  has  been 
found  in  fragments  of  mucosa  gained  from  the  wash-water  of 
perfectly  normal  individuals  so  far  as  any  neuropathic  state  was 
concerned. 

When  the  gastric  nervous  apparatus  is  the  primary  seat  of  the 
disease,  it  is  called  a primary  neurosis,  but  when  the  disease  of  the 
gastric  nerves  is  reflexly  excited  from  the  central  nervous  system, 
or  from  other  organs,  such  as  the  intestines,  liver,  spleen,  and  kid- 
neys, it  is  called  a secondary  or  reflex  neurosis.  Neuroses  may 


N EUROS ES  OF  THE  STOMACH. 


735 


cause  secondary  anatomical  alterations  in  the  stomach — for  in- 
stance, if  anacidity  is  associated  with  impaired  motility,  we  may 
have  a gastritis  develop  from  decomposition  of  a stagnating  ingesta. 
When  hyperacidity,  or  supersecretion,  causes  a persistent  spasm  of 
the  pylorus,  a dilation  may  result  producing  the  same  symp- 
toms. Disturbances  of  the  sensory  nerves  of  the  stomach  may 
extend  to  the  bowels,  and  bring  about  the  so-called  neurasthenia 
or  nervous  dyspepsia  of  the  intestines ; with  persistent  nervous 
atony  of  the  stomach  the  motility  of  the  intestine  frequently  begins 
to  suffer  also.  This,  apparently,  is  a direct  extension  of  the  ner- 
vous trouble  to  the  intestines.  In  achylia  gastrica,  when  the  anti- 
septic effect  of  HC1  is  missing,  an  excessive  putrefaction  of  the 
intestinal  contents  with  abundant  formation  of  gases  is  sometimes 
noticed,  so  that  the  intestinal  wall  becomes  very  much  expanded, 
and  an  atony  can  arise  in  this  manner.  It  is  well  known  that 
strong  psychic  impressions  and  emotions  like  anger,  aggravation, 
fright,  fear,  and  sadness,  as  well  as  excessive  joy,  can  completely 
suppress  the  appetite.  In  very  excitable  people  these  emotions 
may  even  cause  eructation,  nausea,  and  severe  gastralgia.  These 
nervous  disturbances  mend  rapidly,  as  a rule,  when  the  mind 
has  been  quieted;  but  when  the  emotional  excitement  was  great, 
and  frequently  repeated  within  a short  time,  particularly  in  very 
excitable,  neuropathic  individuals,  a lasting  neurosis  may  de- 
velop. 

Gastric  neuroses  which  are  the  result  of  functional  or  anatomical 
diseases  of  the  nervous  central  organs,  of  hysteria  and  neuras- 
thenia, may  be  so  prominent  that  the  fundamental  disease  may  be 
completely  submerged,  and  be  little  regarded  by  the  patient,  and 
is  not  discovered  by  the  physician  until  after  a careful  study  of  the 
case  has  been  made.  In  sclerosis  of  the  posterior  columns  of  the 
spinal  cord  (tabes  dorsalis)  a train  of  gastric  symptoms  has  been 
first  described  by  Charcot  under  the  name  of  “ crises  gastriques.” 
They  are  described  as  intense  cramp-like  pains  occurring  suddenly 
in  the  midst  of  comparative  well-being,  and  radiating  toward  the 
abdomen  and  back  ; they  are  usually  followed  by  copious  vomiting. 
The  vomit  at  first  consists  of  food,  and  later  of  mucus,  bile,  and 
duodenal  secretions,  and  may  occur  several  times  in  the  same  day, 
frequently  every  hour.  These  attacks  appear  and  disappear  very 
rapidly,  and  are  separated  by  long  intervals  of  perfect  freedom 
.from  gastric  disturbances.  Ewald  emphasizes  that  these  attacks 
may  occur  in  tabes  so  early  in  the  disease  that  the  fundamental 


736 


GASTRIC  NEUROSES. 


affection  can  not  in  all  be  diagnosed  because  all  typical  symptoms 
are  wanting.  Sensations  of  a boring  and  burning  character  and 
severe  gastralgia  may  be  present  in  tabic  patients  years  before  the 
spinal  disease  is  recognizable  (Seymour  Basch,  “ Arch.  f.  Verdau- 
ungskr.,”  Bd.  v,  1899).  In  other  anatomical  diseases  of  the  nervous 
central  organs,  in  myelitis  due  to  compression,  meningitis,  brain 
tumors,  and  after  powerful  concussions  of  the  brain  and  spinal  cord, 
nervous  gastric  disturbances  appear.  In  the  progress  of  certain  dis- 
eases of  the  medulla,  repeated  nausea  and  vomiting  may  be  attributed 
to  irritation  of  the  vomiting  center.  Reflex  neuroses  of  the  stom- 
ach may  occur  from  disease  of  the  neighboring  organs : as,  for 
instance,  from  the  liver,  intestines,  bile  passages,  spleen,  and  periton- 
eum, as  well  as  from  the  kidneys,  sexual  organs,  and  heart.  In 
biliary  colic  gastric  symptoms  are  rarely  absent.  We  generally 
find  that  gastralgia,  nausea,  vomiting,  eructation,  and  anorexia  are 
present  during  the  passage  of  gall-stones,  and  rapidly  disappear  as 
soon  as  the  stone  has  passed  through  into  the  intestine.  The  gastric 
complications  of  cholemia  and  cholelithiasis  do  not  disappear  so 
rapidly,  because  the  excretion  of  the  foreign  materials  in  the  blood 
of  cholemia,  and  the  correction  of  anatomical  changes  in  chole- 
lithiasis require  time.  Renal  colic  in  a similar  manner  may  cause 
dyspeptic  symptoms.  Cases  are  reported  in  which  the  renal  symp- 
toms were  so  masked  by  the  gastric  that  the  diagnosis  of  peptic 
ulcer  was  made.  This  may  very  readily  occur  when  the  nephritic 
pains  radiate  toward  the  back  and  shoulders  like  those  of  ulcers. 
Gastric  symptoms  occurring  as  a sequence  to  uremia  are  the  result 
of  a direct  or  indirect  irritation  of  the  central  nervous  organs,  and 
also  of  the  gastric  nerves  by  retained  products  of  catabolism.  In 
cases  of  contracted  kidney  with  chronic  uremia  in  my  clinic  the 
patient  suffered  exclusively  from  gastric  symptoms,  but  test-meals 
showed  that  the  motor  and  secretory  functions  were  normal,  at  times 
at  least,  and  that,  therefore,  the  dyspeptic  complaints  were  disturb- 
ances of  the  sensory  nerves  of  the  stomach.  Diseases  of  the  sexual 
organs,  in  both  sexes,  but  particularly  in  women,  may  bring  about 
reflex  gastric  neurosis.  Kretschy  and  Fleischer  have  found  that 
the  physiological  process  of  menstruation  may  cause  disturbances 
of  gastric  function,  which  naturally  are  also  met  with  in  a 
more  exaggerated  form  in  dysmenorrhea,  in  diseases  of  the  uterus 
and  ovaries,  and  during  pregnancy.  Whatever  may  be  the  etio- 
logical culmination  of  factors  in  vomiting  of  pregnancy , there  is 
no  better  explanation  offered  up  to  the.  present  time  than  that  it  is  a 


ANATOMY  AND  PHYSIOLOGY  OF  GASTRIC  NERVES.  737 

reflex  neurosis  of  the  stomach  induced  by  the  expansion  of  the 
uterus  and  irritation  of  the  sympathetic  fibers  caused  thereby.  R. 
Frommel  (Penzoldt  and  Stintzing’s  “ Handbuch  d.  specielle  Therap. 
innerer  Krankheiten,”  Bd.  iv,  S.  440)  has  obtained  very  good  results 
in  this  disease  with  basic  orexin,  a medicine  which  acts  mainly  in 
nervous  affections,  and  rarely  in  anatomical  alterations  of  the 
stomach. 

Gastric  neuroses  are  much  more  frequently  seen  in  women  than 
in  men.  Women  and  girls  of  the  better  classes  constitute  the  pre- 
vailing number  of  those  affected  with  gastric  neuroses.  The  recog- 
nition of  pure  gastric  neuroses  and  whether  they  exist  as  idiopathic 
independent  diseases,  or  are  in  some  causal  relation  to  a preexist- 
ing disease,  like  those  we  have  mentioned,  is  often  a problem 
presenting  great  difficulties.  The  stomach  is  an  organ  that  is 
very  rich  in  nerves,  and  is  inclosed  in  a widely  connected  net- 
work of  fibers  which  bring  it  into  close  connection  with  other 
vital  organs. 


ANATOMY  AND  PHYSIOLOGY  OF  GASTRIC  NERVES. 

Concerning  the  anatomy  and  physiology  of  the  gastric  nerves, 
we  may  say  that  the  innervation  of  the  organ  is  carried  out  above 
all  by  the  vagi.  The  left  vagus  spreads  over  the  cardiac  portion 
and  the  lesser  curvature,  and  forms  the  anterior  gastric  plexus  with 
fibers  coming  from  the  abdominal  sympathetic.  The  right  vagus 
supplies  mainly  the  liver,  pancreas,  spleen,  kidney,  and  small 
intestine,  and  a small  part  of  its  branches  reaches  the  posterior 
wall  of  the  stomach.  Anastomoses  from  the  abdominal  sympa- 
thetic with  branches  of  the  right  vagus  form  the  posterior  gastric 
plexus.  The  vagi  also  enter  into  the  formation  of  the  celiac  or 
solar  plexus.  Branches  from  the  solar  plexus  form  the  so-called 
superior  coronary  plexus  of  the  stomach  lying  along  the  lesser 
curvature,  while  branches  coming  from  the  hepatic  plexus  and 
running  along  with  the  right  inferior  coronary  artery  form  the 
inferior  coronary  plexus  of  the  stomach.  These  four  plexuses  are 
united  into  a great  network  by  connecting  communicative  branches. 
In  the  pyloric  portion,  the  beginnings  of  the  large  and  important 
intestinal  plexuses  can  be  demonstrated.  The  intestinal  sympa- 
thetic nerves  form  a network  with  close  meshes  in  the  submucosa 
as  well  as  in  the  muscular  layer.  In  the  broadened  points  of  union 
of  this  nervous  network  are  found  numerous  ganglion  cells.  The 


738 


NEUROSES  OF  THE  STOMACH. 


Meissner  network  supplies  the  muscularis  mucosae,  and  the 
mucosa  and  the  intermuscular  plexus  of  Auerbach  supply  the 
muscular  layers  with  very  fine  branches.  Openchowsky  has 
demonstrated  large  masses  of  ganglion  cells  not  only  at  the 
pylorus,  but  all  along  the  fundus  and  cardia  m the  serosa ; these 
ganglia  are  in  communication  with  the  large  vagosympathetic 
fibers. 

Our  knowledge  of  the  physiology  of  the  gastric  nerves  is,  up 
to  the  present  time,  very  limited.  Since  the  publication  of  the 
first  edition,  Pawlow  has  repeated  and  published  his  work  on 
gastric  innervation  and  secretion  (“  Die  Arbeit  d.  Verdauungs- 
driisen,”  S.  71),  which  proves  beyond  a doubt  that  the  vagus 
is  the  secretory  nerve  of  the  gastric  glands.  The  influence  of  the 
vagus  and  sympathetic  fibers  on  peristalsis  is  but  imperfectly 
understood.  Although  we  do  not  know  the  exact  paths  of  vast 
secretory  motor  and  absorptive  impulses,  nor  of  sensation,  it  is 
generally  assumed  on  clinical  grounds  that  each  of  these  functions 
is  represented  by  different  nerves,  and  we  therefore  accept  the  exist- 
ence of  special  nerves  for  motion,  sensation,  secretion,  and  absorp- 
tion. Clinical  experience  has  confirmed  this  assumption  because 
peristaltic,  sensory,  and  secretive  disturbances  may  exist  by  them- 
selves. 

All  gastric  neuroses  may  show  considerable  variation  in  their 
course.  Thus,  the  contents  of  the  stomach  may  one  day  show 
anacidity  or  achylia,  and  on  the  next  day  show  hyperchylia.  In 
the  same  manner  we  may  find  motor  insufficiency  alternating  with 
peristaltic  unrest.  Although  the  neuroses  may  exist  singly  as  in- 
dividual diseases,  we  are  confronted,  as  a rule,  with  combinations 
of  various  disturbances.  Thus,  we  may  find  that  hyperacidity  and 
gastrospasm  are  associated  with  each  other,  that  hyperesthesia  will 
be  combined  with  vomiting,  and  that  supersecretion  may  be  present 
in  atony.  These  diseases  may  develop  pronounced  attacks  at 
periods  when  the  stomach  is  resting.  The  intensity  of  the  attack 
is  very  frequently  entirely  independent  of  the  quantity  or  quality 
of  the  food,  but  the  effect  of  psychic  influences  is  generally  unmis- 
takable. Neuroses  may  exist  side  by  side  with  organic  diseases 
of  the  stomach,  but,  as  a rule,  they  are  part  of  the  symptomatology 
of  neurasthenia  or  hysteria.  The  symptoms  of  a general  neurosis 
are  rarely  absent : that  is,  the  characteristic  changes  of  the  psychic 
indisposition,  the  lassitude,  irritability,  feeble  memory,  indisposition 
to  work,  insomnia,  neuralgia,  migraine,  vertigo,  polyuria,  weakness 


CARDIOSPASM. 


739 


of  the  bladder,  and  a varying  pain.  All  these  neuroses  which  we 
have  mentioned  are  really  not  individual  diseases,  but  rather  symp- 
toms; but,  as  these  symptoms  generally  occur  with  a certain  inde- 
pendence and  are  disturbances  peculiar  to  themselves,  it  will  not 
be  illogical  to  call  -the  complex  anomalies  by  the  name  of  one 
symptom,  so  that  we  will  speak  of  cardiac  spasm  and  nervous 
eructation  and  hyperacidity  as  diseases  peculiar  to  themselves, 
bearing  in  mind,  however,  that  we  are  simply  describing  symptoms. 


CARDIOSPASM  (Cramp  of  the  Cardia). 

The  etiology  of  spasm  of  the  ring  musculature  of  the  cardia 
agrees  fully  with  that  of  cramp  of  the  pylorus.  In  the  great 
majority  of  cases  the  cramp  of  the  cardia  represents  a secondary 
disease,  which  may  appear  with  hyperesthesia  and  very  strong  irri- 
tation of  the  mucous  membrane  of  the  cardiac  region  ; further,  with 
abnormal  dilation  of  the  stomach  through  air  and  gases,  as  well 
as  with  caustic  action  upon  the  mucous  membrane  present  with 
ulcer  and  ulcerating  carcinoma  of  the  cardia  ; hence,  it  is  produced 
by  the  same  causes  as  cramp  of  the  pylorus.  Much  more  rarely  the 
spasm  of  the  cardia  is  due  to  a genuine  symptomatic  or  idiopathic 
neurosis  of  the  motor  apparatus,  which  is  characterized  by  an 
increased  irritability.  It  is  observed  as  a symptom  of  hysteria 
and  neurasthenia,  simultaneous  with  other  nervous  disturbances, 
which  may  facilitate  the  recognition  of  the  neuropathic  basis  of  this 
form  of  cramp.  Whether  cramp  of  the  cardia  as  a pure  neurosis 
of  the  motor  apparatus  is  a functional  impairment  of  the  periph- 
eral motor-nerve  apparatus,  or  whether  it  is  of  central  origin,  is  at 
present  still  a debated  question.  We  may  distinguish  two  forms  of 
cramp  of  the  cardia  : 

1.  Acute  cramp,  which,  appearing  rather  suddenly,  often  spas- 
modically, is  generally  only  of  short  duration. 

2.  Chronic  cramp,  which  is  a very  stubborn  and  serious  dis- 
ease. 

One  of  the  most  frequent  causes  of  the  rare  form  of  secondary 
cramp  is  dilation  of  the  stomach  by  air  and  gases.  An  abnormal 
dilation  of  the  stomach  by  air,  which  may  finally  bring  about  a 
cramp  of  the  cardia,  is  found  mostly  in  those  persons  who  have 
the  nervous  habit  of  swallowing  large  quantities  of  air.  If  the  air 
is  not  soon  removed  through  eructation,  it  keeps  on  collecting  in 
the  stomach  and  expands  on  becoming  warmed,  so  that  finally  a 


740 


NATURE  OF  CARDIOSPASM. 


considerable  dilation  of  the  stomach  is  produced,  and  with  it 
cramp  of  the  cardia,  which  is,  perhaps,  always  complicated  with 
cramp  of  the  pylorus.  Ewald  and  Fleischer  have  had  oppor- 
tunity to  examine,  repeatedly,  cases  of  intentional  swallowing  of  air. 
Fleischer’s  case  was  a girl  who  had  been  practising  it  as  a kind  of 
sport  for  many  years.  The  stomach  was  constantly  dilated,  even 
in  a jejune  state,  and  felt  like  an  air-pillow.  The  rounding  of  the 
region  of  the  stomach  was  plainly  visible,  even  through  the  cloth- 
ing. The  elastic  stomach-tube  introduced  into  the  esophagus  met 
an  obstruction  at  the  cardia,  which  was  not  easily  overcome,  even 
after  the  insertion  of  the  tube  into  the  stomach.  When  the  outer 
end  was  put  into  water,  numerous  bubbles  of  air  escaped  through 
it;  but  even  with  a strong  external  pressure  in  the  region  of  the 
stomach  one  could  not  succeed  in  removing  all  the  air.  The  re- 
sistance in  this  region  continued,  though  to  a less  degree.  With 
repeated  thorough  palpation  it  was  discovered  that  the  cramp  of 
the  cardia  and  pylorus,  occurring  intermittently  for  many  years, 
had  caused  a hypertrophy  of  the  musculature  of  the  stomach;  and 
it  was  this  condition,  probably,  which  prevented  the  formation  of  a 
more  severe  atony  and  ectasia  of  the  stomach,  for  the  lower  limit 
of  the  stomach  was  only  slightly  below  the  normal. 

The  stomach  may  also  be  dilated  by  a very  copious  intragastric 
formation  of  gases  to  such  a degree  that  a cramp  of  the  cardia 
arises ; and  this  happens  very  easily  when  the  formation  of  gases 
is  very  rapid,  as  is  observed  sometimes  with  protracted  stagnation 
of  the  ingesta  in  the  stomach,  as  a result  of  atony,  ectasia,  chronic 
gastritis,  advanced  stenosis  of  the  pylorus  or  duodenum,  as  well 
as  with  primary  and  secondary  cramp  of  the  pylorus,  when  the 
contents  of  the  stomach  are  subject  to  fermentation  and  decom- 
position. If  the  gases  can  not  pass  over  into  the  intestine,  they 
continue  to  collect  in  the  stomach,  which  finally  becomes  very 
much  dilated;  the  region  of  the  stomach  becomes  arched,  and 
troublesome  sensations  of  pressure  and  tension  appear  in  the 
same.  If  the  stomach  presses  the  diaphragm  upward,  and  if  the 
latter  in  turn  presses  on  the  lower  part  of  the  lung  and  the  heart, 
dyspnea,  precordial  oppression,  palpitation  of  the  heart,  and  “ asthma 
dyspepticum  ” may  result.  With  this  there  sometimes  exist  great 
prostration,  rapid,  soft  pulse,  and  headache.  That  these  very 
often  dangerous  symptoms  are  really  caused  by  the  dilation  of 
the  stomach  and  not,  perhaps,  by  autointoxication, — that  is,  by 
toxic  products  of  fermentation  and  putrefaction  of  the  chyme, — is 


SYMPTOMS  AND  COMPLICATIONS  OF  CARDIOSPASM.  74 1 

evident  from  the  fact  that  the  symptoms  cease  quickly  when  the 
cardiac  closure  is  finally  broken  (the  pylorus,  on  account  of  its 
very  n\uch  stronger  ring  musculature,  offers  a much  greater  resist- 
ance to  the  passage  of  the  gases  into  the  intestines),  when  the 
spasm  relaxes,  or  a ‘tube  is  introduced  into  the  stomach,  and  the 
air  or  gases  have  an  opportunity  to  escape  outwardly.  Very  rapid 
distention  of  the  stomach  with  air  pumped  in  through  the  tube  or 
evolved  from  bicarbonate  of  sodium  by  tartaric  acid  may  bring  on 
cardiospasm  of  a short  and  transient  nature.  In  highly  neurotic 
patients  distention  should  be  carried  out  very  slowly. 

On  the  other  hand,  the  cramp  of  the  cardia  may  also  be  primary, 
and  the  dilation  of  the  stomach  (pneumatosis)  may  be  secondary. 
If  the  cramp  of  the  cardia  sets  in  immediately  after  the  meal,  and  if 
the  eructation  of  the  air  which  is  swallowed  during  the  meal  with 
the  food  and  liquids  is  prevented,  then  the  stomach  may  also 
become  abnormally  distended.  Since  the  neuromuscular  apparatus 
of  the  cardia  is  mechanically  irritated  with  strong  distention  of 
the  stomach,  the  cramp  is  prolonged  thereby,  and,  therefore, 
it  probably  lasts  longer  during  digestion  than  with  an  empty 
stomach.  Just  as  the  removal  of  air  and  gases  from  the  stomach 
through  eructation  is  sometimes  made  entirely  impossible  by  a 
primary  or  secondary  cramp  of  the  cardia,  so  the  removal  of  the 
contents  of  the  stomach  by  vomiting  may  also  be  made  impos- 
sible. Even  the  strongest  efforts  at  vomiting  bring  up  nothing, 
and  patients  may  be  much  tormented  by  fruitless  muscular 
exertion.  When  this  is  of  long  duration  and  frequent  repetition, 
it  may  bring  about  atony  of  the  stomach  in  consequence  of  over- 
exertion of  the  musculature.  If  the  cramp  is  caused  as  a second- 
ary or  reflex  neurosis  by  hyperesthesia,  strong  irritation,  or 
ulceration  of  the  mucous  membrane  of  the  cardia,  it  sometimes 
produces  a painful  feeling  of  contraction  in  the  region  of  the  cardia, 
which  may  radiate  toward  the  breast,  the  back,  and  to  the  region 
of  the  heart.  It  has  been  asserted  that  the  cramp  which  appears 
as  a pure  neurosis  of  the  motor  apparatus  may  also  cause  the  same 
sensations  of  pain,  but  this  is  not  very  probable.  At  least  my 
observations  with  that  form  of  cramp  of  the  pylorus  that  is  not 
dependent  upon  the  states  of  disease  before  mentioned,  but  de- 
pends simply  upon  a pure  neurosis  of  the  motor  apparatus,  argue 
against  it,  since  the  latter  is  not  accompanied  by  pain.  The  pains 
described  are  not  a constant  symptom,  and,  therefore,  may  not  be 
used  as  a factor  in  a differential  diagnosis  of  the  two  forms  of  cramp. 

49 


742  SYMPTOMS  AND  PROGNOSIS  OF  CARDIOSPASM. 

Since  with  an  entirely  empty  stomach  the  acute  spasm  produces 
no  symptoms,  it  may  remain  latent  for  some  time,  and  is  sometimes 
recognized  only  by  accident,  when  for  some  reason  a tube  is 
introduced  into  the  stomach  which  meets  an  obstruction  in  the 
region  of  the  cardia,  or  when  food  or  drink  is  taken  by  the  pa- 
tient during  the  cramp,  deglutition  being  then  impeded.  Chronic 
cardiospasm  gives  much  more  significant  symptoms.  Besides 
the  symptoms  mentioned  previously,  very  severe  complaints 
from  deglutition  appear.  The  patients  have  the  unmistakable 
feeling  that  some  of  the  food  becomes  stuck  before  it  reaches  the 
stomach.  If,  in  spite  of  this,  the  meal  is  continued,  the  lower  part 
of  the  esophagus  is  filled  with  food,  which  after  some  time  the 
patients,  with  great  exertion,  succeed  in  bringing  up  again  in  an 
almost  unchanged  condition.  That  it  comes  from  the  esophagus 
and  not  from  the  stomach  is  shown  by  the  absence  of  the  free 
hydrochloric  acid.  The  second  deglutition  sound  (auscultation 
over  the  lower  part  of  the  sternum)  is  always  lacking,  and  in 
its  place  a low,  rippling  noise  may  be  heard,  which  probably 
arises  from  the  circumstance  that  the  cardia  is  not  completely 
closed,  and  liquids  pressed  on  may  still  flow  into  the  stomach. 
With  protracted  duration  of  the  malady,  the  ingesta  remaining  in 
the  lower  part  of  the  esophagus  may  exert  such  a pressure  upon 
its  walls  that  a diverticulum  may  be  formed,  which  prevents 
the  taking  in  of  food.  The  nutrition  of  patients  may  be  much 
reduced,  so  that,  especially  when  the  patients  are  advanced  in  age, 
the  suspicion  may  arise  that  a carcinoma  of  the  cardia  is  developing, 
which,  as  we  know,  can  also  cause  a stenosis  of  the  cardia  as  well 
as  the  formation  of  a diverticulum. 

Fortunately,  chronic  cramp  of  the  cardia  is  a very  rare  malady  ; 
it  may  exist  for  months,  even  years. 

Prognosis. — The  prognosis  of  the  acute  primary  or  secondary 
cramp  of  the  cardia  is,  on  the  whole,  favorable,  especially  when  it  is 
recognized  in  time,  and  if  one  is  successful  in  rapidly  removing  its 
fundamental  causes — swallowing  of  air,  formation  of  gases  in  the 
stomach,  hyperacidity,  hypersecretion,  atony,  hyperesthesia,  etc. 
The  prognosis  is  always  to  be  made  with  caution  when  a diver- 
ticulum of  the  esophagus  which  hinders  the  passage  of  food  has 
already  been  formed. 

Diagnosis. — In  order  to  distinguish  acute  primary  and  second- 
ary cramp,  one  must  learn,  above  all,  whether  one  of  the  diseases 
before  mentioned,  which  can  produce  cramp  of  the  cardia,  is 


DIAGNOSIS  OF  CARDIOSPASM. 


743 


present.  With  repeated  thorough  investigations  one  generally 
succeeds  in  determining  the  cause  of  the  secondary  cramp.  If 
it  is  due  to  hyperesthesia,  to  a strong  irritation,  or  to  loss  of 
substance  of  the  mucous  membrane  of  the  cardia,  then  pains  in 
the  region  of  the  cardia  often  draw  attention  to  this  manner  of 
origin,  and  the  introduction  of  a tube  into  the  stomach  will  then 
cause  pain  also.  But  if  a decided  cause  for  the  cramp  can  not  be 
discovered,  if  it  recurs  periodically,  if  it  is  always  of  rather  short 
duration,  and  if  other  nervous  troubles  are  present,  then  probably 
a symptomatic  functional  neurosis  exists;  and  if  all  these  signs 
are  lacking,  then  there  is  an  idiopathic  functional  motor  neurosis; 
but  this  is  a very  rare  occurrence. 

The  diagnosis  of  the  chronic  cardiospasm  leading  to  a perma- 
nent closure  of  the  cardia  is  more  difficult,  because  it  may  easily 
be  mistaken  for  carcinoma  or  malignant  stenosis  of  the  cardia,  as 
well  as  for  a diverticulum  of  the  lowest  part  of  the  esophagus, 
which,  however,  is  rare. 

Advanced  age,  anemia,  and  cachexia,  appearing  at  a time  in 
which  the  passage  of  food  is  not  yet  hindered  to  a great  extent, 
argue  for  carcinoma  of  the  cardia.  In  the  food  brought  up  by 
regurgitation,  as  well  as  in  the  examination  with  the  tube,  one 
often  finds  traces  of  blood,  and  in  some  few  cases  particles  of  car- 
cinomatous structure  (in  the  aperture  of  the  tube).  In  most  of 
the  patients  free  hydrochloric  acid  is  wanting  in  the  contents  or 
food  that  may  be  drawn  from  the  esophageal  diverticulum.  The 
more  the  stenosis  increases  with  the  progress  of  the  carcinoma, 
the  thinner  the  tubes  that  must  be  used  in  order  to  pass. 
Cicatricial  stenosis  of  the  cardia  is  less  frequent,  a diverticulum  of 
the  lowest  section  of  the  esophagus  much  rarer,  than  carcinoma  of 
the  cardia.  Both  diseases  are  not  connected  with  any  particular 
age.  The  nutrition  of  the  patients  is  decreased  only  when  the  pas- 
sage of  the  food  is  very  much  impeded.  In  the  formation  of  diver- 
ticulum traces  of  blood  in  the  contents  of  the  tube  are  generally 
lacking,  and  with  cicatricial  stenosis  they  are  very  rare.  With  diver- 
ticulum, tubes  of  different  thicknesses  sometimes  penetrate  into  the 
stomach  at  the  first  attempt,  at  other  times  only  after  many  fruit- 
less endeavors,  according  as  the  stomach  is  full  or  empty.  With 
stenosis,  when  there  is  much  difficulty  in  deglutition,  only  thin 
tubes  can  penetrate.  In  both  maladies  there  are  no  anomalies  of 
secretion  in  the  stomach.  With  carcinoma,  as  well  as  with  stenosis 
of  the  cardia  and  with  diverticulum,  the  difficulties  of  deglutition 


744 


CARDIOSPASM. 


increase  very  gradually,  while  in  the  case  of  cramp  they  generally 
come  to  an  acute  stage  in  a short  time.  The  chronic  cramp,  which 
is  very  rare,  may  appear  at  any  age.  The  general  nutrition  suffers 
only  after  protracted  duration.  Traces  of  blood  can  neither  be  found 
in  the  examination  with  the  tube  nor  in  the  food  that  is  eructated. 

The  examination  of  the  contents  of  the  stomach  in  cases  of  sim- 
ple cramp  of  the  cardia  shows  nothing  abnormal.  With  intermit- 
tent relaxation  of  the  cramp,  the  difficulties  of  deglutition  cease  tem- 
porarily, and  a rigid  tube  may  be  pushed  into  the  stomach  without 
meeting  with  any  resistance;  neither  of  these  phenomena  are  ob- 
served with  carcinoma  and  stenosis,  except  in  the  rare  case  of  disin- 
tegration of  the  carcinoma.  An  important  distinction  of  the  cramp 
consists  in  the  fact  that  thick,  rigid  tubes  overcome  the  obstacle  at 
the  entrance  of  the  stomach  much  more  easily  than  thin  tubes. 
The  same  observations  have  been  made  repeatedly  with  spastic 
stricture  of  the  urethra,  which  is  generally  a result  of  hyperes- 
thesia of  the  mucous  membrane  of  the  urethra.  If  in  this  case 
a thin  catheter  is  introduced,  its  point,  with  moderate  pressure, 
irritates  only  one  spot  of  the  mucous  membrane,  and  by  this  a 
cramp  of  the  musculature  is  produced  (or  a previously  existing  one 
is  increased),  which  becomes  so  severe  that  it  may  easily  be  mis- 
taken for  an  organic  stricture.  A wrong  diagnosis  is,  however, 
easily  avoided  if  the  mucous  membrane  is  first  anesthetized 
with  a four  per  cent,  solution  of  cocain.  Then,  after  a short  time, 
one  can  push  the  catheter  further.  If  a much  thicker  catheter  is 
introduced,  the  broader  point  of  the  same  will  exert  an  even  pres- 
sure upon  the  whole  mucous  membrane  at  the  point  in  question, 
which  is  not  so  irritating.  Probably  the  sensory  nerves  are  then 
for  a time  paralyzed,  and  the  cramp  abates.  Very  likely  the  same 
conditions  obtain  in  the  probing  of  the  esophagus.  If  after 
protracted  duration  of  a cramp,  a diverticulum  of  the  esophagus 
has  been  formed,  considerable  quantities  of  food  may  be  retched 
up  at  one  time,  and  a thick  tube  will  then  pass  the  obstacle  at  the 
entrance  of  the  stomach,  the  facility  of  the  passage  depending  on 
the  fullness  of  the  diverticulum,  and  sometimes  the  passage  is  ac- 
complished only  after  many  unsuccessful  endeavors. 

In  all  cases  when  there  is  any  doubt  about  the  differential  diag- 
nosis between  cardiospasm  and  carcinoma  of  the  cardia,  the  patient 
should  be  examined  under  anesthesia.  If  the  passage  becomes 
readily  permeable  to  the  sound  under  narcosis,  carcinoma  can  be 
excluded. 


TREATMENT  OF  CARDIOSPASM. 


745 


Among  the  severest  cases  of  this  type  occurring  in  my  experi- 
ence was  that  of  a girl  ten  years  old.  The  diagnosis  was  difficult 
— it  could  not  be  decided  whether  it  was  a diverticulum,  a cicatri- 
cial stenosis,  or  cardiospasm.  For  two  weeks  the  tube  inevitably 
became  caught  above  the  cardia.  Eventually,  I succeeded  in 
passing  a tube  under  anesthesia,  and  thereafter  the  intubation 
became  less  difficult  of  execution  even  while  the  patient  was 
conscious.  For  a month  previous  to  consulting  me  the  child 
could  not  swallow  any  solid  food,  which  had  resulted  in  extreme 
emaciation.  After  three  intubations  under  anesthesia  she  began 
to  swallow  semisolid  food  material,  and  she  was  ultimately  cured 
by  electricity  and  daily  passage  of  the  tube. 

Naturally,  the  inspection  of  the  esophagus  with  the  esophago- 
scope  would  decide  most  of  such  cases.  (See  p.  183.) 

Therapeutics. — The  patient  must  abstain  from  all  injurious 
influences.  The  abnormal  conditions  which,  according  to  experi- 
ence, produce  cramp  of  the  cardia,  must  be  removed.  Those  who 
swallow  air  must  be  cautioned  against  the  bad  effects  of  the  habit. 
With  strong  dilation  of  the  stomach  through  air  and  gases, 
in  consequence  of  fermentation  and  stagnation  of  the  contents, 
the  air  and  gases  should  be  removed  as  quickly  as  possible  by 
the  introduction  of  a rather  thick,  rigid  tube,  and  a more  copious 
formation  of  gases  must  be  prevented  by  methodical  lavage  of 
the  stomach,  often  with  the  addition  of  antiseptics.  The  diet  must, 
for  some  time,  consist  of  milk,  and  later  of  various  meats  taken  in 
a minced  form.  Other  nervous  disorders  must  receive  suitable 
treatment.  One  of  the  best  methods  of  treatment  for  cramp  of  the 
cardia  is  the  introduction  of  firm,  thick  tubes,  which  are  permitted 
to  remain  in  position  for  thirty  minutes  at  a time.  Sometimes  the 
cramp  ceases  entirely  after  sounding  one  or  more  times.  If  the 
spasm  is  the  consequence  of  the  hyperesthesia  of  the  mucous 
membrane  of  the  esophagus  and  cardia,  the  sensibility  is  blunted 
by  frequent  soundings. 

In  very  stubborn  cases  of  hyperesthesia  with  cardiospasm  it  is  ad- 
visable to  apply  a solution  of  cocain  hydrochlorate  to  the  mucous 
membrane  just  before  the  meal,  in  order  to  prevent  the  appearance  of 
the  cramp.  For  this  purpose  one  had  best  use  a small  sponge,  satu- 
rated with  a three  per  cent,  solution  of  cocain,  and  fastened  to  the 
lower  end  of  an  open,  rather  thick,  firm  tube,  with  rounded  edges,  by 
means  of  a strong  silk  thread  brought  through  the  tube  to  its  upper 
end.  After  introducing  the  tube  into  the  cardia,  the  cocain  solution 
is  forced  out  of  the  sponge  by  pulling  the  silk  thread,  or  by  blow- 


746 


PYLORIC  SPASM. 


ing  air  into  the  tube,  and  the  mucous  membrane  may  thus  be  anes- 
thetized. Another  way  of  accomplishing  this  is  with  the  Einhorn 
intragastric  spray,  by  which  the  lower  part  of  the  esophagus  and 
the  cardia  may  be  sprayed  with  cocain  and  menthol.  With  chronic 
cardiospasm  also  the  methodical  introduction  of  firm  tubes  is  the 
most  successful  remedy.  The  effect  may  be  aided  by  external  or 
internal  galvanization  (the  anode  in  the  tube).  According  to  an  in- 
teresting observation  of  Boas,  solid  foods  are  sometimes  introduced 
more  easily  than  liquid  ones.  Before  meals  the  foods  lying  in  front 
of  the  cardia  are  to  be  removed  as  completely  as  possible,  especi- 
ally when  a diverticulum  should  have  developed  (rare). 

In  both  acute  and  chronic  cardiospasm  we  have  obtained  the  most 
permanent  relief  by  the  galvanic  current.  The  length  of  the  esopha- 
gus is  determined  by  methods  devised  by  Penzoldt  (/.  c.)  and  Isert 
Perl,  and  a rather  large  spiral  electrode  (Stockton’s)  is  introduced  to 
a distance  compelling  it  to  be  in  or  near  the  cardia;  the  cathode 
is  placed  on  the  cervical  region,  the  anode  in  the  cardia,  and  a cur- 
rent of  twenty-five  milliamperes  is  turned  on  for  ten  minutes.  Then 
the  same  procedure  is  repeated  with  the  anode  on  the  epigastrium 
and  cathode  in  the  cardia. 

PYLORIC  SPASM  (Pylorospasm,  Cramp,  Convulsion,  Spasm  of  the 
Pylorus). 

Cramp  of  the  ring  musculature  of  the  pylorus  is  brought  on 
by  entirely  different  causes  : it  may  appear  with  hyperesthesia, 
with  very  strong  chemical  irritation  of  the  mucous  membrane 
of  the  pylorus  by  means  of  hydrochloric  acid  (hyperacidity,  super- 
secretion), by  excess  of  organic  acids,  as  well  as  with  dilation  of 
the  stomach  by  gases  (as  a reflex  neurosis),  and  finally  also  after 
the  caustic  action  of  toxic  substances,  and  further  as  a secondary 
disease  accompanying  ulcer  and  ulcerating  carcinoma  of  the 
pylorus.  While  the  existence  of  a secondary  cramp  of  the  pylorus 
is  generally  recognized,  strange  to  say  the  existence  of  a primary 
cramp  of  the  pylorus,  caused  by  an  independent  motor  neurosis, 
restricted  to  the  pylorus  alone,  is  still  generally  denied.  If  one 
grants,  however,  that  the  insufficiency  of  the  pylorus  may  appear 
also  as  a genuine  motor  neurosis,  due  to  a decrease  of  the  irrita- 
bility of  the  motor  nerve  apparatus  of  the  pylorus,  there  is  no 
reason  to  deny  entirely  the  occurrence  of  a primary  cramp  of  the 
pylorus,  which  is  due  to  an  abnormally  increased  irritability  of  the 
motor  nerves,  even  though  this  be  rare.  Indeed,  Stiller,  one  of 


RESULTS  OF  PYLOKOSPASM. 


747 


the  most  competent  judges  of  neuroses  of  the  stomach,  assumes  a 
primary  cramp  of  the  pylorus  for  the  explanation  of  peristaltic 
unrest  of  the  stomach.  It  is  true  its  detection,  as  well  as  that 
of  the  secondary  spasm,  is  very  difficult,  since  the  most  important 
result  of  the  same — namely,  an  increased  peristalsis  of  the  stomach 
— can  not  be  proved  with  normal  location  and  size  of  the  stomach 
except  by  Hemmeter’s  or  Einhorn’s  method.* 

The  existence  of  a primary  cramp  of  the  pylorus  becomes  proba- 
ble if,  after  the  exclusion  of  the  before-mentioned  causes  (secondary 
cramp  of  the  pylorus),  as  well  as  of  organic  disease  of  the  stomach, 
the  reaction  for  iodin  in  the  saliva  occurs  much  later  than  under 
ordinary  circumstances,  after  the  introduction  of  o.i  iodoform  into 
the  stomach  with  the  test-breakfast.  According  to  A.  Lockhart 
Gillespie  (Brit.  Med.  Assoc.,  July,  1898),  salol  was  absorbed  from 
the  stomach  in  a dog  in  whom  he  produced  a fistula  in  the 
duodenum  near  the  pylorus.  He  still  found  the  salicyluric  reac- 
tion in  the  urine,  although  no  salol  reached  the  small  intestine. 
Stein  (“  Wien.  Med.  Wochenschr.,”  43,  1892)  found  that  salol  was 
absorbed  from  the  stomach,  and,  although  not  decomposed  in  that 
organ,  it  may  appear  as  salicyluric  acid  in  the  urine.  For  these 
reasons  the  salol  test  can  not  be  relied  upon  as  informing  us  con- 
cerning the  presence  or  absence  of  pyloric  stenosis.  The  diagnosis 
becomes  probable  also  when  atony  of  the  stomach  appears  without 
any  assignable  cause.  The  results  of  a primary  cramp  of  the  pylorus 
are  the  same,  naturally,  as  those  of  the  secondary.  Since  contents 
of  the  stomach  can  not  pass  into  the  intestine  during  the  entire 
duration  of  the  spasm,  there  must  result  a stagnation  of  the  ingesta 
and  a protracted  burdening  of  the  stomach,  causing  atony  of  mus- 
culature, which  also  becomes  gradually  exhausted  through  the 
energetic  exertions  for  overcoming  the  increased  resistance  at  the 
pyloric  orifice.  If  the  neurosis  is  very  stubborn,  the  atony  may 
pass  over  into  a pronounced  dilation,  particularly  if  the  stagnating 
ingesta  decompose  rapidly  and  the  atonic  stomach  is  abnormally 
distended  with  gases. 


*In  a singular  case  of  periodic  pylorospasm  occurring  in  a hysterical  female  regularly 
at  the  menstrual  period,  we  obtained  a record  with  our  triple  intragastric  bag  which  may 
be  characteristic  of  these  cases.  This  bag  (•*  N.  Y.  Med.  Jour.,”  June  22,  1896)  records 
the  pyloric,  fundic,  and  cardiac  peristalsis  separately  on  three  tambours  on  the  kymograph 
(see  p.  80),  and  in  this  case  the  pyloric  pen  showed  great  spastic  contractions,  and  tenes- 
mus lasting  from  three  to  five  minutes  before  they  relaxed.  The  pens  recording  the 
fundic  and  cardiac  contractions  were  quiet  during  this  period  except  for  slight  passive 
movements  due  to  respiration  and  impulse  of  aorta. 


748 


PERISTALTIC  UNREST. 


Therapeutics. — If  a primary  cramp  of  the  pylorus  is  suspected, 
a digestible,  non-irritating  diet  is  to  be  prescribed  (see  chapter  on 
Diet);  every  immoderate  burdening  and  dilation  of  the  stomach 
through  very  abundant  meals,  which  might  heighten  the  irritability 
of  the  motor  nerves,  is  to  be  avoided.  With  this  the  bromids,  pre- 
ferably the  bromid  of  strontium,  in  liberal  doses  (3.0  (45  grs.)  to  5.0 
(75  grs0  Per  diem),  extractum  belladonnae  (0.02  (J-  of  a gr.)  to  0.03 
( y2  of  a gr.)),  and  codein  phosphate  (0.02  (^-  of  a gr.)  to  0.03  of 
a gr.)),  chloral  hydrate  (10  grs.  t.  i.  d.)  are  to  be  prescribed.  Elec- 
tricity is  a valuable  adjuvant  to  the  treatment,  and  should  be  used 
in  the  same  manner  as  indicated  for  cardiospasm.  Spraying  the 
pylorus  with  cocain  and  menthol  is  a satisfactory  treatment.  Under 
narcosis  the  pylorospasm  relaxes.  The  pylorus  may  be  intubated 
by  the  author’s  method : A large  tube  once  passed  through  the 
pylorus  will,  if  allowed  to  rest  there  for  ten  minutes,  in  some  cases 
act  in  a very  gratifying  manner,  allaying  the  spasm  without  any 
other  treatment.  This  method  constitutes  a means  of  recognizing 
pylorospasm. 


GASTROSPASM  (Convulsions  of  the  Stomach). 

Gastrospasm  is  a neurosis  in  which  the  musculature  of  the 
stomach  is  so  strongly  contracted  that  the  whole  organ  may  be- 
come hardened  like  a board,  and  may  be  recognized  by  palpation 
as  a resistant  mass  through  the  lax  abdominal  integuments.  It  is 
a very  rare  disease.  Whether  it  ever  occurs  as  an  independent  genu- 
ine neurosis  of  the  motor  apparatus,  or  whether,  as  is  generally 
supposed,  it  occurs  only  as  a secondary  nervous  affection,  with 
hyperesthesia  of  the  sensory  nerves  of  the  stomach,  or  as  a conse- 
quence of  a cramp  of  the  pylorus,  combined  with  hypertrophy  of 
the  musculature  of  the  stomach,  is  still  an  open  question.  In 
the  very  rare  cases  observed  thus  far  the  single  paroxysms  of 
gastrospasm  invariably  lasted  but  a short  time,  and  the  quick 
intermission  might  be  sufficiently  explained  by  the  enormous  over- 
exertion of  the  musculature  during  the  attack.  The  treatment  is 
the  same  as  for  hyperperistalsis  (Kussmaul). 


GASTRIC  HYPERPERISTALSIS  (Peristaltic  Unrest  (Kussmaul)— 
Tormina  Ventriculi  Nervosa). 

General  Considerations. — Peristaltic  unrest  is  the  name  given 
by  Kussmaul  to  a state  of  the  stomach  first  described  by  him,  which 


ETIOLOGY  OF  H YPERPEKISTALSIS. 


749 


is  characterized  by  the  appearance  of  extraordinarily  rapid  con- 
tractions of  the  stomach,  following  close  upon  one  another,  which 
appear  especially  after  meals,  continuing  also  during  the  day  and 
sometimes  through  the  night  with  an  entirely  empty  stomach.  This 
excess  of  peristalsis  brings  about  very  disagreeable  sensations  of 
heaving  to  and  fro,  of  unrest,  and  contractions  in  the  region  of  the 
stomach  which,  without  being  really  painful, — as,  for  example,  the 
so-called  cramps  of  the  stomach  with  cardialgia, — may  nevertheless 
annoy  the  patient  very  much.  When  there  is  an  ectasia  or  a dis- 
location of  the  stomach  present  simultaneously,  as  was  the  case  in 
all  the  observations  up  to  date,  these  abnormally  strong  contrac- 
tions of  the  stomach  can  be  seen  and  felt  externally  through  the  lax 
abdominal  integument  as  distinct  undulatory  motions.  The  peris- 
taltic waves  generally  run  from  the  fundus  to  the  pylorus : that  is, 
from  left  to  right.  Besides  the  peristaltic  motions,  in  a small  pro- 
portion of  cases  antiperistaltic  motions  were  observed  also ; 
sometimes  the  latter  were  observed  to  exist  alone,  but  this  is  rare 
(Schiitz,  Cohn,  Glax).  If  the  size  and  location  of  the  stomach  are 
normal,  the  objective  symptoms  are  lacking  entirely,  and  only  the 
subjective  complaints,  particularly  the  feeling  of  unrest,  are  evident. 
Sometimes,  also,  peristaltic  unrest  of  the  small  intestine  coexists 
with  that  of  the  stomach. 

Increased  irritability  of  the  motor  nerves  of  the  stomach  is 
looked  upon  as  the  cause  of  peristaltic  unrest. 

Etiology. — An  abnormally  increased  activity  of  the  stomach 
may  be  brought  about  by  different  causes : 

1.  As  a reflex  process,  through  hyperesthesia  of  the  sensory 
nerves  of  the  stomach. 

2.  By  a very  strong  stimulation  of  the  mucous  membrane  of 
the  stomach  by  HC1  (hyperacidity,  supersecretion),  by  organic 
acids,  the  result  of  an  abnormal  fermentation  of  the  contents  of 
the  stomach,  by  gases  which  distend  the  stomach  to  a considerable 
degree. 

3.  With  an  advanced  stenosis  of  the  pylorus  and  of  the  duo- 
denum, and,  finally,  it  may  be  due  to  an  increased  irritability  of 
the  motor  nerves,  and  may  thus  be  the  result  of  an  independent 
functional  neurosis. 

The  question  arises,  Which  of  the  motor  nerves  of  the  stomach 
take  part  in  the  merely  functional  illness  in  the  case  of  peristaltic 
unrest  ? 

While  Stiller,  who  has  paid  much  attention  to  neuroses  of  the 


750 


HYPERPERISTALSIS. 


stomach,  traces  back  peristaltic  unrest  to  a cramp  of  the  ring 
musculature  of  the  pylorus,  other  authors  explain  it  by  an  in- 
creased irritability  of  those  motor  nerves  which  innervate  the 
musculature  of  that  region  of  the  stomach  lying  between  the 
cardia  and  the  pylorus. 

In  severe  cases  the  anomaly  of  function  is  probably  extended 
over  all  the  motor  nerves  of  the  stomach,  since  with  cramp  of  the 
pylorus  alone  the  peristaltic  motions  are  not  so  intense  as  with 
peristaltic  unrest.  Fleischer  had  opportunity  of  convincing  him- 
self of  this  in  a case  of  dilation  of  the  stomach  in  which  the 
greatly  contracted  pylorus  could  each  time  be  felt  distinctly  through 
the  lax  abdominal  integuments. 

With  normal  size  and  location  of  the  stomach  the  peristaltic 
motions  are  not  visible  in  the  epigastrium,  in  spite  of  the  pres- 
ence of  peristaltic  unrest,  on  account  of  the  thickness  of  the 
abdominal  integument  and  because  a part  of  the  stomach  is  under 
the  liver;  it  is  thus  very  probable  that  many  cases  escape  detection. 
Sexual  excesses,  repeated  intense  emotions,  an  unsuitable  mode  of 
living,  general  nervousness,  as  well  as  anemia,  increase  the  dispo- 
sition to  this  disease. 

Symptomatology. — If  a stomach  which  is  dilated  or  dislocated 
downward  is  seized  with  peristaltic  unrest,  the  symptoms  are,  in 
decided  cases,  so  characteristic  that  they  can  not  easily  be  over- 
looked or  mistaken.  The  very  strong  contractions  of  the  gastric 
musculature,  repeating  quickly,  can  be  distinctly  seen  and  felt  as  un- 
dulatory  motions,  especially  when  abdominal  integument  is  relaxed. 
If  the  stomach,  at  the  same  time,  contains  liquids  and  gases,  the  peris- 
taltic waves  are  often  accompanied  by  strong,  gurgling  noises  which 
can  be  heard  at  some  distance.  These  undulatory  motions,  caused 
by  restless  action  of  the  muscles,  generally  run  in  the  direction  from 
fundus  to  pylorus:  that  is,  from  the  left  above  to  the  right  below, 
more  rarely  also  in  the  reverse  direction  of  right  to  left.  In  some 
cases  only  antiperistaltic  waves  have  been  observed.  By  the  con- 
traction of  the  muscles,  the  fundus  of  the  stomach  may  at  times 
be  distended  to  the  size  of  a child’s  head,  so  that  it  strongly  arches 
up  the  abdominal  walls. 

After  a time  the  elevation  sinks,  to  appear  in  another  region  of 
the  stomach.  At  the  height  of  the  contraction  of  the  muscles 
there  may  be  a slight  circular  constriction  or  furrow  seen  in  the 
middle  of  the  stomach,  dividing  the  organ  into  two  nearly  equal 
parts,  so  that  it  temporarily  assumes  the  shape  of  an  hour-glass. 


SY  M PTO  M ATO  LOGY. 


75  * 


Since  the  muscular  undulations  can  be  observed  only  with  a 
dilated  or  dislocated  stomach,  they  naturally  extend  beyond  its 
normal  location  ; if  peristaltic  unrest  of  the  small  intestine  exists 
simultaneously,  the  undulations  extend  also  over  a part  of  the  hy- 
pogastric region,  and  even  with  an  empty  stomach  a rolling  and 
rumbling  noise,  originating  in  the  intestines,  can  be  heard. 

Slight  degrees  of  peristaltic  unrest  occurring  when  the  stomach 
is  in  a normal  position  are  recognizable  by  the  aid  of  the  X-rays 
and  fluoroscope.  The  patient’s  stomach  must  contain  about  one 
liter  of  milk  mixed  with  one  teaspoonful  of  subnitrate  of  bis- 
muth. 

While  energetic  contractions  of  the  stomach  hasten  the  execu- 
tion of  its  normal  functions,  an  excessive  peristalsis  has  a directly 
injurious  effect,  and  causes  manifold  disturbances  of  digestion. 
Patients  frequently  complain  of  a lack  of  appetite,  belching,  nausea, 
and  vomiting.  If  the  peristaltic  unrest  is  very  stubborn,  the 
patients  may  suffer  a loss  in  nutrition,  so  that  the  suspicion  seems 
justified  that  malignant  neoplasm  is  developing.  If  the  peristaltic 
unrest  continues  also  through  the  night,  the  state  of  mind  is 
generally  much  depressed,  because  patients  are  constantly  re- 
minded of  their  stomach  and  their  disease ; any  neurasthenia 
which  may  be  present  is  often  considerably  increased.  If  the 
small  intestine  is  also  the  seat  of  active  peristaltic  unrest,  intestinal 
gases  and  liquid  contents  sometimes  regurgitate  into  the  stomach. 
The  eructations  are  then  very  foul-smelling,  and  often  feculent 
masses  are  vomited,  which  may,  exceptionally,  even  contain 
scybala. 

The  demonstration  of  scybala  in  vomited  matter  indicates  that 
the  peristalsis  of  the  colon,  which  generally  is  not  concerned  in 
peristaltic  unrest,  is  considerably  increased.  In  spite  of  peristaltic 
unrest  of  the  small  intestine,  very  stubborn  constipation  and 
meteorism  often  occur,  because  the  colon  is,  as  a rule,  pacific 
during  these  enteric  contortions. 

With  normal  size  and  location  of  the  stomach  the  objective  signs 
of  peristaltic  unrest  are  wanting,  and  sometimes  the  disagreeable 
sensations  of  unrest  in  the  region  of  the  stomach  constitute  the 
only  subjective  symptom  of  the  disease. 

Prognosis. — If  the  peristaltic  unrest  is  the  result  of  a genuine, 
independent,  or  symptomatic  neurosis,  the  prognosis  on  the  whole 
is  favorable.  When  injurious  substances  before  mentioned  are 
kept  away,  and  the  primary  diseases — neurasthenia,  anemia — can  be 


752 


HYPERPERISTALSIS. 


removed,  the  peristaltic  unrest,  as  a rule,  soon  recedes  with  suitable 
mode  of  living,  diet,  and  with  methodical  use  of  electricity. 

Diagnosis. — In  order  to  diagnose  with  certainty  that  type  of 
peristaltic  unrest  which  is  an  independent,  genuine  motor  neurosis, 
it  is  necessary  first  to  exclude  those  other  diseases  which  also  cause 
an  increased  peristalsis  of  the  stomach.  The  so-called  cramps  of 
the  stomach  with  cardialgia  are  accompanied  with  more  or  less 
severe  boring,  gnawing,  or  cramp-like  pains,  and,  therefore,  are 
generally  easily  recognized.  Whether  the  increased  peristalsis  is 
the  result  of  a very  strong  irritation  of  the  mucous  membrane  of 
the  stomach  by  hydrochloric  acid,  organic  acids,  or  by  gases  which 
distend  the  organ  to  excess,  may  generally  be  easily  determined  by 
a repeated  chemical  analysis  of  the  stomach  contents ; further,  the 
gastralgia  sometimes  ceases  entirely  when  the  stomach  has  been 
emptied  by  the  tube  and  is  thoroughly  cleansed  (which  is  not  the 
case  with  peristaltic  unrest).  The  increased  peristalsis  of  dila- 
tion resulting  from  stenosis  of  the  pylorus  or  duodenum  is  also 
arrested  by  lavage.  The  diagnosis  is  very  difficult  with  normal 
size  and  location  of  the  stomach.  In  these  cases  the  author’s 
method  of  graphically  recording  the  motor  functions  by  the  deglut- 
able  stomach-shaped  bag  is,  perhaps,  the  only  reliable  means  of 
settling  the  differential  diagnosis  between  peristaltic  unrest  of  the 
stomach  and  that  of  the  intestines.  In  fact,  in  all  neuroses  of  motility 
the  intragastric  stomach-shaped  bag  gives  most  valuable  informa- 
tion of  the  nature  and  intensity  of  the  peristalsis.  (See  p.  80.) 

One  may  suspect  peristaltic  unrest  when  the  symptoms  recede 
rapidly  after  methodical  application  of  electricity,  arid  when  other 
nervous  disturbances  occur  coincidently.  In  the  distinction  of 
peristaltic  unrest  of  the  stomach  from  that  of  the  intestine  one 
should  ascertain  whether  the  rolling  and  rumbling  is  still  audible 
with  an  empty  stomach,  and  whether  the  peristaltic  motions  can 
also  be  perceived  outside  of  the  limits  of  the  stomach.  If,  with  an 
empty  stomach,  every  splashing  noise  is  constantly  absent,  and  if 
the  sounds  appear  again  shortly  after  drinking  water,  this  argues 
for  peristaltic  unrest  of  the  stomach.  If  dilation  or  dislocation 
of  the  stomach  can  be  excluded,  the  visible  peristaltic  motions  are 
to  be  ascribed  to  the  intestines. 

Leube  has  described  cases  in  which  loops  of  small  intestine 
were  evidently  pushed  up  between  the  stomach  and  the  abdominal 
wall  while  in  active  peristalsis. 

Sedatives,  like  the  bromids,  opium,  and  belladonna,  are  said  to 


TREATMENT  OF  H YPEKPEK ISTA LSIS.  753 

exert  a more  controlling  effect  on  the  intestinal  than  on  gastric 
hyperperistalsis. 

Therapeutics. — The  sufferer  must  be  urged  to  keep  away  from 
injurious  influences,  such  as  sexual  excesses,  mental  shocks,  and 
overexertions,  etc.,  and  lead  a quiet,  regular  mode  of  life.  If  the 
peristaltic  unrest  is  a partial  or  resultant  effect  of  a decided  neuras- 
thenia or  anemia,  a protracted  sojourn  in  the  country,  in  the 
mountains,  at  the  seashore,  and  hydropathic  procedures  (cold  rub- 
bings, baths)  will  influence  favorably  the  nervous  system  and  the 
composition  of  the  blood  ; the  anemia  must  also  be  fought  by  a 
strengthening,  easily  digestible  diet  (scraped  meats),  and  by  iron 
and  arsenic  preparations. 

In  severe  cases  in  which  the  peristaltic  unrest  continues  through 
the  night,  resting  in  bed  and  a mild  diet  (milk,  soups)  are  recom- 
mended, and  cold  bandages  or  packings  of  the  stomach  should  be 
tried,  and  if  these  do  not  relieve,  then  warm  cataplasms.  Every 
immoderate  loading  of  the  gastric  walls,  as  well  as  every  severe 
dilation  of  the  stomach  by  means  of  gases,  is  to  be  strictly 
avoided,  in  order  not  to  increase  the  irritability  of  the  motor 
nerves.  Kussmaul  obtained  very  favorable  results  by  the  internal 
and  external  applications  of  electricity.  In  the  former  case  the 
anode,  by  means  of  the  tube,  is  inserted  into  the  stomach,  partially 
filled  with  a small  quantity  of  a normal  salt  solution  (0.6  per  cent.), 
and  then  slow  rubbing  motions  are  to  be  made  with  the  cathode 
externally  in  the  region  of  the  stomach  ; in  external  galvanization 
the  anode  is  used  for  the  last-mentioned  movements,  while  the 
cathode  is  placed  on  the  sternum.  I have  had  satisfactory  results 
with  exclusive  rectal  feeding  in  two  cases  of  peristaltic  unrest  in 
which  the  stomach  was  in  the  normal  position.  The  rectal  nutri- 
tive enemata  were  continued  for  sixteen  days;  thereafter  the  symp- 
toms disappeared. 

Of  the  medicines,  sodium,  ammonium,  or  strontium  bromid, — 
in  doses  of  three  to  five  gm.  (45  to  75  grs.)  in  twelve  hours, — 
extract  of  belladonna,  dose,  0.008  to  0.013  (%  °f  a gr-  to 

of  a gr.),  or  codein  phosphate,  dose,  0.02  to  0.03  gm.  of 
a gr.  to  y2  of  a gr.),  are  to  be  recommended.  The  bromid  of 
strontium,  20  grs.  four  times  daily,  has  my  preference.  Exclu- 
sive feeding  by  the  rectum  for  one  week  is  more  effective  when 
combined  with  rest  in  bed  and  the  use  of  the  bromids.  In  a per- 
sistent case  of  peristaltic  unrest  in  a gouty  patient  I obtained 


754 


NEUROSES  OF  THE  STOMACH. 


very  good  results  from  salicylate  of  sodium  i scruple,  with  bismuth 
subnitrate  16  grs.,  three  times  daily. 

NERVOUS  ERUCTATION. 

This  is  a frequent  symptom  in  hysteria,  neurasthenia,  and  allied 
neuropathic  conditions.  It  is  said  to  be  particularly  frequent  in 
the  sexual  neuroses.  The  belching  up  of  tasteless  or  offensive 
gases  is  a frequent  symptom  in  most  gastric  diseases.  In  fact,  it 
occurs  at  times  in  every  normal  person,  and  then  consists  of  the 
sporadic  expulsion  of  air  that  has  been  swallowed  with  the  food, 
or  of  C02  that  has  been  taken  in  with  beverages,  or  has  been  formed 
by  fermentation  of  the  food.  The  pathological  condition  which 
occurs  in  neurasthenia  consists  of  the  explosive  evacuation  of 
tasteless  gas  in  large  quantities.  The  attacks  are  usually  parox- 
ysmal, and  the  gas  that  is  expelled  is  generally  air,  which  is  not 
formed  in  the  stomach,  but  which  has  been  swallowed.  Every  time 
air  is  eructated  from  the  stomach  the  closure  of  the  cardia  must  be 
opened,  and  with  a frequent  repetition  of  this  a permanent  relaxa- 
tion of  the  cardia  may  develop.  The  muscular  development  of  the 
pylorus  being  much  stronger,  this  orifice  is  not  so  easily  opened  by 
gas.  We  have  known  nervous  individuals,  particularly  hysterical 
patients,  to  belch  up  air  during  the  entire  day,  and  often  during 
the  night.  Air  can  be  aspirated  into  the  stomach  when  the  cardia 
is  relaxed  and  the  esophagus  is  closed,  either  in  consequence  of  a 
negative  thoracic  pressure  when  the  vocal  cords  are  closed,  or  be- 
cause the  lumen  of  the  stomach  expands  and  dilates  under  nervous 
influence.  On  the  other  hand,  some  nervous  patients  have  the 
bad  habit  of  intentionally  or  unconsciously  swallowing  air  until 
the  stomach  is  expanded,  when  the  same  air  is  eructated  with  explo- 
sive violence.  In  one  of  the  patients  of  Cartellieri  (“  Wiener  allge- 
meine  med.  Zeitung,”  1885,  S.  3),  2500  eructations  occurred  in  one 
hour.  Some  patients  have  dyspeptic  symptoms,  while  in  others 
digestion  is  not  disturbed.  I have  personally  known  a neuras- 
thenic colleague  who  could  eructate  whenever  called  upon  to  do 
so.  It  is  probable  that  in  this  case  the  air  that  is  swallowed 
does  not  reach  his  stomach,  but  gets  no  further  than  the  upper  part 
of  the  esophagus,  when  it  is  again  expelled.  Oser  has  explained 
the  aspiration  of  air  into  the  stomach,  assuming  that  it  acts  on  the 
principle  of  an  elastic  balloon — the  contraction  of  the  longitudinal 
muscle  enlarging  the  gastric  lumen  and  thereby  sucking  in  air, 


NERVOUS  ERUCTATION. 


755 


and  the  circular  muscle  contracting  it  again  and  thereby  expelling 
it.  This  would  not  explain  all  cases,  because  in  some  hysterical 
patients  the  eructation  is  so  rapid  and  uninterrupted  that  there 
seems  to  be  no  time  left  for  swallowing  air  in  this  manner.  It  is 
probable  that  a clonic  spasm  of  the  pharyngeal  muscles  may  exist 
here,  persistently  pressing  air  into  the  esophagus,  which  eventually 
reaches  the  stomach,  but  generally  is  expelled  from  the  esophagus. 
(Bouveret,  /.  c.,  “ Aerophagia.”)  Esophageal  eructation  and  vom- 
iting may  be  produced  by  hysterical  patients  at  will.  Cartellieri 
asserted  that  his  patient  (/.  c .)  had  no  time  to  swallow  air  during 
the  attack,  and  Ewald  raises  the  question  whether  these  attacks 
are  really  nervous  eructations,  or  only  simulate  them. 

Pneumatosis. — This  is  a condition  of  the  foregoing  disease,  in 
which  the  stomach  is  abnormally  expanded  with  air,  producing  a 
sensation  of  unpleasant  distention  and  dyspnea.  When  the  air 
escapes  into  the  mouth  or  intestines,  the  torturing  feelings  cease. 
The  suffering  may  be  permanent  or  only  periodical,  and  has  been 
attributed  to  a spasmodic  closure  of  the  cardia  and  pylorus.  The 
dyspnea  that  occurs  in  these  cases  has  much  similarity  to  the 
“ asthma  dyspepticum  ” of  Henoch.  Pneumatosis  may  be  easily 
recognized  by  an  inspection  and  percussion  of  the  inflated  stomach, 
which,  of  course,  should  be  differentiated  from  a possible  distended 
transverse  colon.  In  many  cases  persistent  constipation  will  be 
found  to  be  an  etiological  factor,  for  in  these  cases  the  pneumatosis 
rapidly  improves  when  the  bowels  become  regular.  A possible 
gastric  dilation  and  atony  must  be  excluded. 

Treatment. — The  patient  and  his  attendants  must  be  instructed 
that  the  eructation  and  the  pneumatosis  are  largely  a habit,  and 
that  by  close  observation  of  the  patient  he  or  she  can  be  inter- 
rupted in  the  act  of  swallowing  air.  Penzoldt  cured  a patient  of 
this  kind  who  had  been  uninterruptedly  swallowing  and  eructating 
air,  by  making  him  keep  his  mouth  open  for  a half-hour,  as  it  is 
impossible  to  swallow  air  when  the  mouth  is  open.  The  eructation 
ceased  entirely,  and  the  patient  became  convinced  that  the  swallow- 
ing of  air  was  the  cause  of  his  suffering.  The  explosive  eructa- 
tions of  hysterical  patients  are  best  treated  by  methods  directed 
toward  the  psychical  condition  of  the  case.  Quincke  has  seen  cures 
by  introducing  a thick,  soft  stomach-tube,  and  permitting  it  to  rest 
for  a while  in  the  esophagus.  The  cases  that  depend  upon  aspira- 
tion by  alternate  expansion  and  contraction  of  the  stomach  are,  in 
my  experience,  benefited  by  the  intragastric  application  of  the  gal- 


756 


NEUROSES  OF  THE  STOMACH. 


vanic  current.  The  neurasthenic  foundation  of  the  disease  should 
receive  careful  attention — thus  nervous  eructation  and  pneumatosis 
have,  in  my  experience,  been  repeatedly  cured  by  a course  of  surf- 
bathing, as  well  as  the  Scotch  douche  applied  to  the  epigastrium. 
Cold  sponging  and  massage  are  very  useful  aids  in  treatment. 
Among  the  drugs  that  have  been  recommended  are  small  and 
frequently  repeated  doses  of  arsenic,  belladonna,  or  atropin,  hypo- 
dermic injections  of  morphin,  and  cocain.  Boas  obtained  good 
results  from  the  following  pill : 


R.  Extract,  physostigmatis, o.  13  gr.  ij 

Extract,  belladonnse  (Ale.), 0.25  gr.  iv 

Strychnin  sulphate, 0.03  gr.  ss.  M. 

Fiant  pill,  No.  xx. 

SiG.— One  pill  three  times  a day. 


Spraying  the  pharynx  with  solutions  of  cocain  and  menthol,  and 
the  internal  administration  of  bromid  strontium  are  available  thera- 
peutic measures.  Neurasthenia  depending  on  uric  acid  diathesis 
frequently  causes  nervous  eructations,  for  which  salicylate  of 
sodium  is  of  more  value  than  the  bromids. 


NERVOUS,  HABITUAL,  OR  REFLEX  VOMITING. 

In  the  classical  experiments  of  Magendie  the  stomach  of  an 
animal  was  replaced  by  a pig’s  bladder,  and  after  tartar  emetic  was 
injected  into  the  blood,  the  contents  of  the  bladder  were  vomited ; 
this  experimenter,  accordingly,  concluded  that  the  stomach  had 
nothing  to  do  with  the  act  of  emesis,  but  that  it  was  brought  about 
by  action  of  the  abdominal  muscles.  Tintani,  however,  showed 
later  on  that  the  experiment  of  Magendie  no  longer  succeeds  when 
the  cardia  still  remains  intact  and  is  not  cut  away ; therefore  the 
cardia,  inasmuch  as  it  can  prevent  vomiting,  must  be  concerned  in 
the  act  of  emesis,  which  was  found  to  consist  of  firm  closure  of  the 
pylorus,  opening  of  the  cardia,  while  powerful  peristaltic  and  anti- 
peristaltic  waves  traveled  over  the  stomach.  The  main  force  for 
emesis  is  then  furnished  by  the  abdominal  muscles,  which  are  ener- 
getically assisted  by  the  contractions  of  the  stomach  itself.  There 
are  three  forms  of  nervous  vomiting  : (1)  The  cerebral  or  spinal 
vomiting  (also  known  as  central  vomiting),  which  is  caused  by  di- 
rect or  indirect  stimulation  of  the  vomiting  center  in  the  medulla 
oblongata  from  other  irritated  foci  in  the  brain  and  spinal  mar- 
row. (2)  Nervous  vomiting,  occurring  as  a symptom  of  hysteria 
or  neurasthenia.  (3)  The  reflex  vomiting,  in  a more  restricted 


NERVOUS  VOMITING.  757 

sense,  brought  about  by  reflex  irritations  from  various  other  organs 
in  the  body. 

Cerebral  vomiting  is  a frequent  symptom  in  organic  diseases 
of  the  brain  and  its  membranes,  particularly  when  they  are  asso- 
ciated with  circulatory  disturbances  or  changes  in  intracranial 
pressure  occurring  more  or  less  suddenly.  It  has  been  observed 
in  acute  inflammatory  processes,  like  encephalitis  and  meningitis, 
also  with  cerebral  abscesses,  tumors,  and  focal  diseases.  It  may 
result  from  acute  anemia  or  hyperemia,  and  after  concussion  of 
the  brain.  It  is  said  to  occur  also  with  vivid  emotional  affections, 
and  after  intoxication  by  opium,  chloroform,  ether,  nicotin,  and 
also  in  uremia.  Spinal  vomiting  in  diseases  of  the  cord  is  rarer, 
but  it  is  quite  frequent  in  exophthalmic  goiter  and  in  tabes 
dorsalis,  in  which  it  occurs  in  form  of  the  gastric  crises,  first 
described  by  Charcot. 

Gastric  Crises.  — In  a majority  of  cases  the  gastric  crises 
are  accompanied  not  only  with  severe  vomiting,  but  with  gastric 
hyperesthesia  and  hyperchylia.  According  to  Leyden,  the  vomit- 
ing may  be  absent  entirely.  The  attack  begins  without  any  pro- 
dromal symptoms.  In  the  midst  of  well-being  the  patients  complain 
of  intense,  spasm-like  pains  in  the  stomach,  particularly  in  the  epi- 
gastrium, which  radiate  to  the  sides  and  to  the  back.  The  face 
is  pale,  the  pulse  is  small,  soft,  and  rapid,  there  are  vertigo  and 
palpitation  of  the  heart.  The  bowels  are  constipated,  the  ap- 
petite is  lost,  and  thirst  is  great.  At  the  same  time  there  are  great 
prostration  and  weakness  and  a clinical  picture  of  severe  collapse. 
Although  the  patients  drink  large  quantities  of  water,  they  pass 
very  little  urine,  partly  because  the  water  is  again  vomited,  or 
because  it  can  not  enter  the  intestines  on  account  of  an  existing 
pyloric  spasm.  The  abdomen  is  much  retracted  on  account  of 
clonic  contractions  of  the  stomach  and  intestines,  as  well  as  of  the 
abdominal  wall.  Very  soon,  copious  vomiting  begins.  First  food, 
then  bile,  mucus,  and  particles  of  blood  are  vomited.  The  reaction 
of  the  vomit,  as  a rule,  shows  hyperacidity.  Von  Noorden 
(“  Charite  Annalen,”  1890,  S.  166)  and  Seymour  Basch  have  re- 
ported attacks  of  gastric  crises  in  which  the  acidity  for  free  HC1 
was  normal  or  subnormal.  The  degree  of  acidity  will  natur- 
ally vary  with  the  length  of  time  that  the  vomited  ingesta  have 
remained  in  the  stomach.  After  abundant  vomiting  transient 
relief  is  generally  experienced,  and  in  mild  attacks  this  may  be 
the  end  of  the  crisis  ; but  in  severe  attacks  the  vomiting  may  occur 

50 


758 


NEUROSES  OF  THE  STOMACH. 


hourly,  continuing  to  the  evening,  with  very  short  intermissions. 
During  the  night  the  attacks  generally  cease,  to  return  again  on  the 
following  day.  This  course  of  symptoms  may  repeat  itself  in  eight 
to  ten  days,  by  which  time  the  debility  of  the  patient  is  very  great. 
The  suffering  may  cease  just  as  rapidly  and  suddenly  as  it  came. 
The  vomiting  stops,  the  appetite  improves,  and  the  general  condi- 
tion of  the  patient  slowly  convalesces.  If  gastric  crisis  occurs  in  a 
case  of  advanced  tabes,  its  recognition  is  not  difficult,  but  when  it 
occurs  as  one  of  the  very  first  symptoms  of  tabes,  the  correct  diag- 
nosis may  be  difficult.  In  that  case  we  must  test  the  patellar  re- 
flexes, the  reflexes  of  the  pupil,  Romberg’s  symptom  (increased 
incoordination  of  movements  by  placing  feet  together  and  closing 
eyes),  and  inquire  concerning  the  existence  of  lancinating  pains.  In 
case  the  connection  with  tabes  is  not  established,  gastric  crises  may 
be  mistaken  for  gastroxynsis,  hemicrania,  or  hyperacidity.  Hemi- 
crania — intense,  one-sided  headache — is  rarely  complained  of  in 
gastric  crises.  The  gastric  pains  in  hemicrania  are  insignificant. 
Gastroxynsis  occurs  only  in  men,  after  severe  mental  exertion  or 
after  well-known  toxic  influences,  and  is  always  incited  by  certain 
opportune  and  traceable  causes,  which  is  not  the  case  with  gastric 
crisis. 

Periodical  Vomiting  (Leyden). — This  is  a combination  of 
symptoms  in  which  the  prominent  feature  is  vomiting  that  returns 
in  regular  intervals.  In  some  cases  the  days  of  the  paroxysm  of 
the  attack  may  be  predicted  with  tolerable  accuracy.  The  attacks 
begin  without  any  marked  prodromal  symptoms,  in  the  midst  of 
apparently  good  health.  Gastralgia  may  introduce  the  attack  or 
may  follow  it.  The  appetite  is  lost,  pulse  small  and  frequent, 
tongue  coated  and  dry.  The  patients  may  have  intense  headache 
and  even  slight  delirium.  The  clinical  picture  is  very  similar  to 
that  of  the  gastric  crisis.  The  character  and  the  reaction  of  the 
vomit  are  essentially  the  same.  The  duration  of  the  attack  varies 
between  twenty-four  hours  and  fourteen  days  ; some  patients  have 
lancinating  pains  in  the  extremities  in  place  of  gastralgia.  Toward 
the  end  of  the  attack  the  vomiting  gradually  ceases,  and  the  remain- 
ing complaints  slowly  disappear.  The  characteristic  of  periodical 
vomiting  is  that  the  attacks  occur  at  certain  definite  intervals  of 
from  two  to  ten  weeks.  The  repetition  occurs  with  great  regularity, 
and  the  disease  may  last  many  years. 

The  prognosis  is  therefore  a very  doubtful  one.  The  distinction 
from  gastric  crisis  is  made  by  the  typical  periodicity,  and  the  pres- 


NERVOUS  VOMITING. 


759 


ence  of  great  hyperacidity  of  the  vomit  in  the  crisis.  Periodical 
vomiting  appears  occasionally  as  a primary,  idiopathic  neurosis  of 
the  vagi.  It  has  been  known  to  occur  with  hydronephrosis,  with 
floating  kidney,  diseases  of  the  uterus  and  ovaries,  with  intestinal 
entozoa,  and  nicotin  poisoning. 

Nervous  Vomiting  in  the  Course  of  Neurasthenia  and  Hys- 
teria.— This  vomiting  is  found  more  frequently  in  hysteria  than  in 
neurasthenia.  If  it  occurs  in  neurasthenia.it  is  associated  with 
marked  sensitiveness  of  the  lower  thoracic  and  the  upper  lumbar 
vertebrae  to  the  electrical  current  (M.  Rosenthal).  The  patients 
frequently  complain  of  severe  pain  in  the  gastric  region,  pointing 
to  a hyperesthesia  of  the  sensory  nerves,  which  may  probably 
be  the  cause  of  this  kind  of  vomiting.  Stiller  gives  the  fol- 
lowing points  which  are  characteristic  of  vomiting  of  nervous 
origin:  (i)  The  facility  of  the  emesis.  (2)  The  independence  of 
the  quality  and  quantity  of  the  ingesta.  (3)  The  capricious- 
ness with  which  very  bizarre  articles  of  diet  are  frequently 
retained  to  the  exclusion  of  others.  (4)  Sometimes  the  elec- 
tive vomiting  of  certain  substances  which  seemingly  are  sepa- 
rated from  the  mixed  chyme.  (5)  The  carelessness  with  which 
the  patient  endures  the  habitual  sickness.  (6)  The  tolerance  of 
the  body  to  the  effect  of  inanition  caused  by  the  habitual  vomiting, 
even  when  the  metabolism  is  much  reduced.  (7)  The  extraordin- 
ary influence  of  the  slightest  external  and  internal  causes  that  act 
on  mood  or  temperament.  (8)  The  frequent  occurrence  of  emesis 
when  no  food  has  been  taken  and  the  stomach  is  apparently  empty. 
{9)  The  presence  of  other  nervous  symptoms  alternating  or  con- 
temporaneous with  the  vomiting.  To  these  Boas  adds  (10)  the 
absence  of  important  secretory  or  motor  disturbances.  In  some 
of  these  cases  the  vomiting  occurs  almost  every  day,  occasionally 
after  each  meal.  In  other  cases  the  attacks  occur  at  longer  or 
shorter  intervals,  either  spontaneously  or  after  severe  influences 
exerted  upon  the  psychical  sphere.  Cases  have  been  repeatedly 
observed  in  which  only  the  liquids  have  been  expelled,  and  in  others 
only  the  solids.  Sometimes  the  vegetable  and  carbohydrate  foods 
are  vomited  and  proteid  food  retained,  or  vice  versa.  Nausea  and 
retching  are  absent  in  the  vomiting  of  hysterics,  which  occurs  with- 
out any  exertion. 

Juvenile  vomiting  rarely  occurs  by  itself,  but  is  rather  an  expres- 
sion of  a dyspepsia  developed  in  school-children  as  a result  of 
mental  overexertion.  The  symptoms  are  the  following : dyspeptic 


760 


NEUROSES  OF  THE  STOMACH. 


complaints,  gastralgia,  vomiting,  great  pallor,  dilation  of  pupils, 
slowing  of  the  pulse,  constipation.  In  all  of  these  cases  improve- 
ment follows  when  the  children  are  removed  from  school  and 
allowed  to  rusticate  in  the  fresh  country  air  (Leyden,  “ Ueber 
period.  Erbrechen,”  etc.,  “ Zeitschr.  f.  klin.  Med.,”  1882,  Bd.  iv, 
S.  605). 

Reflex  Vomiting  in  a More  Restricted  Sense. — Strictly 
speaking,  vomiting  is  almost  always  a reflex  act,  and  the  separation 
of  other  forms  of  vomiting  from  reflex  vomiting  is  justifiable  only 
on  didactic  grounds.  There  is  hardly  an  organ  which  could 
not  produce  this  form  of  vomiting  when  it  is  in  a state  of 
irritation.  The  peripheral  irritations  which  cause  this  reflex  vomit- 
ing are,  among  the  first,  those  which  strike  the  sensory  and  motor 
nerve-endings  in  the  esophagus,  the  posterior  pharyngeal  wall,  the 
epiglottis,  the  soft  palate,  and  the  root  of  the  tongue.  All  organs  that 
are  supplied  by  branches  of  the  vagus — so  particularly  the  abdominal 
organs — may,  under  pathological  conditions,  excite  an  attack  of  re- 
flex vomiting.  It  may  occur  as  a result  of  constipation,  meteorism, 
lead  colic,  irritation  by  foreign  bodies,  and  intestinal  parasites.  It  is 
one  of  the  first  symptoms  of  strangulated  hernia,  and  of  conditions  of 
irritation  in  the  peritoneum.  Abscess  of  the  liver,  perityphlitis, 
renal  and  hepatic  colic  are  associated  with  reflex  vomiting.  It  has 
been  known  to  occur  by  the  invasion  of  the  ascaris  lumbricoides 
into  the  ductus  choledochus,  emboli  in  the  kidney,  liver,  pancreas, 
and  spleen,  floating  kidney,  and  severe  concussion  or  contusion  of 
any  abdominal  organ.  Diseases  of  the  female  sexual  organs  are  a 
prolific  source  of  this  form  of  emesis.  It  is  not  the  severe  ana- 
tomical diseases  of  these  organs  that  most  often  cause  these  attacks, 
but  preferably  the  slight,  inconsiderable  affections.  Normal  men- 
struation and  pregnancy  are  occasionally  accompanied  by  emesis. 
The  so-called  pernicious  vomiting  of  pregnancy  may  be  caused  by 
a variety  of  conditions,  although  its  pathogenesis  is  still  obscure. 
When  vomiting  is  uncontrollable  in  a female  in  whom  the  evidences 
of  pregnancy  are  unmistakable,  the  embryo  should  be  removed 
and  the  uterus  curetted  before  prostration  becomes  too  great. 
Fleischer  states  that  this  should  be  done  in  order  to  save  the  life 
of  the  mother  and  eventually  that  of  the  child  (/.  c .,  p.  977) ; the 
pernicious  vomiting  of  pregnancy  occurs,  however,  at  such  an 
early  period  in  our  experience  that  the  child  would  not  be  viable. 
Every  form  of  severe  vomiting,  when  it  continues  for  a week  or 
more,  will  eventually  produce  hematemesis  from  local  ischemias 


PROGNOSIS  AND  DIAGNOSIS  OF  NERVOUS  VOMITING.  761 

produced  by  the  convulsive  gastric  contractions  during  the  emesis. 
In  a patient  that  died  at  the  Maryland  General  Hospital  in  April, 
1897,  the  young  woman,  who  was  undoubtedly  pregnant,  and  who 
refused  to  be  curetted,  vomited  and  purged  blood  in  the  second 
week  so  that  the  practitioner  who  presented  her  for  admission 
stated  that  she  had  undoubtedly  a gastric  ulcer.  At  the  autopsy, 
which  occurred  three  weeks  after  the  beginning  of  the  attack,  an 
embryo  between  two  and  three  months  old  was  found  within  the 
uterus,  while  nowhere  in  the  stomach  could  a lesion  be  found  ex- 
cepting large  ecchymoses,  some  of  them  attaining  the  size  of  a 
five-cent  piece,  and  scattered  over  the  entire  surface  of  the  stomach, 
which,  in  our  opinion,  had  been  caused  by  the  intensely  spastic 
contractions  of  the  stomach,  producing  ischemia.  Displacements 
of  the  uterus,  pelvic  exudates,  parametritis,  inflammations  and 
ulcerations  of  the  uterine  mucosa,  myomata,  and  ovarian  diseases 
may  cause  reflex  vomiting,  which  is  much  rarer  with  the  diseases 
of  the  male  sexual  organs.  Nevertheless,  it  is  occasionally  ob- 
served with  injury  or  inflammations  of  the  testicles  and  in  epididy- 
mitis. Chronic  inflammation  about  the  nasal  mucous  membrane, 
polypi,  and  hyperplasia  of  the  upper  air-passages  have  been  re- 
corded as  producing  the  disease.  Eichhorst  has  repeatedly  ob- 
served reflex  vomiting  in  certain  individuals  on  hearing  very  shrill 
tones.  Von  Troeltzsch  has  called  attention  to  the  fact  that  irrita- 
tion of  the  external  auditory  canal  may  cause  emesis. 

Prognosis  of  Nervous  Vomiting. — The  prognosis  will  vary 
with  the  fundamental  causative  disease.  Gastric  crises,  when  they 
occur  in  advanced  tabes,  may  cease  entirely  after  a time,  although 
the  fundamental  disease  continues  and  even  becomes  worse.  Peri- 
odical vomiting,  which  occurs  after  insignificant  disturbances  in 
other  organs,  which  get  well  without  difficulty,  may  stubbornly 
persist  after  the  fundamental  disease  has  been  cured.  The  prog- 
nosis is  favorable  whenever  the  causes  can  be  recognized  and 
completely  removed.* 


* A case  of  severe  nervous  vomiting  which  had  persisted  for  two  years  under  my 
observation  defied  all  treatment : electricity,  lavage,  Weir-Mitchell  rest-cure,  sedatives. 
All  foods  were  vomited.  For  two  months  a membranous  colitis  prevented  rectal  feeding, 
and  the  life  of  the  patient  was  maintained  by  hypodermic  injections  of  sterile  olive  oil. 
Periodical  pyloric  spasm  existed  at  the  same  time.  Professor  Howard  A.  Kelly,  after  an 
exploratory  incision,  found  nothing  abnormal  with  the  stomach  or  intestines,  no  adhesions, 
pelvic  organs,  liver,  and  spleen  normal.  But  the  pylorus  seemed  somewhat  smaller  than 
it  should  be,  and  a pyloroplastic  operation  was  done  (January  19,  1900).  It  is  too  early 
to  judge  of  the  effects  of  this  operation,  but  one  week  thereafter  the  vomiting  had  not  re- 


762 


NEUROSES  OF  THE  STOMACH. 


Diagnosis. — The  majority  of  the  forms  of  nervous  vomiting  can 
be  determined  after  an  exhausting  examination  of  the  entire  body, 
the  urine,  the  blood,  and  gastric  contents.  A careful  study  of  the 
previous  history  is  indispensable.  Nervous  vomiting,  as  has  been 
said,  may  be  in  rare  cases  an  idiopathic  vagus  neurosis  (Leyden), 
but  in  most  cases  some  palpable  cause  for  the  vomiting  can  be 
detected.  Prominent  among  these  are  dislocated  kidneys,  hydro- 
nephrosis, uterine  and  ovarian  diseases,  entozoa,  and  nicotin 
poisoning.  A careful  examination  of  the  fundus  of  the  eyes,  of  the 
ears,  and  of  the  nose,  mouth,  pharynx,  and  larynx  should  never  be 
omitted. 

Treatment. — Whenever  possible,  the  treatment  must  be  di- 
rected to  the  underlying  causal  disease.  When  the  various  morbid 
states  of  other  organs,  which  have  been  mentioned  in  the  etiology 
and  symptomatology,  can  be  excluded  after  application  of  all 
methods  of  diagnostic  technic,  only  then  is  a purely  symptomatic 
treatment  justifiable.  Hysteria  and  neurasthenia  are  to  be  met  by 
hydropathic  procedures,  or  by  absolute  rest,  abstention  from  mental 
and  emotional  excitement,  and  a sojourn  in  the  mountains  or  at 
the  seashore.  In  most  cases  the  greatest  possible  rest,  and  strict 
avoidance  of  psychical  disturbances  will  be  indispensable.  Gastral- 
gic  pains  and  hyperesthesia  can  be  relieved  by  a hot  cataplasm  on 
the  stomach,  but  the  application  of  the  galvanic  current  anode  on 
the  stomach  or  in  the  stomach,  and  cathode  alternately  on  the 
sternum  or  spinal  column  will  be  more  efficacious.  The  internal 
gastric  douching  with  warm  water,  and,  as  we  have  found,  spraying 
of  the  inside  of  the  stomach  with  solutions  of  menthol  and  cocain, 
are  also  generally  followed  by  cessation  of  the  pain.  In  vomiting 
of  pregnancy  rectal  feeding  and  six  grains  of  the  basic  orexin  in  a 
gelatin  capsule  three  or  four  times  a day  should  be  tried  first,  but 
cureting  of  the  uterus  should  not  be  delayed  too  long.  The  fol- 
lowing formula  we  have  found  efficacious  in  the  treatment  of  this 
form  of  vomiting  of  the  non-pernicious  type : 


R- 

Cerii  oxalatis,  .... 

gr.  lx 

Cocain  hydrochlor. , . . 

0. 2 

gr.  iij 

Menthol,  

gr.  xij 

Bismuth  salicylatis,  . . 

4.0 

Elixir  simpl.,  . . . . 

q.  s.  180.0 

f^vj. 

SlG.- 

— One-half  fluidounce  on 

an  empty  stomach  four  times  daily. 

turned.  The  case  is  mentioned  only  to  show  that  very  severe  cases  of  nervous  vomiting 
may  exist  without  observable  anatomical  lesions  ; may  endanger  life  by  progressive  emaci- 
ation. 


TREATMENT  OF  NERVOUS  VOMITING. 


763 


Hypodermic  injection  of  -J-  of  a grain  of  morphin,  together  with 
of  a grain  of  atropin  sulphid,  proved  helpful  in  a number  of 
cases. 

The  idiosyncrasy  of  the  patient  concerning  diets  should  be  care- 
fully studied.  A priori,  “ no  diet  can  be  suggested  that  shall  be 
universally  applicable  to  all  cases.”  The  ingestion  of  liquids  must, 
as  a rule,  be  very  much  limited,  and  thirst  relieved  by  colon  enemata. 
If  every  meal  is  vomited,  it  is  best  not  to  permit  the  ingestion  of 
larger  quantities  of  food,  but  simply  to  give  nourishment  in  very 
small  quantities — iced  milk,  champagne,  cold  tea  or  coffee,  or  egg- 
albumen  with  brandy,  or  clam  bouillon  in  tablespoonful  doses. 
Superacidity  must  be  treated  according  to  principles  laid  down  in 
the  chapter  on  this  subject.  When  there  is  abnormal  hyperesthesia 
of  the  stomach,  it  is  well  to  feed  the  patient  by  rectal  enemata  for 
about  a week  to  ten  days,  according  to  methods  described  in  the 
chapter  on  Dietetics.  The  most  effective  sedative  that  we  have  is 
morphin,  particularly  the  hypodermic  injection  of  of  a grain, 
together  with  of  a grain  of  atropin  sulphate.  The  following 
suppositories  are  useful  when  we  do  not  wish  to  create  an  adapta- 
tion to  morphin  : 

R.  Extract,  belladonnse, 0.2  gr.  iij 

Codein  phosphatis,  0.8  gr.  xij 

Butyr.  cacao, q.  s. 

Supposit.  No.  xii. 

Sig. — Insert  one  suppository  every  two  hours  during  the  attack. 


When  the  nervous  vomiting  persists,  even  during  the  night,  the 
bromids,  together  with  chloral  hydrate,  are  of  approved  efficacy. 
I am  in  the  habit  of  giving  thirty  grains  of  bromid  of  strontium 
with  ten  grains  of  chloral  in  peppermint  water,  repeated  every 
three  hours  until  sleep  supervenes.  We  have  also  found  the  fol- 
lowing combination  to  be  a reliable  means  of  combatting  this  neu- 
rosis : 


R.  Menthol, 1.0  gr.  xv 


Cocain  hydrobromatis,  . . . 

0.4 

gr.  vj 

Aquae  chlorofbrmi, 

f^iv 

Spir.  vini  gallic., 

60.0 

Sig. — One  tablespoonful  three  times 

a day,  largely  diluted. 

M. 


In  the  treatment  of  the  gastric  crises  Boas  has  found  that  iodid 
of  potassium  and  bromid  of  sodium  exert  very  favorable  influ- 
ences in  diminishing  the  frequency  and  intensity  of  the  attacks. 


76  4 


NEUROSES  OF  THE  STOMACH. 


The  use  of  the  constant  current,  with  the  anode  within  the  stomach 
and  the  cathode  over  the  spinal  cord  in  the  cervical  region,  is  gen- 
erally followed  by  a very  marked  palliative  effect.  Chloroform, 
three  to  five  drops  given  on  sugar,  ammoniated  tincture  of  valerian, 
twenty-five  drops  p.  r.  n.,  and  the  compound  spirits  of  ether,  fifteen 
to  twenty  drops  p.  r.  n.,  might  be  tried,  but  in  our  experience  they 
are  rarely  efficacious.  Basch  (/.  c.)  made  comparative  therapeutic 
studies  with  cerium  oxalate,  strychnin,  and  antipyrin  in  the  treat- 
ment of  tabic  gastric  crises.  The  results  were  not  encouraging 
with  any  of  these.  For  the  control  of  vomiting  in  tabic  gastric 
crises  the  following  is  about  the  most  effective  combination  I have 
experience  with : 

R . Strontium  bromid, 


Sodium  bromid, aa  3.0  gr.  xlv 

Morphin  sulphat., 0.065  gr.  j 

Essentiae  pepsin. , 200.0  ^viss.  M. 


Sic. — One  tablespoonful  every  two  hours. 


INSUFFICIENCY  OR  INCONTINENCE  OF  THE  CARDIA. 

Incontinence  of  the  cardia,  due  to  paresis  or  paralysis  of  the 
motor  nerves  of  the  ring  muscle,  is  a comparatively  rare  malady, 
though  somewhat  more  frequent  than  that  of  the  pylorus.  It 
appears  either  as  an  independent  disease,  or  as  a partial  or  result- 
ant phenomenon  of  other  neuroses.  The  relaxation  of  the  cardia 
produces  an  effect  directly  opposite  to  that  of  cramp  of  the  cardia. 
While  the  latter,  as  is  well  known,  prevents  the  removal,  by  eruc- 
tation, of  the  air  and  gases  introduced  into  the  stomach  during 
meals,  as  well  as  that  of  liquid  or  solid  contents  of  the  stomach, 
insufficiency  of  the  cardia,  on  the  other  hand,  much  facilitates  it. 
When  the  relaxation  of  the  cardia  is  accompanied  by  an  increased 
irritation  of  those  motor  nerves  which  innervate  the  dilator  of  the 
cardia,  so  that  by  the  spasm  of  the  latter  the  esophageal  orifice  of 
the  stomach  is  actively  enlarged,  energetic  peristalsis  of  the 
stomach,  with  the  additional  influence  of  the  abdominal  pressure, 
will  raise  portions  of  the  gastric  contents  into  the  esophagus,  and 
even  into  the  mouth. 

The  firmness  of  the  cardial  closure,  even  under  normal  circum- 
stances, seems  to  vary  greatly  in  different  individuals.  While  many 
persons  vomit  only  with  difficulty, — since  the  resistance  at  the 
esophageal  orifice  of  the  stomach  is  greater,  so  that  they  have  to 


REGURGITATION. 


765 


make  use  of  almost  all  known  remedies  and  devices  in  order  to 
overcome  it, — and  even  then  eject  only  a portion  of  the  contents  of 
the  stomach,  others  vomit  with  exceeding  ease,  and  they  succeed, 
with  only  a moderate  contraction  of  the  abdominal  muscles,  in 
emptying  the  stomach  entirely  through  vomiting.  In  one  and  the 
same  individual  the  closure  of  the  cardia  may  vary  at  different 
times.  At  times  small  quantities  of  ingesta  come  up  again  into 
the  mouth  after  eating,  while  at  other  times,  with  the  same  food 
and  the  same  fullness  of  the  stomach,  this  does  not  occur. 

If  only  small  quantities  of  the  contents  of  the  stomach  come  up 
into  the  mouth,  now  and  then,  this  does  not  yet  constitute  an  abnor- 
mal condition  ; one  should  only  consider  it  abnormal  when  large 
quantities  of  ingesta  come  up  after  eating,  and  when  this  is  repeated 
frequently,  almost  regularly  every  day  for  a considerable  period  of 
time.  If  the  masses  which  come  up  are  expectorated,  the  whole 
process  is  called  regurgitation  ; but  if,  on  the  other  hand,  they  are 
swallowed  again,  it  is  called  rumination  (merycism,  remastication), 
even  when  the  regurgitated  foods  are  not  chewed  again,  which  is 
observed  in  a small  number  of  patients. 

Concerning  the  causes  of  regurgitation  and  rumination,  opinions 
still  differ  greatly  at  the  present  time.  Some  authors  trace  both 
conditions  to  a permanent  relaxation  of  the  cardia,  but  the  presence 
of  the  deglutition  sounds  is  an  argument  against  a permanent  incon- 
tinence, according  to  Ewald  ; other  authors  assume  a temporary 
insufficiency  of  the  cardia,  and  still  others,  in  addition,  an  increased 
irritation  of  the  motor  nerves — and  eventually  also  of  the  sensory 
nerves — of  the  stomach.  According  to  M.  Rosenthal,  regurgitation 
and  rumination  are  caused  by  an  increased  irritability  of  the  vagus, 
and  with  this  also  an  increased  irritability  of  the  motor  nerves  lead- 
ing from  it  and  supplying  the  dilator  cardiae,  which  causes  a spasm 
of  the  latter,  and  through  this  an  active  enlargement  of  the  esopha- 
geal orifice  of  the  stomach.  Whether  the  disease  is  of  central  or 
peripheral  origin  is  at  present  also  impossible  to  decide. 

Regurgitation. — At  a longer  or  shorter  period  after  meals  large 
quantities  of  the  liquid  and  solid  contents  of  the  stomach  are  at 
first  involuntarily  brought  up  again  into  the  mouth,  and  are 
then  expectorated.  With  protracted  duration  of  regurgitation 
the  patient  generally  learns  how  to  facilitate  the  ascension  of  the 
ingesta  by  means  of  rather  severe  contractions  of  the  musculature 
of  the  abdomen.  According  as  regurgitation  takes  place  in  the 
first  or  second  period  of  the  digestion  of  the  stomach,  the  regurgit- 


766 


NEUROSES  OF  THE  STOMACH. 


ated  food  particles  have  either  the  same  taste  as  in  eating,  or  they 
taste  sour  (HC1)  or  bitter  (peptone).  Regurgitation  is  not  easily 
mistaken  for  vomiting,  since  the  sensations  of  nausea  experienced 
before  and  after  the  latter  are  entirely  lacking  with  regurgitation. 
Regurgitation  takes  place  without  any  especial  exertion  on  the  part 
of  the  patients,  and  is  easily  distinguished  from  the  retching  forth 
of  foods  previously  eaten,  in  cases  of  stenosis  or  the  formation  of 
diverticula  in  the  esophagus — that  is,  from  the  rising  up  of  the 
same  into  the  mouth,  when  the  diverticulum  is  full  and  runs  over. 
The  difficulties  of  deglutition,  the  result  of  sounding  the  esopha- 
gus, as  well  as  the  constant  absence  of  hydrochloric  acid  in  the 
regurgitated  masses,  make  a sure  differentiation  of  the  two  first- 
mentioned  diseases  possible.  Most  patients  are  able  to  suppress 
regurgitation,  but  in  a few  cases  they  do  not  succeed  in  this,  how- 
ever much  they  try.  If  copious  quantities  of  the  contents  of  the 
stomach  are  regurgitated  in  quick  succession  and  are  expectorated, 
the  general  nutrition  may  suffer  considerably;  but  generally  these 
patients  have  a very  hearty  appearance.  Other  nervous  disturb- 
ances— signs  of  hysteria  or  neurasthenia — may  be  present  coinci- 
dently.  With  protracted  duration,  regurgitation  may  develop  into 
rumination. 

The  prognosis  is  generally  favorable  with  regurgitation,  since  the 
state  of  nutrition  remains  good,  and  if  disturbances  of  nutrition 
appear,  the  patient  often  can  be  induced  to  swallow  the  ingesta 
which  have  risen  into  the  mouth  and  to  energetically  prevent  their 
coming  up  again. 

Therapeutics. — Regurgitation  is  promoted  by  hasty  eating  and 
quick  swallowing  of  insufficiently  chewed  foods,  especially  when 
the  latter  are  of  difficult  digestion  ; a diet  should,  therefore,  be  pre- 
scribed which  is  easily  digestible,  and  the  patients  should  be 
directed  to  eat  slowly  and  chew  thoroughly.  Gladstone’s  sug- 
gestion is  to  give  each  morsel  of  food  one  bite  or  grind  for  every 
tooth  in  the  mouth — i.  e.,  32 — before  it  is  swallowed.  It  is  best 
for  the  patients  to  eat  in  the  company  of  such  persons  whose  good 
opinion  they  value,  so  that  they  avoid  expectorating  the  ingesta 
which  have  risen  into  the  mouth,  and  will  rather  swallow  them 
again  endeavoring  to  combat  regurgitation  to  the  utmost  of  their 
power.  If  indications  of  hysteria  or  neurasthenia  can  be  shown, 
these  diseases  are  first  to  be  treated.  In  stubborn  cases  the  swallow- 
ing of  small  pieces  of  ice  is  recommended  (Alt),  which  may  reflexly 
induce  the  musculature  of  the  cardia  to  contract.  In  addition,  mas- 


RUMINATION. 


767 


sage  of  the  epigastrium,  internal  and  external  galvanization  and 
faradization,  as  well  as  internal  administration  of  strychnin  nitrate 
(0.003-0.006)  are  indicated.  The  galvanic  current  should  be 
applied  in  the  same  manner  as  in  cardiospasm. 


RUMINATION,  OR  MERYCISM. 

Patients  afflicted  with  this  neurosis  return  the  ingesta  from  the 
stomach  through  the  esophagus  back  into  the  mouth  sooner  or 
later  after  they  have  been  swallowed.  This  is  not  only  done  without 
nausea,  but  apparently  with  a certain  enjoyment.  The  raised  food 
is  rechewed,  and  either  swallowed  again  or  expectorated.  This  occurs 
habitually  several  hours  after  meals  and  without  the  least  exertion. 
Rumination  in  the  human  subject  has  been  known  for  a long  time. 
Fabricius  Ab.  Aquapendente  described  the  disease  in  1618.  As 
the  knowledge  of  physiology  of  older  practitioners  was  very 
limited,  and  they  had  no  conception  of  the  functions  and  mechanism 
of  gastric  digestion,  the  most  peculiar  hypotheses  were  developed 
in  explanation  of  this  very  interesting  neurosis.  It  was  firmly 
believed  that  ruminants  descended  from  parents  with  horns,  or  that 
they  at  least  had  a horned  father,  or  had  been  nursed  from  the 
udder  of  ruminating  horned  animals.  It  was  also  believed  that  the 
stomach  of  human  ruminants  was  divided  into  several  sections 
by  partitions,  as  we  find  them  in  cattle.  After  it  was  found  at 
autopsies  that  ruminants  possessed  stomachs  of  the  same  structure 
as  all  other  human  beings,  the  profession  gradually  accepted  the 
neurotic  explanation  of  the  malady. 

Etiology. — A neuropathic  constitution  is  a frequent  factor  in  the 
development  of  rumination.  Heredity  seems  to  have  some  effect 
in  the  matter,  as  ruminating  fathers  have  been  known  to  have  rum- 
inating children.  The  element  of  imitation  and  suggestion  can, 
however,  not  well  be  eliminated  under  this  question  of  heredity. 
Freund  and  Korner  have  described  a case  in  which  two  children 
developed  this  habit  in  imitation  of  their  ruminating  governess. 
The  disease  seems  to  be  more  frequent  in  men  than  in  women.  It 
occurs  in  all  classes  of  society  and  at  all  ages.  The  following  are 
some  of  the  causes  assigned  to  rumination  : Sexual  excesses,  mas- 
turbation, fear,  terror,  anger,  psychical  irritations,  and  the  very  hasty 
deglutition  of  badly  masticated  food,  particularly  when  it  exists 
exclusively  of  vegetables,  injury  to  the  epigastrium,  achlorhydria, 
obstinate  constipation,  and  gastro-enteritis.  It  is  claimed  by  Dehio 


;68 


NEUROSES  OF  THE  STOMACH. 


that  whooping-cough  may  be  followed  by  this  disease  ; this  is  very 
plausible,  because  pertussis  brings  on  frequent  vomiting,  and  there- 
by an  incontinence  of  the  cardia.  Although  the  disease  has  been 
known  to  occur  in  persons  of  high  intellectuality,  a large  number  of 
ruminating  patients  belong  to  the  class  of  neurasthenics,  and  hys- 
terical, hypochondriacal,  epileptic,  anemic,  choreic,  and  idiotic  indi- 
viduals. The  disease  has  been  studied  by  Bourneville  and  Seglas, 
Dehio,  Alt,  Boas,  Bear,  Ducasse,  Decker,  Einhorn,  Oser,  Ponsgen, 
Johannessen,  Lebert,  M.  Rosenthal,  and  E.  Singer. 

In  the  “ N.  Y.  Med.  Record  ” for  June  12,  1896,  Dr.  H.  A.  Minas- 
sian  reports  an  interesting  case  of  merycism  with  achlorhydria  and 
hyperperistalsis  which  was  cured  by  hydrochloric  acid,  exclusion  of 
fluids,  and  exercise  of  self-control.  In  the  same  journal  for  July 
10,  1897,  Andrew  Halliday,  M.B.,  a physician  of  Nova  Scotia,  who 
personally  has  the  power  of  regurgitation  and  rumination  at  will, 
gives  the  analysis  of  his  own  stomach-contents:  Forty-five  to  sixty 
minutes  after  a Ewald  test-meal  the  total  acidity  was  45  to  55. 
The  free  HC1  was  0.124  to  0.1604  per  cent.  His  motility  seems 
normal.  These  two  cases  suffice  to  show  the  variability  of  the 
state  of  secretion  and  motility  in  merycism. 

Symptomatology. — The  regurgitation  of  ingesta  from  the 
stomach  into  the  mouth  is  usually  at  first  voluntary,  but  later  on 
involuntary.  The  rumination  differs  from  simple  regurgitation  in 
that  the  raised  food  is  expectorated  in  the  latter  disease,  but  is  swal- 
lowed again  in  the  former.  The  ascent  of  the  food  from  the 
stomach  causes  a pleasurable  sensation  to  these  patients,  and  they 
assist  the  act  by  bringing  into  effect  the  pressure  of  their  abdominal 
muscles.  In  severe  cases  the  rumination  occurs  after  every  meal, 
and  lasts  either  only  for  the  first  hour  or  for  five  or  six  hours. 
The  condition  of  the  secretory  function  is  variable.  Jurgensen 
found  no  free  HC1,  Bear  and  Boas  found  subacidity,  while  Alt 
demonstrated  hyperacidity  in  one  of  his  cases.  In  some  patients 
secretion  was  found  to  be  normal.  In  three  of  such  cases  I ob- 
served that  the  state  of  the  secretion  varied,  as  expressed  in 
the  chemical  analysis  of  the  raised  masses  according  to  the  time 
after  the  ingestion  in  which  they  were  regurgitated,  and  the  com- 
bining power  for  HC1  which  the  particular  food  possessed.  If  they 
were  regurgitated  immediately  after  the  meal,  they  were  faintly  acid 
or  neutral,  contained  no  free  HC1  nor  ferments,  which,  however, 
were  present  within  forty-five  minutes  of  the  first  ingestion  of  food. 
It  is  probable  that  many  of  the  discrepancies  concerning  the  state  of 


SYMPTOMS  OF  RUMINATION. 


769 


the  secretion,  as  stated  by  the  various  authors  mentioned,  can  be  ex- 
plained on  the  same  grounds.  Alt  has  suggested  a very  interesting 
theory  in  explanation  of  the  ruminating  habit  (“  Berlin,  klin.  Woch- 
enschr.,”  Bd.  lxxxviii,  Nos.  26  and  27) : he  suggests  that  the  object 
of  the  act  may  be  the  correction  of  defective  chewing  and  insaliva- 
tion of  the  food,  and  the  hyperacidity  caused  thereby.  Acting  ac- 
cordingly, Alt  treated  his  patient  with  alkalies,  and  claims  to  have 
found  that  the  case  ruminated  less  frequently  and  by  and  by  could 
suppress  the  habit.  Boas  (“  Berlin,  klin.  Wochenschr.,  ” 1886,  No. 
831)  has  published  a case  of  rumination  with  subacidity,  and  in 
this  case  improvement  followed  the  administration  of  HC1.  Ac- 
cording to  Einhorn,  but  106  cases  of  this  malady  have  been 
described  up  to  1896,  which  cases  occurred  chiefly  among  the  pro- 
fessional and  educated  classes — physicians,  lawyers,  and  philolo- 
gists. This  observation  was  also  made  in  a report  by  Johannessen 
(“  Zeitschr.  f.  klin.  Med.,”  Bd.  x,  S.  274). 

The  following  is  a brief  account  of  a case  occurring  in  my  private  practice : 
A.  F.,  aged  thirty-eight,  mother  has  been  a highly  nervous  woman,  much 
afflicted  with  insomnia  and  neuralgia  ; father  died  at  the  age  of  fifty-six  from 
Bright’s  disease.  He  was  a very  irascible  and  eccentric  man.  A.  F.  has  had 
no  severe  disease,  except  gout  four  years  ago.  He  is  a pianist  of  exceptional 
ability,  and  has  played  in  foreign  countries  as  well  as  in  the  larger  cities  of 
the  United  States.  Ordinarily  and  when  in  a quiet  frame  of  mind  he  rarely 
ruminates,  but  when  he  gives  instruction,  particularly  when  he  has  to  perform 
at  a concert,  or  at  other  times  when  he  is  emotionally  excited  or  disturbed,  he 
begins  to  raise  food  into  his  mouth,  which  he  at  first  swallows  for  about  two 
hours.  He  confesses  that  he  chews  the  food,  and  actually  enjoys  it,  but  at  the 
expiration  of  two  hours  the  muscles  of  mastication  become  so  exhausted  that 
he  can  no  longer  chew  the  raised  masses.  He  would  then  like  to  put  an  end 
to  the  ruminating,  or  rather  to  the  rising  of  the  food,  but  then  can  not  stop  it, 
as  it  persists  in  coming  up  from  his  stomach.  He  then  terminates  the  rumina- 
tion by  voluntarily  evacuating  his  stomach  through  vomiting,  which  he  accom- 
plishes very  easily. 

The  masses  begin  to  ascend  within  ten  to  fifteen  minutes  after  a meal,  and 
are  then  very  faintly  acid.  He  is  also  aware  that  they  begin  to  taste  salty  sour, 
as  he  calls  it,  forty-five  minutes  to  an  hour  after  the  meal.  The  total  acidity 
one  hour  and  a quarter  after  a meal,  as  judged  from  the  regurgitated  masses, 
is  70;  free  HC1  30.  Erythrodextrin  present;  achroodextrin  present.  Gas- 
tric' motility,  as  determined  by  Hemmeter’s  method,  is  evidently  exaggerated. 
Physical  examination  of  the  thoracic  and  abdominal  organs  negative.  Urine 
negative.  Examination  of  blood  negative.  On  one  occasion  this  patient  had 
not  ruminated  for  three  weeks,  when  the  time  came  for  him  to  fulfil  an  engage- 
ment at  a concert.  The  author,  for  the  sake  of  study,  was  present  when  he 
took  his  supper  on  the  evening  of  this  concert.  Within  fifteen  minutes  after 
the  supper  we  observed,  by  the  movements  of  his  throat,  he  had  begun  his  old 


7;o 


NEUROSES  OF  THE  STOMACH. 


bad  habit,  which  kept  up  during  the  entire  evening,  and  was  plainly  observable 
while  he  was  performing  at  the  piano  during  the  concert. 

Atony  and  dilation  may  be  present,  together  with  rumination, 
and  the  state  of  the  motility  seems  to  vary  as  much  as  that  of 
secretion.  The  general  nutrition  is  not,  as  a rule,  affected,  although 
the  disease  may  have  existed  a long  time  ; but  when  the  patients 
persistently  spit  out  the  ascending  masses  of  food,  instead  of  swal- 
lowing them  again,  or  when  severe  disturbances  of  secretion  and 
motility  exist,  the  patients  rapidly  lose  strength  and  weight. 
According  to  von  Hacker  and  G.  Singer,  an  insufficiency  of  the 
cardia,  and  a dilation  of  the  esophagus  immediately  above  the 
cardia,  may  be  caused  by  mechanical  expansion,  resulting  from  the 
regurgitation  of  large  bits  of  food.  This  esophageal  expansion 
has  been  demonstrated  by  these  authors  with  the  esophagoscope. 

Prognosis. — This  is  not  a serious  disease,  as  the  general  nutri- 
tion remains  good,  and  if  the  patient  really  does  begin  to  suffer,  he 
may  be  relieved  by  a rational  psychical  and  symptomatic  treatment, 
particularly  if  the  patient  himself  will  aid  the  therapeutic  measures 
by  self-control.  The  diagnosis  presents  no  difficulties  whenever  the 
physician  can  observe  a patient  in  the  act  of  rumination ; regurgi- 
tation and  emesis  imply  the  spitting  out  of  food,  and  are  always 
associated  with  nausea  or  some  other  unpleasant  sensation. 

Treatment. — Medicinal  treatment  in  this  disease  is  of  little 
value.  The  state  of  the  secretions  should  be  carefully  determined, 
and  subacidity  or  achylia  corrected  by  the  administration  of  HC1, 
and  hyperchylia  by  the  use  of  calcined  magnesia  and  bicarbonate 
of  sodium.  Korner  is  enthusiastic  on  the  value  of  small  pieces  of 
ice  given  directly  after  meals.  The  stomach-tube  has  been  used 
for  the  lavage  and  artificial  feeding,  but  the  relief  has  been  only 
temporary.  The  physician  should,  however,  in  all  cases  insist  on 
slow  eating  and  careful  chewing;  the  food  should  be  easily  digest- 
ible and  largely  composed  of  gruels  and  diet  of  a soft  consistency. 
The  patient  should  always  take  his  meals  in  the  presence  of  persons 
for  whom  he  has  considerable  respect,  and  who  understand  to  op- 
pose the  morbid  habit  with  kindness  and  yet  with  emphatic  per- 
sistence. The  success  of  the  treatment  will  depend  upon  the  will- 
power of  the  patient  himself.  Whenever  the  patient  feels  a desire 
to  ruminate,  he  should  be  prompted  to  resist  the  temptation  with 
all  the  self-control  at  his  command.  He  should  be  guarded  against 
using  the  contraction  of  the  abdominal  muscles  to  assist  the  act. 


INSUFFICIENCY  OF  THE  PYLORUS. 


77 1 


Ponsgen,  Boas,  and  Einhorn  report  permanent  cures  resulting  from 
such  persistent  autosuppression.  A trial  might  be  made  with  the 
intragastric  use  of  the  faradic  and  galvanic  currents.  Hydropathic 
methods  are  sometimes  useful.  In  one  case  observed  by  myself, 
in  which  every  meal  was  persistently  ruminated,  I carried  out 
rectal  alimentation  for  twelve  days,  not  allowing  anything  to  enter 
the  stomach  during  this  time.  Since  then  nearly  two  years  have 
elapsed  and  rumination  has  not  thus  far  returned.  I hesitate  in 
attributing  this  recovery  to  the  rectal  alimentation,  although,  of 
course,  it  was  impossible  for  the  patient  to  regurgitate  and  ruminate 
when  no  food  was  contained  in  the  stomach.  However,  the  psychical 
effect  of  hospital  treatment,  the  entirely  new  surroundings,  and 
attendance  by  intelligent  nurses,  the  constant  rest  in  bed,  may 
have  contributed  as  much  as  the  rectal  feeding  toward  the  re- 
covery. In  another  case  the  author  cured  the  patient  by  giving 
ten  grains  of  quinin  after  each  meal.  The  good  result  is  not  at- 
tributed to  the  antimalarial  effect,  but  rather  to  the  fact  that  the 
quinin  rendered  the  food  so  disgustingly  bitter  that  the  patient 
suppressed  the  regurgitation.  Rossier  claims  to  have  cured  one 
case  by  muriate  of  morphin,  and  another  by  large  doses  of  opium. 
In  my  experience  these  remedies  have  been  useless. 

INSUFFICIENCY  OR  INCONTINENCE  OF  THE  PYLORUS. 

It  has  been  known  for  a long  time  that  an  insufficiency  or  incon- 
tinence of  the  pylorus  may  be  caused  by  organic  diseases  of  the 
stomach  and  intestines,  by  carcinoma  and  ulcer,  by  bringing  about 
a partial  or  complete  obliteration  or  carcinomatous  infiltration  of 
the  annular  muscle,  so  that  the  latter  becomes  incapable  of  function- 
ing; or  it  may  be  caused  by  a stenosis  of  the  duodenum  leading 
to  advanced  dilation  of  the  initial  part  of  the  same.  Attention 
was  first  called  by  Ebstein  to  those  interesting,  though  very 
rare,  cases  of  insufficiency,  which  appear,  in  the  absence  of  ana- 
tomical changes,  genuine  neuroses — paralysis  of  the  motor  nerves 
of  the  annular  muscle.  It  had  been  previously  observed  by 
Ebstein  as  a concomitant  phenomenon  of  myelitis  due  to  compres- 
sion, and  also  in  hysteria  and  gout;  but  it  may,  perhaps,  occur 
also  as  an  idiopathic  malady.  If  the  muscular  insufficiency  is  con- 
fined to  the  pylorus,  then  the  foods  and  liquids,  according  to  the 
degree  of  the  insufficiency,  either  remain  a very  much  shorter 
time  than  usual  in  the  stomach,  or  enter  the  intestines  immediately 


772 


NEUROSES  OF  THE  STOMACH. 


after  their  ingestion.  The  nutriments  then  are  not  at  all  digested 
in  the  stomach,  or  only  to  a slight  degree,  so  that  the  whole,  or 
almost  the  whole,  burden  of  digestion  falls  upon  the  intestine. 
Since,  however,  repeated  experiments  upon  human  beings  and 
animals  have  proved  that  the  intestine,  in  normal  conditions,  may 
entirely  make  up  for  the  lack  -of  digestion  in  the  stomach — and 
the  experience  gained  from  the  treatment  of  persons  that  have 
undergone  a resection  of  the  pylorus  confirms  this  ; therefore  even 
with  protracted  duration  of  the  pyloric  insufficiency  disturbances 
of  nutrition  generally  fail  to  appear,  especially  when  an  easily 
digestible  diet  is  prescribed,  suitable  to  the  malady,  and  provided 
that  the  intestinal  functions  are  normal. 

The  symptoms  of  pyloric  insufficiency  are,  in  brief,  the  following — 
viz. : If  frequent  vomiting  and  belching  existed,  these  suddenly  cease 
after  the  setting  in  of  the  insufficiency.  If  rather  large  particles  of 
food  get  into  the  intestine  which  mechanically  irritate  its  mucous 
membrane  more  than  usual,  then  the  increased  peristalsis  may  cause 
diarrhea.  This  may  also  be  brought  about  by  very  cold  or  very 
hot  foods  or  drinks,  which  are  gradually  warmed  or  cooled  by  the 
stomach,  as  the  case  may  be,  before  their  entrance  into  the  intes- 
tine, when  the  closure  of  the  pylorus  is  normal.  If  a quantity  of 
air  was  swallowed  with  the  foods,  or  if  drinks  rich  in  carbonic  acid 
have  been  imbibed  (beer,  seltzer  water,  champagne),  a very  acute 
tympanites  of  the  intestine  may  develop  from  the  escape  of  air  or 
carbonic  acid  gas. 

According  to  Ebstein,  one  can  not  succeed  in  distending  the 
stomach  with  the  artificial  production  of  carbon  dioxid  in  the 
organ  by  acid,  tartrate  and  sod.  bicarb.,  one  teaspoonful  of  each  in  4 
ounces  of  water  in  separate  tumblers  ; but  Ewald,  Boas,  and  other 
authors  justly  contend  that  this  evidence  is  not  conclusive;  since, 
even  when  the  musculature  of  the  pylorus  functions  in  a normal 
manner,  every  attempt  at  distending  the  stomach  by  means  of 
gases  may  remain  unsuccessful,  because  the  amount  of  the  gases 
formed  is  too  small.  Further,  with  an  empty  stomach  the  pylorus 
(Kussmaul)  is  normally  so  relaxed  that  a portion  of  the  carbonic 
acid  gas  may  easily  pass  over  into  the  intestine,  without  the  pres- 
ence of  any  real  insufficiency.  This  source  of  error  may,  however, 
be  removed  by  letting  the  patient  eat  a test-breakfast  before  the 
distention  of  the  stomach  (Fleischer),  since  then,  under  normal  cir- 
cumstances, the  closure  of  the  pylorus  becomes  so  firm  that  the 
carbonic  acid  gas  set  free  can  not  at  once  escape  into  the  intestine ; 


INSUFFICIENCY  OF  THE  PYLORUS. 


773 


or  if,  instead  of  C02,  air  is  forced  into  the  stomach  by  means  of  a 
tube  and  a pump,  increasing  the  supply  according  to  necessity.  If 
the  air  passes  quickly  into  the  intestine,  the  inflated  ascending  colon 
appears  as  a thick  swelling  on  the  right  side  of  the  abdomen.  For 
a proof  of  the  purely  nervous  origin  of  insufficiency  it  is  necessary 
to  exclude  the  above-mentioned  diseases  of  the  stomach  and  intes- 
tine, and  such  organic  diseases  of  the  stomach  as  chronic  gastritis, 
which  probably  bring  about  a serous  infiltration  of  the  annular 
muscle,  and  may  lead  to  a temporary  insufficiency  (Eichhorst, 
Boas).  If  the  insufficiency  be  due  to  a stenosis  of  the  duodenum, 
the  stomach  may  very  well  be  distended  by  C02  or  air,  in  spite  of 
insufficiency.  If,  after  finding  out  the  lower  limits  of  the  stomach, 
quantities  of  water  are  introduced  through  the  tube,  and  no  dullness 
appears  in  the  lower  parts,  while  gurgling  noises,  before  lacking, 
now  become  audible  in  the  intestine,  and  if  the  intestinal  loops, 
just  before  this,  gave  a tympanitic  resonance,  and  after  the  intro- 
duction of  water  exhibit  a muffled  sound,  insufficiency  is  to  be 
inferred.  It  has  been  claimed  that  after  the  introduction  of  one 
grain  of  salol  or  o.i  gr.  of  iodoform  with  the  test-breakfast,  sali- 
cyluric acid  can  be  shown  in  the  urine  after  taking  the  former, 
and  iodin  in  the  saliva  after  taking  iodoform,  much  sooner  than 
with  continence  of  the  pylorus,  as  these  chemicals  enter  more 
quickly  into  the  intestine,  and  on  account  of  the  neutralization  of 
the  hydrochloric  acid  by  the  alkaline  intestinal  juice,  they  are 
immediately  converted  into  soluble  compounds  which  may  be 
absorbed.  I have  explained  the  fallacy  of  these  tests. 

Insufficiency  of  the  pylorus  may  be  recognized  by  the  author’s 
method  of  intubating  the  duodenum  (“  Archiv  f.  Verdauungskrank- 
heit.,”  Bd.  n,  S.  85),  and  by  the  spiral  revolving  sound  of  F.  Kuhn, 
of  Giessen,  and  of  F.  B.  Turck,  either  of  which  may  be  used  for 
sounding  the  pylorus.  This  operation  was  first  performed  by  the 
author  and  also  by  Dr.  F.  B.  Turck,  and  Kuhn’s  claims  of  priority  of 
sounding  the  pylorus  are  unfounded  (Hemmeter,  “ Die  Prioritat 
d.  Pylorus-Sonderung,”  “ Centralblatt  f.  innere  Medicin,”  1897, 
No.  2).  The  interesting  observation  of  a case  of  insufficiency, 
reported  by  Schiitz,  in  which  it  was  possible  to  distend  the 
stomach  by  means  of  C02  but  not  by  air,  so  that  by  the  increased 
irritation  of  the  mucous  membrane  of  the  pylorus  by  the  carbonic 
acid  gas  a contraction  of  the  annular  muscle  was  brought  about, 
but  with  the  forcing  in  of  air  the  stomach  did  not  become  distended, 
points  to  the  fact  that  different  degrees  of  insufficiency  occur.  If, 
5i 


774 


NEUROSES  OF  THE  STOMACH. 


as  easily  happens  in  a case  of  pyloric  insufficiency,  some  of  the 
contents  of  the  intestine  go  back  into  the  stomach,  causing  dys- 
peptic complaints  by  the  irritation  of  the  mucous  membrane  and 
neutralization  of  the  HC1,  this  can  be  recognized  by  testing  for 
bile. 

Therapeutics. — If  symptoms  of  irritation  of  the  intestine — 
namely,  diarrhea — are  absent,  only  dietetic  treatment  is  necessary. 
In  order  to  relieve  the  intestine  of  its  excessively  burdensome  task, 
we  must  prescribe  easily  digestible,  well-prepared  foods,  which 
are  to  be  carefully  masticated,  and  are  not  to  be  taken  too  hot  or 
too  cold. 

If,  on  the  other  hand,  complaints  such  as  diarrhea  appear,  we 
must  attempt,  in  addition  to  the  treatment  of  the  causal  disease,  to 
get  rid  of  the  insufficiency  by  means  of  massage,  internal  and  ex- 
ternal galvanization  and  faradization  applied  directly  to  the  pylorus 
by  the  author’s  method  (a  spiral  electrode  contained  within  a 
rubber  tube,  and,  after  introduction,  brought  into  contact  with  the 
pylorus,  as  demonstrated  by  X-rays),  douches,  and  eventually  also 
by  giving  strychnin,  gr.  3V,  t-  K If  flatulence  and  constipation 
arise  on  account  of  suppression  or  loss  of  hydrochloric  acid  secre- 
tion, which,  as  is  well  known,  has  a stimulating  effect  upon  the 
peristalsis  of  the  intestine,  and,  further,  acts  as  an  antiseptic,  then 
the  massage,  as  well  as  the  galvanization,  is  to  be  applied  also  to 
the  intestine,  and  dilute  HC1  should  be  administered  in  doses  of 
30  drops  largely  diluted  and  taken  after  meals  through  a tube  or 
the  double  Aaron  capsules.  In  all  other  indications  the  treatment 
must  be  directed  to  the  cause. 

ATONY  OF  THE  STOMACH  (Myasthenia  Gastrica;  Mechanical 
Insufficiency  of  the  Stomach). 

In  the  consideration  of  dilation  of  the  stomach  we  have  fully 
quoted  the  classifications  of  Riegel,  Schreiber,  Boas,  Naunyn,  and 
Rosenbach.  By  simple  atony  we  mean  that  combination  of  symp- 
toms in  which  there  exists  a disproportion  between  the  peristaltic 
work  the  stomach  has  to  perform  and  its  real  expelling  muscular 
force.  Objectively,  the  disease  makes  itself  known  by  the  fact 
that  the  ingesta  are  retained  in  the  stomach  beyond  the  normal 
time,  but  although  the  muscular  action  of  the  organ  is  weakened, 
the  food  is  eventually  expelled  into  the  duodenum.  By  this  it  is 
distinguished  from  the  mechanical  insufficiency  of  the  second 


ATONY  OF  THE  STOMACH. 


775 


degree,  the  pronounced  dilation,  in  which  the  food  is,  as  a rule,  per- 
manently retained  in  the  stomach,  and  only  exceptionally  reaches  the 
bowels.  Every  relaxation  of  the  muscular  wall  that  is  not  due  to  any 
pyloric  or  other  mechanical  obstruction  may  be  justly  designated  as 
an  atony.  In  simple  atony  the  stomach  is  not  considerably  enlarged 
in  the  empty  state,  but  only  becomes  so  with  increasing  burdening 
of  the  ingesta,  but  in  atonic  dilation  the  diseased  organ  remains  in 
a dilated  state  even  after  it  is  empty,  (i)  This  disease  may  occur 
as  a typical,  primary,  idiopathic  neurosis,  as  a consequence  of  per- 
sistent overloading  of  the  stomach  with  indigestible  food,  particu- 
larly with  liquids.  It  may  appear  very  suddenly  as  a transient  affec- 
tion, under  the  influence  of  violent  emotional  disturbances, — fright, 
anger,  grief,  etc., — occurring  in  this  way  principally  in  neurasthenic 
persons.  It  is  probable  that  gastric  myasthenia  may  be  inherited, 
and  may  be  transmitted  through  several  generations.  It  is  gener- 
ally referred  to  as  the  so-called  “ weak  stomach  ” in  some  families. 
The  abuse  of  alcoholic  liquors,  particularly  of  beer,  and  even  of 
coffee  and  soups,  has  been  assigned  as  a cause.  (2)  Myasthenia 
occasionally  appears  as  a reflex  neurosis  evolved  from  other  dis- 
eased organs — for  instance,  diseases  of  the  liver,  bile  passages, 
peritoneum,  intestines,  kidney,  and  sexual  apparatus.  (3)  It  occurs 
as  a secondary  neurosis,  constituting  part  of  the  symptoms  of  hys- 
teria, neurasthenia,  gastrospasm,  cardiospasm,  and  pylorospasm. 
It  has  been  observed  as  a complication  of  gastroptosis,  nervous 
dyspepsia,  ulcer,  and  chronic  gastritis.  There  are  a number  of 
intestinal  affections  which  may  be  complicated  with,  or  even  cause, 
atony.  These  are  stenosis  in  the  inferior  horizontal  portion  of  the 
duodenum,  or  stenosis  of  the  jejunum,  enteroptosis,  and  stenosis  of 
the  colon ; passive  congestions  and  enlargements  of  the  liver  and 
cholelithiasis  are  definitely  known  to  be  etiological  factors.  Criti- 
cally speaking,  we  designate  only  such  cases  gastric  atony  in  which 
the  organ  retains  its  normal  size  when  it  is  empty.  As  soon  as  the 
stomach  remains  permanently  enlarged,  even  when  it  is  empty,  it 
is  more  logically  classed  with  the  motor  insufficiency  of  the  second 
degree,  as  atonic  dilation.  As  we  have  seen  in  the  section  referred 
to,  Riegel  makes  a separate  class  for  stenotic  dilation. 

The  final  cause  of  simple  atony,  or  myasthenia,  is  malnutrition, 
overstretching  of  the  muscles  and  motor  nerves  of  the  stomach,  or 
an  early  and  progressed  exhaustion  after  undue  and  improper  ex- 
ertion. Occasionally  unknown  neurotrophic  influences  may  be  re- 
sponsible for  the  origin  of  atony.  As  secretion  and  absorption  depend 


776 


NEUROSES  OF  THE  STOMACH. 


more  or  less  upon  energetic  contraction  of  the  gastric  muscularis, 
they  are  in  most  cases  interfered  with  in  the  absence  of  effective 
muscular  tonicity.  The  gastric  contents  do  not  diminish  in  quantity 
as  rapidly  as  they  should,  and  in  consequence  of  this  the  gastric 
wall  is  excessively  expanded  by  the  prolonged  weight  of  food.  If 
fermentation  of  the  ingesta  occurs  with  abundant  formation  of  gases, 
the  expansion  will  be  still  greater.  The  gaseous  distention  may 
secondarily  produce  spasm  of  the  pylorus  and  cardia,  thus  adding 
another  etiological  factor  to  the  causation.  If  the  atony  is  very 
far  advanced  and  has  persisted  for  a long  time,  it  may  develop  into 
an  irreparable  dilation,  particularly  if  dietetic  and  hygienic  regula- 
tions are  disregarded.  We  have  observed  a number  of  cases  of 
this  kind,  in  which  permanent  dilation  was  developed  when  long- 
standing gastric  distress  was  left  unheeded.  Myasthenia — by 

diagnostic  methods  for  judging  the  motility — may  be  found  to  be 
very  pronounced,  and  still  remain  latent  and  unnoticed  even  by 
the  patient  for  a long  time. 

The  following  is  an  example  of  this  class  of  cases : 

Miss  S.,  aged  twenty-two,  a well-built  and  apparently  healthy  girl,  moving 
in  the  best  circles  of  social  life,  complains  of  only  one  symptom,  that  is  a 
severe  headache,  occurring  two  or  three  times  of  every  week,  and  lasting  for 
twenty -four  hours.  On  being  questioned  about  her  stomach,  she  asserts  that 
her  digestion  is  good,  appetite  excellent,  and  bowels  regular.  She  eats  all 
kinds  of  food  apparently  without  distress.  On  passing  the  tube  in  the  morn- 
ing, on  an  empty  stomach,  200  c.c.  of  a slightly  yellowish  mucous  liquid  were 
obtained  which  shows  free  HC1  by  Congo  paper.  The  next  day  she  was 
directed  to  take  the  double  test-meal.  One  hour  after  the  second  meal  the 
contents  were  drawn,  and  rice  and  egg  of  the  early  breakfast,  which  was  taken 
six  and  a half  hours  before,  were  still  present  in  her  stomach,  together  with 
a considerable  amount  of  mucus.  Total  acidity,  60  ; free  HC1,  20.  Subse- 
quently the  same  state  of  affairs  was  found  after  other  test-meals.  Peristole 
by  author’s  method  decidedly  impaired. 

The  striking  feature  of  this  case  is  that,  although  there  was  a pro- 
nounced gastric  atony,  the  patient  was  not  at  all  conscious  of  it,  and 
regularly  expressed  surprise  when  she  recognized  food  in  the  lavage 
that  had  been  taken  eight  to  twelve  hours  before.  It  is  very  prob- 
able that  such  cases  as  this  one  would  develop  the  unmistakable 
symptoms  of  myasthenia  in  a very  short  time  if  left  untreated.  The 
author  examined  100  members  out  of  a medical  class  of  140  stu- 
dents ; of  these,  five  had  gastric  atony  and  were  unaware  of  it. 
Superacidity  and  supersecretion  may  cause  cardiospasm  and 
pylorospasm,  and  subsequently  gastric  atony,  by  the  irritation 


SYMPTOMS  OF  GASTRIC  ATONY. 


777 


of  the  muscular  structures  of  the  orifices.  But,  reversely,  gastric 
atony  may  cause  superacidity  and  supersecretion  by  the  fact  that 
the  ingesta  are  retained  in  the  stomach  for  an  unduly  long  period, 
and  thereby  excite  the  gastric  glands  to  stronger  functioning. 
Stiller  and  Boas  assert  that  gastric  atony  rarely  develops  into  per- 
manent gastric  dilation.  The  subjective  symptoms  of  gastric 
atony  are  very  similar  to  those  of  gastritis  and  incipient  dilation. 
The  patients  complain  of  pressure  and  pain  in  the  head,  the  feeling 
of  pressure  and  distention  in  the  stomach,  a premature  sensation 
of  fullness  during  eating  by  which  the  appetite  becomes  appeased 
very  rapidly,  very  frequent  eructation,  and  persistent  constipation. 
The  feeling  of  pressure  is  intimately  associated  with  the  ingestion 
of  food.  When  the  stomach  is  empty,  the  patient  feels  quite  well. 
The  headache  is  very  frequently  observed,  together  with  the 
so-called  stomach  vertigo.  We  agree  with  Boas  that  this  so- 
called  gastric  vertigo  (Trousseau,  “ Gazette  des  Hopitaux,”  1862) 
is  much  more  frequently  found  in  atony  and  dilation  than  in  any 
other  gastric  disease.  The  feeling  of  pressure  and  distention  may 
persist  as  long  as  there  is  food  in  the  stomach : in  recent  cases, 
about  one  hour;  in  advanced  cases,  it  continues  from  one  meal  to 
the  other.  One  of  the  most  frequent  symptoms  is  eructation  of  air, 
which  generally  has  the  taste  of  the  food  that  has  been  last  taken. 
We  have  noticed  that  the  most  annoying  sensations  of  pressure  in 
the  advanced  cases  are  felt  after  breakfast,  at  a time  when  one  would 
presume  that  they  should  be  absent,  since  the  stomach  should  have 
been  rested  during  the  night.  The  duration  of  the  time  after  meals 
during  which  the  eructations  continue  is  generally  a good  indica- 
tion of  the  extent  and  degree  of  the  myasthenia.  In  some  cases, 
however,  we  may  be  confronted  with  typical  neurotic  regurgitation 
and  eructation,  that  has  existed  before  the  atony  developed,  and 
then  this  indication  is  invalid.  If  there  is  hyperacidity,  the  atony 
may  be  associated  with  attacks  of  vomiting,  and  pyrosis  is  gener- 
ally present.  The  constipation  is  undoubtedly  an  expression  of 
the  general  atony  of  the  entire  gastro-intestinal  tract. 

Objective  Symptoms. — The  most  important  distinguishing  sign 
between  simple  atony  and  dilation  consists  in  the  fact  that  the 
stomach,  in  the  former,  should  be  empty  in  the  morning,  when 
nothing  has  been  taken  since  the  previous  supper;  in  other  words, 
the  jejune  stomach  of  atony  contains  no  food  particles,  while  the 
stomach  in  a state  of  dilation  does  contain  them.  The  splashing 
sound  in  the  epigastric  region  is  absent  in  the  morning  with  simple 


77  8 


NEUROSES  OF  THE  STOMACH. 


atony,  but  it  is  present  in  dilation.  The  size  and  location  of  the 
stomach  vary  physiologically.  A myasthenic  stomach  yields  and 
distends  with  greater  readiness  when  it  is  filled  with  water  or  air 
than  a normal  stomach.  Boas  asserts  that  even  an  atonic  stomach 
may  react  more  normally  to  the  distending  force  of  water  and  air 
in  such  cases  in  which  the  superimposed  layers  are  swelled  and 
much  thickened  by  inflammatory  infiltration.  The  methods  of  in- 
vestigation and  diagnosis  which  we  have  found  useful  are,  in  addi- 
tion to  inspection,  palpation,  percussion,  and  auscultation,  the  dis- 
tention of  the  stomach  by  air  or  carbon  dioxid  gas,  the  Hemmeter 
intragastric  stomach-shaped  bag,  and  the  gastrodiaphane.  Very 
frequently  the  contour  of  the  greater  curvature  may  be  recog- 
nized on  the  outside  of  the  abdomen.  Palpation  may,  in  some 
cases,  instruct  us  concerning  the  limits  of  the  organ,  and  enable  us 
to  separate  it  from  adjacent  organs.  The  so-called  splashing  sound 
may  be  elicited  by  permitting  the  patient  to  drink  a glass  of  water, 
and  then,  placing  the  palm  of  the  left  hand  firmly  over  the  right 
hypochondriac  region,  and  by  gently  tapping  the  epigastrium  with 
the  right  hand,  the  sound  is  generally  very  evident  if  atony  is 
present.  In  most  cases  of  gastric  atony  a splashing  sound  can  be 
heard  with  binaural  stethoscope  on  shaking  the  stomach  from  the 
outside.  Dehio  has  given  a very  expedient  method  for  judging 
the  elasticity  of  the  gastric  walls  by  means  of  gradually  increasing 
quantities  of  water : at  first  ^ of  a liter  is  taken,  and  the  location 
of  the  greater  curvature  determined  ; then,  in  short  intervals,  of 
a liter  is  taken  at  three  successive  periods,  and  after  each  ^ of  a 
liter  increment  the  further  descent  of  the  greater  curvature  is  de- 
termined by  palpation  and  percussion,  and  the  niveau  of  the  water 
in  the  stomach  ascertained  by  holding  the  funnel  against  the  ab- 
dominal wall  and  observing  the  level  at  which  water  either  flows 
into  or  out  of  the  organ.  A healthy  stomach  will  not  reach  the 
line  of  the  umbilicus  under  these  conditions,  while  an  atonic 
stomach  may  have  transgressed  far  beyond  it.  Auscultation  elicits 
sounds  only  when  the  stomach  contains  liquids  or  shortly  after 
they  are  ingested.  It  is  best  to  use  the  binaural  stethoscope  in 
these  cases,  as  then  both  hands  are  free  to  palpate  and  move  the 
stomach  to  obtain  the  percussion-sound.  Boas  holds  that  we  have 
no  reliable  method  to  test  the  gastric  elasticity  and  tonicity  (/.  c., 
p.  76).  We  consider  that  our  method  of  recording  the  gastric 
peristalsis  on  the  kymograph,  as  described  in  the  first  part  of  this 
book,  is  also  an  excellent  method  for  investigating  the  gastric 


SYMPTOMS  OF  GASTRIC  ATONY. 


779 


tonicity,  for,  as  our  stomach-shaped  intragastric  bag  on  being  dis- 
tended gradually  fills  out  the  lumen  of  the  stomach  exactly,  the 
indications  of  pressure  which  are  obtained  on  the  kymograph  are 
reliable  representations  of  the  tonicity.  Moreover,  we  have  experi- 
mented with  an  electrodiaphane  contained  within  our  stomach-bag, 
so  that  when  the  bag  was  distended  in  a dark  room,  the  gradual 
descent  of  the  greater  curvature  could  very  plainly  be  seen.  By 
reference  to  the  description  of  the  apparatus  on  pages  76  to  78,  it 
will  become  evident  that  we  can  easily  determine  the  amount  of 
air  or  water  with  which  the  bag  is  distended  within  the  stomach  ; 
so  with  this  method,  which  in  a modified  form  was  also  used  inde- 
pendently, after  our  first  publication,  by  Professor  Moritz,  of 
Munich,  for  studying  the  gastric  motility,  we  may  determine  also 
the  elasticity  and  tonicity  of  the  stomach. 

Percussion. — In  percussion  of  the  stomach  we  must  attempt  to 
define  its  four  limits — viz.,  the  upper,  lower,  right,  and  left  limits. 
The  lower  limit  may,  on  percussion,  be  confounded  with  the  trans- 
verse colon  if  the  latter  still  be  in  its  normal  position.  The  way  out 
of  this  difficulty  is  to  fill  the  transverse  colon  with  water,  which 
gives  a dull  percussion-note  through  the  abdominal  wall,  while  the 
stomach  may  be  distended  with  air  or  gas,  giving  a clear  tympanitic 
sound.  When  both  the  stomach  and  the  colon  are  filled  with  gas 
or  with  solid  material  simultaneously,  it  is  almost  impossible  to  dis- 
tinguish between  the  two  by  percussion.  It  is  best  to  evacuate  the 
colon  and  fill  the  stomach  with  water,  or  vice  versa  to  evacuate 
the  stomach  and  fill  the  colon  with  water.  In  our  clinic  we  use  the 
rubber  stomach-shaped  intragastric  bag  methodically,  and  when  it 
is  distended,  there  is  no  difficulty  at  all  to  percuss  and  palpate  the 
stomach.  The  determination  of  the  upper  border  of  the  stomach 
is,  in  our  experience,  no  easy  matter,  since  there  are  no  very  striking 
differences  in  the  percussion-note  of  the  lower  edge  of  the  left 
lung  and  the  highest  portion  of  the  gastric  fundus  which  is  nor- 
mally covered  over  anteriorly  by  the  lung  in  inspiration.  The  upper 
border  may  be  best  determined  by  filling  the  stomach  with  water 
and  then  percussing  over  the  left  lung  along  the  parasternal  line 
from  above  downward.  Pacanowski  ( “ Deutsche  Arch.  f.  klin. 
Medicin,”  Bd.  XL,  S.  342)  gives  the  following  determinations  of  the 
upper  limit  of  the  stomach  : In  the  left  parasternal  line  it  is  at  the 

lower  edge  of  the  fifth  rib  or  in  the  fifth  intercostal  space.  In  the 
left  mammillary  line  the  limit  is  in  the  fifth  intercostal  space  extend- 
ing to  the  sixth  rib,  or  into  the  seventh  rib.  In  the  anterior  left 


NEUROSES  OF  THE  STOMACH. 


780 

axillary  line  the  upper  limit  is  at  the  lower  edge  of  the  seventh  or 
eighth  rib,  rarely  under  the  eighth  rib.  The  determination  of  the 
left  and  right  gastric  limits  seems  most  impractical  to  us,  and  not 
of  diagnostic  value,  because  here  we  may  confound  the  percussion- 
notes  of  organs  superimposed  upon  the  stomach. 

In  our  experience  a clear  conception  of  the  size  and  location  of 
a normal  stomach  can  be  obtained  only  when  it  is  distended  by 
gas,  air,  or  water.  Naturally,  this  can  not  be  done  if  there  is 
suspicion  of  recent  ulcer  or  perigastritis.  In  such  cases  we  now 
coat  the  inside  of  the  stomach  with  bismuth  subnitrate  with  a 
gastric  powder-blower,  and  observe  the  size  of  the  organ  by  means 
of  the  X-  rays  and  skiagraph — the  rays  being  cut  off  by  the  bismuth. 
The  powder  can  readily  be  blown  in  through  an  ordinary  soft 
stomach-tube.  We  have  already  spoken  of  the  value  of  the  elec- 
trodiaphane  in  ascertaining  the  size  and  location  of  the  stomach, 
and,  notwithstanding  numerous  objections,  consider  the  method 
practical. 

After  all,  the  most  convenient  method  of  determining  gastric 
atony,  and  that  which  is  available  for  every  practitioner,  is  by  means 
of  the  double  test-meal  used  in  our  clinics.  (See  pp.  120  and  121.) 
According  to  Boas’  suggestion,  a full  meal  is  preferably  given  in 
the  evening,  when  a healthy  stomach  will  show  no  demonstrable 
signs  of  food  particles  the  next  morning.  It  should  not  be  forgot- 
ten, in  this  connection,  that  even  healthy  stomachs  may  contain 
mucus,  gastric  juice,  and  bile  in  the  morning  before  food  is  taken. 
The  chemical  analysis  of  the  stomach-contents  in  gastric  atony 
yields  no  results  useful  for  diagnosis,  because  the  state  of  the 
secretion  varies  considerably  according  to  the  degree  of  the 
mechanical  insufficiency.  In  the  primary  stages  of  gastric  atony 
superacidity  is,  as  a rule,  present;  at  other  times  the  secretions 
may  be  normal,  and,  in  the  latter  stage,  we  may  have  subacidity  or 
even  achylia.  The  drawn  stomach-contents  in  atony,  on  settling 
in  a glass  vessel,  do  not  show  the  three  characteristic  layers  of 
solid,  liquid,  and  froth  which  are  usually  found  in  the  drawn  con- 
tents of  the  dilated  stomach.  We  have  never  observed  processes 
of  fermentation  in  simple  atony.  The  secretion  of  pepsin  and  ren- 
nin  is  generally  found  to  be  proportionate  to  the  secretion  of  HG1. 
Thirst  is  normal,  and  the  amount  of  urine  passed  is  not  reduced. 
Disturbances  in  nutrition  may  gradually  develop  if  the  diet  is  inap- 
propriate or  if  the  patient  refuse  to  eat  sufficiently  for  fear  of 
causing  gastric  distress. 


TREATMENT  OF  ATONY. 


78i 


The  course  of  gastric  atony  is  a chronic  one,  and  the  symptoms 
are  subject  to  many  deviations.  Stiller  and  Boas  hold  that  gastric 
atony  comparatively  rarely  develops  into  dilation.  Notwithstand- 
ing this,  the  disease  generally  produces  considerable  systemic 
weakness.  A variety  of  nervous  disturbances  accompany  the 
malady. 

Prognosis. — In  recent  cases  the  prognosis  is  favorable,  provided 
that  they  are  systematically  treated  and  the  fundamental  causatives 
of  the  disease  can  be  removed  ; but  in  pronounced  atony,  and  that 
of  long  standing,  complete  recovery  is  rare. 

Diagnosis. — Gastric  atony  and  myasthenia  may  be  confounded 
with  chronic  gastritis,  nervous  dyspepsia,  dilation,  and  megalogas- 
tria.  In  chronic  gastritis  the  stomach  is  not  enlarged,  as  a rule, 
since  the  motility  is  good  ; excess  of  mucus  is  common  in  gastritis 
and  rare  in  atony  ; but  as  atony  may  predispose  to  gastritis,  the  two 
affections  may  sometimes  exist  side  by  side.  Nervous  dyspepsia 
is  characterized  by  a great  deviation  and  uncertainty  in  the  symp- 
toms ; even  the  motility  may  be  at  times  seemingly  much  affected, 
but  at  others,  if  the  case  be  strictly  watched,  the  motility  will  be 
found  to  be  perfect.  In  nervous  dyspepsia  there  are  painful  points 
in  the  district  supplied  by  the  great  abdominal  sympathetic  plexuses 
— the  celiac,  solar,  and  hypogastric.  The  painful  spots  are  rare  in 
simple  atony.  Nervous  dyspepsia  and  atony  may  exist  simulta- 
neously, and  one  may  cause  the  other;  in  such  cases  it  will  be  diffi- 
cult to  determine  which  is  the  primary  disease.  The  differential 
diagnosis  between  dilation  and  simple  atony  should  present  no 
difficulties  when  modern  methods  of  determining  the  size  and  capac- 
ity and  motility  of  the  stomach  are  used  (pp.  98  to  1 12);  neither 
should  there  be  any  difficulty  in  distinguishing  atony  from  megalo- 
gastria,  since  the  latter  is  not  a disease,  but  simply  a condition  of 
big  stomach,  which  performs  its  functions  normally. 

Treatment. — The  most  important  part  of  the  management  of 
gastric  atony  is  prophylaxis,  which  includes  the  avoidances  of  all 
known  causes  of  the  affection  : defective  teeth,  irregular  mode 
of  life,  hasty  eating,  and  abnormal  burdening  of  the  stomach  with 
food  and  drink,  constipation,  as  well  as  the  frequent  abuse  of 
purgatives.  Even  when  the  distinct  cause  of  the  malady  is  not 
known,  one  will  do  best  to  prevent  the  full  development  of  myas- 
thenia by  rational  dietetic  and  hygienic  treatment  before  functional 
disturbances  become  manifest.  We  have  already  remarked  that 
atony  may  be  inherited.  Whenever  this  is  noticed,  such  persons 


782 


NEUROSES  OF  THE  STOMACH. 


should  be  particularly  guarded  and  careful  in  the  selection  ol 
their  diet.  There  are  a number  of  constitutional  diseases  which, 
in  our  experience,  undoubtedly  predispose  to  this  state.  These 
are  tuberculosis,  syphilis,  anemia,  chlorosis,  and  cholelithiasis.  It 
is  present  also  after  exhaustive  hemorrhages,  and  is  particularly 
ominous  when  the  condition  occurs  after  hemorrhages  from  gastric 
ulcer. 

Typhoid  fever  has,  in  our  experience,  frequently  been  followed 
by  gastric  atony  ; the  same  is  true  of  infectious  diseases  generally, 
particularly  scarlet  fever,  malaria,  diphtheria,  and  influenza.  We 
have  also  noticed  gastric  atony  follow  a number  of  operations  for 
abdominal  tumors,  and  particularly  ovarian  neoplasms.  It  is  very 
probable  that  the  relaxation  of  the  gastric  walls  is  here  largely  due 
to  mechanical  causes,  similar  to  that  which  occurs  after  very  fre- 
quent and  rapidly  consecutive  pregnancies.  In  all  of  these  instances 
the  abdominal  walls  do  not  regain  their  tonicity.  We  have  described 
this  condition  fully  in  the  section  on  Gastroptosis.  Prophylaxis 
consists  in  appropriate  hygienic  living,  much  sleep  (at  least  nine 
hours  in  the  twenty-four),  and  strengthening  of  the  abdominal  mus- 
cles— the  latter  is  one  of  the  most  important  elements,  not  only  in 
prophylaxis,  but  also  in  the  treatment  of  atony.  The  training  of 
the  abdominal  muscles  should  be  carried  out  according  to  rules  laid 
down  in  Illoway’s  work  on  “ Constipation,”  and  Sandow’s  book  on 
physical  culture.  The  treatment  proper  of  a fully  developed  atony 
must  have  regard  for  the  fundamental  cause — for  instance,  in 
syphilis  specific  treatment  will  be  the  only  proper  course  to  pur- 
sue; in  anemia  we  must  have  recourse  to  preparations  of  iron 
which  have  no  direct  deleterious  effect  upon  the  mucosa.  Among 
these  preparations  we  prefer  the  iron  albuminates  and  peptonates, 
also  ferratin  and  extract  of  bone-marrow.  With  pronounced 
enteroptosis,  particularly  in  women,  abdominal  gymnastics  can 
not  be  effectively  carried  out,  on  account  of  the  great  exhaustion 
of  the  patient. 

In  some  cases  of  this  type  palliative  results  may  be  obtained  by 
abdominal  massage,  faradization  of  the  abdominal  muscles,  baths, 
and,  last  but  not  least,  a well-fitting  abdominal  bandage.  In  a few 
cases  it  will  not  be  possible  to  trace  any  cause  whatever,  though 
even  in  these  it  is  well  to  carefully  study  the  alimentary  tract  itself 
before  giving  up  the  hope  of  determining  the  etiology.  The  most 
important  factors  of  direct  treatment  are  : (1)  diet,  (2)  hydriatic, 
(3)  electric  procedures,  (4)  massage,  and  (5)  medicines.  The  prin- 


DIETETIC  MANAGEMENT  OF  ATONY. 


783 


ciple  underlying  the  diet  in  gastric  atony  is  that  of  frequent  and 
very  small  meals,  which,  although  quite  nutritious  and  digestible, 
must  not  be  voluminous.  The  diet  should,  as  a rule,  consist  of  fats, 
carbohydrates,  and  proteids,  mixed.  If  there  is  an  excess  of  HC1, 
there  is  no  objection  to  increasing  the  proteid  food,  but  in  doing 
so  it  is  well  to  watch  the  ratio  of  the  ethereal  to  the  combined 
sulphates,  and  the  indican  in  the  urine.  If  the  ratio  of  the  pre- 
formed to  the  combined  sulphates  is  very  high,  and  there  is  an 
excess  of  indigo  in  the  urine,  it  is,  in  our  experience,  worth  the  trial 
of  adding  more  fats  and  artificially  prepared  amylaceous  foods,  such 
as  dextrinized  flours,  etc.,  for  it  has  been  found  that  the  general 
symptoms,  as  well  as  the  aforementioned  indications  in  the  urine 
(in  rare  instances,  in  which  proteid  diet  does  not  agree  in  hyper- 
acidity), will  improve  if  the  proteids  are  cut  down  and  the  other 
food  substances  increased.  Together  with  this  diet  in  hyper- 
acidity the  use  of  alkalies,  magnesia  usta,  sodium  bicarbonate,  etc., 
and  of  ptyalin,  or  of  malt  or  taka-diastase,  is  sometimes  service- 
able. The  diet  which  we  recommend  for  gastric  atony  is  the  fol- 
lowing : 

8 A.  m. — 250  gm.  of  bouillon,  oatmeal,  or  100  gm.  of  milk  and  100  gm.  of  tea 
or  coffee. 

10  a.  m. — One  soft-boiled  egg,  or  70  gm.  of  finely  scraped  tenderloin,  either 
raw  or  broiled,  and  20  gm.  of  toast. 

12  m. — A broiled  sweetbread,  or  150  gm.  of  broiled  oysters,  or  little-neck 
clams,  or  100  gm.  of  finely  scraped  beef  slightly  fried  in  butter;  200  gm. 
of  potato  puree,  and,  if  hyperacidity  is  present,  we  give  half  a wineglassful 
of  some  reliable  malt  extract. 

3 p.  m. — 200  gm.  of  Mosquera’s  beef  chocolate  (P.,  D.  & Co.). 

6.30  p.  m. — 60  gm.  of  scraped  raw  ham,  or  the  same  amount  of  fried  perch  or 
carp  ; 50  gm.  of  toast,  and  30  gm.  of  butter. 

10  p.  m. — 100  gm.  of  some  approved  light  Moselle  wine. 

This  list  calls  for  six  small  meals  in  the  day,  and  is  modeled 
after  those  recommended  in  European  text-books.  We  have  found 
that  very  frequently  the  atonic  stomach  is  unable  to  evacuate  one 
meal  before  another  is  taken.  This  danger  should  be  studiously 
avoided,  and  if  detected,  it  is  best  to  allow  only  two  meals  a day — 
a breakfast  and  a late  dinner — according  to  principles  laid  down  in 
the  chapter  on  the  Use  and  Abuse  of  Rest,  etc. 

In  the  section  on  Dietetics  we  have  given  other  diet-lists  suitable 
for  this  affection.  A number  of  competent  authors  consider  the 
treatment  of  atony  and  a chronic  dilation  together  in  the  same 


7§  4 


NEUROSES  OF  THE  STOMACH. 


chapter.  Personally,  we  draw  a very  sharp  distinction  between 
these  two  affections  and  their  treatment.  The  therapy  of  dilation 
is  considered  in  the  chapter  devoted  to  this  subject. 

The  total  quantity  of  liquids  should  be  limited  to  I y2  liters  a 
day.  This  includes  the  soups,  coffee,  tea,  milk,  alcoholic  beverages, 
and  water.  Alcohol,  except  in  the  quantities  suggested  in  the  diet- 
list,  should  not  be  allowed.  Purgatives  and  narcotics  are  forbidden. 
If  the  thirst  is  intense,  which,  however,  is  rarely  the  case,  water  may 
be  introduced  by  enema.  When  milk  is  well  digested,  and  no 
idiosyncrasy  exists  against  it,  so-called  milk  cures  may  have  a bene- 
ficial effect.  There  is  no  doubt  that  an  exclusive  milk  diet  insures 
rest  and  is  very  sparing  upon  the  stomach,  but  it  is  a two-edged 
sword.  We  have  seen  cases  in  which  the  atony  undeniably 
became  aggravated  by  the  milk  diet.  The  diet  must  vary  also  with 
the  amount  of  HC1  secreted.  With  increased  secretion  of  HC1  the 
meats  may  be  permitted  to  prevail.  All  meats  should  be  run  through 
the  meat-chopper.  Eggs  in  all  forms  are  permissible  in  this  state. 
When  the  secretion  of  HC1  is  diminished,  we  permit  the  use  of  spin- 
ach, carrots,  beans,  cauliflower,  and  asparagus.  All  vegetables 
should  be  cooked  and  given  in  the  form  of  purees ; among  these 
are  the  potato,  rice,  sago,  pea,  and  bean  puree.  The  use  of  beer 
should  be  forbidden  or  very  greatly  limited ; we  do  not,  as  a rule, 
forbid  small  doses  of  good  wine.  Where  good  wine  can  not  be 
obtained,  it  is  safest  not  to  prescribe  wine  of  a doubtful  quality, 
but  to  order  dilute  whisky  or  brandy.  Constipation  should  be 
met  with  proper  diet,  and  medicines  should  not  be  used  unless 
they  are  positively  unavoidable.  We  have  already  spoken  of  the 
diet  best  suited  for  constipation.  In  very  stubborn  and  pro- 
tracted cases  glycerin  suppositories  and  water  injections  will  be 
more  effective  than  medicines  given  by  the  mouth.  (See  Illoway 
on  “ Constipation,”  and  E.  A.  Ewald,  “ Ueber  d.  habituelle  Obsti- 
pation u.  ihre  Behandlung,”  1897.)  An  advantage  is  gained  by 
going  to  stool  at  a definite  hour.  There  are  cases,  however,  in 
which  a natural  stool  that  occurs  every  two  or  even  every  three 
days  spontaneously  is  much  better,  and  will  do  more  toward 
gradual  recovery  from  the  evil  of  constipation  than  a stool  pro- 
duced artificially  every  day.  Where  the  patient  insists  on  medi- 
cine, and  it  is  really  unavoidable,  aloes,  strychnin,  and  cascara 
sagrada  are  most  favored  by  the  author.  (The  syrup  cascara, 
“ active,”  Clinton  Pharm.  Company,  and  the  elixir  and  fluid  ex- 
tract of  cascara  sagrada,  P.,  D.  & Co.,  or  S.  & D.,  can  be  safely 


MASSAGE  AND  MEDICINAL  TREATMENT.  785 

recommended.)  Podophyllin  in  the  form  of  pills  is  a proper  medi- 
cation. The  following  formula  is  the  one  which  we  favor: 


IJ . Podophyllin, 0.26  gr.  iv 

Strychnin,  sulphate,  0.2  gr. 

Glycyrrhizoe,  q.  s. 

F.  pil.  No.  xii.  M. 

SlG. — One  pill  before  supper  and  one  at  bedtime.  Dose  increased  to  two  pills 
the  next  day  if  necessary. 

The  compound  extract  of  rhubarb  is  also  an  effective  combi- 
nation ; but  calomel,  colocynth,  jalap,  and  scammony,  and  the  very 
concentrated  purgative  waters,  such  as  the  Hunyadi  Janos,  the 
Rubinat-Condal,  aftd  Veronica,  must  be  avoided  if  possible.  Boas, 
in  contrast  to  other  authors,  states  that  lavage  is  not  only  unneces- 
sary, but  harmful  in  simple  atony,  because  stagnation  does  not 
occur  in  this  disease  and  there  is  therefore  no  necessity  for  washing 
out  the  stomach.  I employ  lavage,  however,  not  to  combat  any  pre- 
sumable stagnation,  but  as  a sort  of  intragasjtric  hydropathic  mas- 
sage. For  this  purpose  I use  an  intragastric  douche  with  hot 
and  cold  water  alternating.  The  instrument  devised  by  F.  B.  Turck 
is  useful  for  this  purpose.  The  electrical  treatment  with  which 
Einhorn  has  achieved  remarkable  results  is  undeniably  a valuable 
means  of  therapeusis  in  this  affection.  It  may  be  applied  externally 
with  large  felt-covered  plates  applied  to  the  abdomen  directly,  or 
by  the  intragastric  electrode.  We  usually  apply  the  current  fifteen 
minutes  and  repeat  it  daily  for  three  weeks.  Massage  should  be 
applied,  not  only  to  the  stomach,  but  to  the  entire  abdomen.  The 
method  of  application  (concerning  abdominal  massage,  see  Illoway 
on  “ Constipation  Hoffa,  “ Technik  d.  Massage,”  Stuttgart,  Enke, 
1893,  also  Penzoldt  and  Stintzing,  “ Handbuch,”  Bd.  iv,  S.  34-39) 
is  described  on  pages  290-299. 

Treatment  by  Medicines. — The  only  drug  which  one  may  depend 
on  for  improving  the  gastric  tonicity  is  strychnin.  When  atony  is 
accompanied  with  suppression  of  gastric  juice  and  anacidity,  we 
can  practically  associate  it  with  HC1  and  gentian  in  the  following 
manner : 

J&  • Strychnin  sulphate, 0.02  gr.  ^ 

Dil.  hydrochloric  acid, . ......15.6  f 3 iv 

Elixir  of  gentian, q.  s.  180.0  f^vj.  M. 

SlG. — One- half  of  an  ounce  in  two  ounces  of  water,  after  meals,  through  a glass 
tube,  three  times  a day. 


786 


NEUROSES  OF  THE  STOMACH. 


When  there  is  excess  of  HC1,  it  is  well  to  combine  the  strychnin 
in  the  following  manner: 


Strychnin  sulphate, 

gr-  A 

Bismuth  salicylate, 

• 7-5 

3b 

Sodium  bicarbonate, 

• 1125 

3^ 

Magnes.  ustae, 

. 4.0 

3i 

Peppermint  water  enough  to  make  . 

. 180.0 

Zvi- 

Sig. — A tablespoonful  in  a wineglassful  of  water  after  each  meal  t.  i.  d. 

Creosote  has  been  recommended  by  Klemperer  (“  Berlin,  klin. 
Wochenschr.,”  1889,  No.  n)  and  A.  Pick  (“Vorl.  fiber  Magen-  u. 
Darmkrankh.,”  1895),  but  Fleischer  has  found  that  the  motility  is 
still  more  reduced  under  creasote,  and  in  the  author’s  experience  it 
proved  useless.  Ergotin,  which  is  recommended  by  Leube,  is,  in 
my  opinion,  a dpubtful  remedy  for  this  purpose.  Ichthyol  has 
been  claimed  by  Pick  to  benefit  atony,  particularly  when  it  is  asso- 
ciated with  fermentative  processes  in  the  bowel.  In  severe  cases 
of  gastric  atony  with  recurrent  gastric  distress  we  have  had  very 
gratifying  results  by  rectal  feeding  for  from  six  to  eight  days,  and 
total  exclusion  of  food  from  the  stomach  : that  is,  we  treated  the 
atony  as  we  would  treat  a severe  gastric  ulcer.  The  good  results 
were  permanent.  During  the  period  of  rectal  feeding  the  patient 
must  remain  in  bed. 


LITERATURE  ON  NERVOUS  DISEASES  OF  THE  STOMACH. 

1.  Adler  and  Stern,  “ Berl.  klin.  Wochenschr.,”  1889,  Nr.  33- 

2.  Alt,  Konrad,  “ Ueber  das  Bestehen  von  Neurosen  und.  Psychosen  auf 
dem  Boden  von  chronischen  Magenkrankheiten,”  “ Archiv  f.  Psychiatrie  u. 
Nervenkrankheiten,”  Bd.  xxiv,  1892. 

3.  Alvermann,  “ Die  nervose  peristaltische  Unruhe  des  Magens  und 
Darms,”  Dissert.,  Bonn,  i895~’96. 

4.  Arany,  S.  A.,  “ Ueber  Dyspepsia  nervosa  und  was  als  solche  diagnosticirt 
wird,”  “Ungar.  med.  Presse,”  1898,  in,  706-711. 

5.  Bamberger,  “ Tetanie  bei  Magendilatation,”  Bericht  der  “Contracture 
Mortelle  d’Origine  Gastrique,”  “ Gaz.  Hebdom.,”  1889. 

6.  Bentejac,  “These  de  Paris,”  1888. 

7.  Berlizheimer,  “ Ueber  einen  Fall  von  Magentetanie,”  “Berl.  klin.  Woch- 
enschr.,” 1897,  xxxiv,  773-775. 

8.  Biernacki,  “ Berl.  klin.  Wochenschr.,”  1891,  Nr.  25  u.  26. 

9.  Boas,  “ Ueber  periodische  Neurosen  des  Magens,”  “ Deutsche  med. 
Wochenschr.,”  1889. 

10.  Bourneville  et  Seglas,  “ Du  Merycisme,’-  “ Arch,  de  Neurologie,”  Paris, 
1883. 

11.  Bouveret,  L.,  “ Traite  des  Maladies  de  l’Estomac,”  Paris,  1893,  p.  654. 


LITERATURE  ON  GASTRIC  NEUROSES.  787 

12.  Bouveret  et  Devic,  “ Recherches  Cliniques  et  Experimentales  sur  la 
Tetanie  d'Origine  Gastrique,”  “ Revue  de  M<5d.,”  1892,  xn. 

13.  Brieger,  “ Deutsche  med.  Wochenschr.,”  1880,  Nr.  14. 

14.  Briigelmann,  W.,  “ Ueber  Hemicrania  gastrica,”  “ Berl.  klin.  Wochen- 
schr.,” 1883. 

15.  Buch,  “ Wirbelweh  eine  neue  Form  der  Gastralgie,”  “ Petersb.  med. 
Wochenschr.,”  1889. 

16.  Burkart,  “ Zur  Pathologie  der  Neurasthenia  gastrica,”  Bonn,  1892. 

17.  Cahn,  “ Deutsches  Archiv  f.  klin.  Med.,”  1884,  S.  402. 

18.  Cantarono,  G.,  “ Neurolog.  Centralbl.,”  Bd.  iv,  1885. 

19.  Cartier,  “Action  de  la  Feinture  de  Sode  Centre  le  Vomissement,” 
“ L’Union  Med.,”  1889. 

20.  Chantemesse  et  Le  Noir,  “ Nevralgies  Bilaterales  et  Dilatation  de  l’Es- 
tomac,”  “ Arch.  G6n.  de  Med.,”  1885. 

21.  Charcot,  “ Des  Crises  Gastriques  Tabetique  avec  Vomissements  Noirs,” 
“ Gaz.  Med.  de  Paris,”  Sept.,  1892. 

22.  Charcot,  “ Letjons  sur  les  Maladies  du  Systeme  Nerveux,”  1886. 

23.  Claus,  “ Hysterisch  onbedwing  baar  braken  hyprotherapie,”  “ Medisch. 
Weekblad,”  1896,  30,  v. 

24.  Cordes,  “ Die  Platzangst, — Symptom  einer  Erschopfungsneurose,” 
“ Arch.  f.  Psych.,”  Bd.  ill,  1872. 

25.  Cordes,  “ Einiges  iiber  Platzangst,”  “ Archiv  f.  Psych.,”  Bd.  x,  1880. 

26.  Debove,  “ Crises  Gastriques  non  Fabetiques,”  “ Bull,  de  la  Soc.  Med. 
des  Hop.,”  1889. 

27.  Dehio,  “ Singultus  als  Reflexneurose,”  “ Berl.  klin.  Wochenschr.,”  1889. 

28.  Delamarre,  “ Des  Crises  Gastriques  dans  l’Ataxie  Locomotrice,”  “These 
de  Paris,”  1866. 

29.  Demange,  “ Revue  de  Medecine,”  1892. 

30.  De  Sere,  L.,  “ Du  Relachement  du  Pylore,”  “ Gaz.  des  Hop.,”  1864,  No. 
62. 

31.  Doyen,  “ Les  Spasmes  du  Pylore,  ses  Rapports  avec  l’Hyperstenie  Gas- 
trique,” “ Med.  mod.,”  Paris,  1897,  vm. 

32.  Dubois,  “ Crises  Gastriques  dans  l’Ataxie  Locomotrice,”  “ These  de 
Paris,”  1888. 

33.  Ebstein,  “ Deutsches  Archiv  f.  klin.  Med.,”  Bd.  xxvi,  S.  295. 

34.  Edinger,  “ Deutsches  Archiv  f.  klin.  Med.,”  1881. 

35.  Edlefsen,  “Ueber  Husten  und  Magenhusten,”  “Deutsches  Archiv  f. 
klin.  Med.,”  Bd.  xx. 

36.  Edwards,  L.  B.,  “Gastralgia:  Its  Forms,  Recognition,  and  Treatment,” 
“ Practice,”  Richmond,  1897,  xi,  62-74. 

37.  Einhorn,  Max,  “A  Case  of  Dysphagia  with  Dilation  of  the  Esopha- 
gus,” “ Med.  Record,”  1888. 

38.  Einhorn,  “ Eine  neue  Methode  der  directen  Magenelektrisation,”  “ Berl. 
klin.  Wochenschr.,”  1891. 

39.  Einhorn,  “Weitere  Erfahrung  iiber  die  directe  Elektrisation  des  Ma- 
gens,”  “ Zeitschr.  f.  klin.  Med.,”  1893. 

40.  Erb,  “ Handbuch  der  Elektrotherapie,”  2.  Aufl.,  Leipzig,  1886. 

41.  Erb,  “ Ueber  die  wachsende  Nervositat  unserer  Zeit,”  Prorectoratsrede, 
Heidelberg,  1893. 


;88 


NEUROSES  OF  THE  STOMACH. 


42.  Ewald,  “ Neurasthenica  dyspeptica,”  “ Verhandlungen  des  Congresses 
fiir  innere  Medicin,”  1884. 

43.  Ewald,  “ Enteroptose  und  Wanderniere,”  “ Berl.  klin.  Wochenschr.,” 
1890. 

44.  Ewald,  “ Some  Forms  of  Gastralgia,”  “ Internat.  Clin.,”  Philadelphia, 
1898,  11. 

45.  Fenwick,  “ On  Atrophy  of  the  Stomach  and  on  Nervous  Affections  of 
the  Digestive  Organs,”  London,  1880. 

46.  Fenwick,  “ Hyperacid  Dyspepsia,”  “ Med.  Press  and  Circ.,”  London, 
1897,  LXIV. 

47.  Fenwick,  “ Paroxysmal  Hyperacidity  in  Children  Simulating  Migraine,” 
“ London  Lancet,”  January  8,  1898. 

48.  Fenwick,  “ Hyperesthesia  of  the  Mucous  Membranes  of  the  Stomach,” 
“Med.  Press  and  Circ.,”  London,  1898,  lxv,  327. 

49.  Fenwick,  “ Ueber  spasmodische  Strictur  der  Cardiaoffnungdes  Magens,” 
“Wien.  med.  Bl.,”  1898,  XXI,  327-344. 

50.  Ferrari,  E.,  “Ectasia  e tetania  gastrica,”  “ Practico,”  Firenzo,  1897-98, 

in. 

51.  Fleiner,  “Ueber  die  Veranderungen  des  Nervensystems  bei  Addison- 
scher  Krankheit,”  “ Zeitschr.  f.  Nervenheilk.,”  1892. 

52.  Fleiner,  “ Ueber  die  Behandlung  einiger  Reizerscheinungen  und  Blut- 
ungen  des  Magens,”  “Verhandlungen  des  XII.  Congresses  f.  innere  Medicin,” 
Wiesbaden,  1893. 

53.  Fleiner,  “ Erfahrungen  fiber  die  Therapie  der  Magenkrankheiten,” 
“ Sammlung  klin.  Vortrage,”  1894,  Nr.  103. 

54.  Fleiner,  “ Ueber  Neurosen  gastrischen  Ursprungs,  mit  besonderer 
Beriicksichtigung  der  Tetanie  und  ahnlicher  Krampfanfalle,”  “Archiv  f.  Ver- 
dauungskrankh.,”  Bd.  1,  1895. 

55.  Flemming,  “ Ueber  Pracordialangst,”  “Allgem.  Zeitschr.  f.  Psychiatrie,” 
Bd.  v,  1848. 

56.  Fothergill,  cf.  Krakauer,  “ Der  Chron.  Morb.  Brightii  der  atherom. 
Process  und  das  Blut  in  ihren  Wechselbeziehungen,”  Berlin  und  Neuwied, 
1892. 

57.  Frankl-Hochwart,  V.,  “ Die  Tetanie,”  Berlin,  1889. 

58.  Freund,  E.,  “ Ueber  Intoxications  erythyme,”  “Wien.  med.  Wochen- 
schr.,” 1894. 

59.  Fiirbringer,  “Ueber  Magenschwache,”  “ Deutsche  med.  Zeitung,”  1893. 

60.  Gans,  Edg.,  “IX.  Congress  f.  innere  Medicin,”  Wiesbaden,  1890. 

61.  Garrigues,  “Des  Dyspepsies  Hypo  et  Hypersteniques,”  These  de  Mont- 
pelier, 1896. 

62.  Gassner,  “ Ueber  die  bei  Dilat.  ventric.  vorkommenden  tonischen 
Muskelkrampfe  und  epileptiformen  Anfalle,”  Inaug. -Dissert.,  Strassburg,  1868. 

63.  Geigel  und  Abend,  “ Die  Salzauresecretion  bei  Dyspepsia  nervosa,” 
“ Virchow’s  Archiv,”  Bd.  cxxx. 

64.  Gerhardt,  D.,  “ Zur  Lehre  von  der  Achylia  gastrica,”  “Berl.  klin. 
Wochenschr.,”  1898,  xxxv,  765-768. 

65.  Glax,  G.,  “ Ueber  den  Zusammenhang  nervoser  Storungen  mit  den 
Erkrankungen  der  Verdauungsorgane  ” und  “Ueber  nervose  Dyspepsie,” 
“ Sammlung  klin.  Vortrage,”  1882,  Nr.  223. 


LITERATURE  ON  GASTRIC  NEUROSES.  789 

66.  Godart-Danhieux,  “ La  gastralgie  nerveuse,”  “ La  Policlinique,”  I,  II, 
1896. 

67.  Goldschmidt,  E.,  “ Ueber  den  Einfluss  der  Elektricitat  auf  den  gesunden 
und  kranken  menschlichen  Magen,”  “ Deutsches  Archiv  f.  klin.  Med.,”  1895, 
Bd.  lvi. 

68.  Gull,  “ Lancet,”  1868. 

69.  Gumprecht,  “ Magentetanie  und  Autointoxikation,”  “ Centralbl.  f.  innere 
Med.,”  Leipzig,  1897,  xvm,  569-593. 

70.  Hadra,  B.  E.,  “Neurosis  of  the  Stomach  from  a Surgical  Standpoint,” 
“Texas  Med.  Jour.,”  Austin,  i897~’98,  3cm,  319-344. 

71.  Halipre,  “ Un  cas  de  Dyspepsie  Nervomotrice,”  “ Normandie  Medicale,” 
1,  vii,  1896. 

72.  Halliday,  A.,  “The  Condition  of  the  Gastric  Secretion  in  Merycism,” 
“ Med.  Record,”  New  York,  1897,  lii. 

73.  Hamilton,  H.  J.,  “ Hyperchlorhydria,”  “ Canad.  Pract.,”  Toronto,  1897, 

XXII. 

74.  Havel,  “ Des  Crises  Gastriques  dans  l’Ataxie  Locomotrice,”  “These  de 
Paris,”  1882. 

75.  Hayem,  “ Bull.  Medicale,”  1891,  No.  87. 

76.  Hayem,  “ Sur  Un  cas  de  Chloro-dyspepsie  avec  Neurasthenie,”  “ Med. 
Mod.,”  20  Janvier,  1897. 

77.  Hayem,  “ De  l’Hyperchlorhydrie  par  Saturation  Alcaline,”  Soc.  Med. 
du  Hop.,  15  Avril,  1898. 

78.  Hayem,  “ Sur  la  Gastralgie,”  “ Rev.  Gen.  de  Clin,  et  de  Therap.,”  Paris, 
1898,  xii,  353-357. 

79.  Henoch,  “ Ueber  Asthma  dyspepticum,”  “ Berl.  klin.  Wochenschr.,” 
1876,  Nr.  18. 

80.  Herz,  M.,  “ Fall  von  motorischer  Magenneurose,”  “ Wien.  klin.  Wochen- 
schr.,” 1897,  x,  S.  1041. 

81.  Hildebrandt,  W.,  “Nervose  Storungen  im  Gefolge  von  Magenkrank- 
heiten.” 

82.  Hoffmann,  A.,  “ Ueber  den  Einfluss  des  galvanischen  Stromes  auf  die 
Magensaftabscheidung,”  “ Berl.  klin.  Wochenschr.,”  1890. 

83.  Hoffmann,  J.,  “ Zur  Lehre  von  der  Tetanie,”  “ Heidelberger  Habilita- 
tionsschrift,”  1888. 

84.  Honigmann,  G.,  “ Ueber  die  Neurosen  des  Magens,”  “ Zeitschr.  f. 
prakt.  Aerzte,”  1897,  iv,  pp.  833-857. 

85.  Hubbard,  W.  A.,  “ Medical  Record,”  July  31,  1886,  p.  122. 

86.  Huefler,  “ Miinch.  med.  Wochenschr.,”  1889,  Nr.  33* 

87.  Hunt,  B.,  “ On  Nervous  Vomiting,”  “Clin.  Jour.,”  London,  1898,  xii, 
pp.  238-240. 

88.  Hyde,  “ Twentieth  Century  Practice  of  Medicine,”  vol.  v,  p.  170. 

89.  Immermann,“Verhandlungen  des  Congresses  fur  innere  Medizin,”  Wies- 
baden, 1889. 

90.  Jacobi,  A. .“Transactions  of  the  Association  of  American  Physicians,”  1894. 

91.  Jacobson  and  Ewald,  “Ueber  Tetanie,”  “Verhandlungen  des  Congresses 
fur  innere  Medizin,”  1893. 

92.  v.  Jaksch,  “ Epilepsia  acetonica,”  “ Zeitschr.  f.  klin.  Med.,”  Bd.  x. 

93.  Johannessen,  “ Zeitschr.  f.  klin  Med.,”  Bd.  x,  S.  274. 

52 


790 


NEUROSES  OF  THE  STOMACH. 


94.  Jones,  Allen  A.,  “Gastric  Conditions  in  Renal  Disease,”  “ N.  Y.  Med. 
Jour.,”  Jan.  19,  1895. 

95.  Joslin,  E.  P.,  “ Hyperacidity  of  the  Stomach  and  its  Treatmeat,”  “ Bos- 
ton Med.  and  Surg.  Jour.,”  1898,  cxxxvm,  pp.  389-392. 

96.  Jiirgensen,  “ Ueber  Abscheidung  neuer  Formen  nervoser  Magenkrank- 
heiten,”  “ Deutsches  Archiv  f.  klin.  Med.,”  Bd.  xliii. 

9 7.  Jiirgensen,  C.,  “ Ueber  die  Diat  bei  der  Superaciditat : eine  kritische 
Litteraturstudie,”  “ Archiv  f.  Verdauungskrankh.,”  Berlin,  1897,111. 

98.  Kahler,  “ Prager  Zeitschr.  f.  Heilkunde,”  Bd.  11. 

99.  Kaufmann,  J.,  “ Zwei  Falle  geheilter  pernicioser  Anamie,  nebst  Bemer- 
kungen  zur  Diagnose  und  Therapie  dieser  Krankheit,”  “ Berl.  klin.  Wochen- 
schr.,”  1890,  Nr.  10. 

100.  Klemperer,  “ Berl.  klin.  Wochenschr.,”  1899,  Nr.  11. 

101.  Koerner,  “ Deutsches  Archiv  f.  klin.  Med.,”  Bd.  X,  S.  274. 

102.  Koziczkowsky,  E.  von,  “ Beitrag  zur  Aetiologie  der  Magenneurosen,” 
“ Berl.  klin.  Wochenschr.,”  Nr.  7,  1897. 

103.  Kussmaul,  “ Ueber  die  Behandlung  der  Magenerweiterung  durch  die 
Magenpumpe,”  “ Deutsches  Archiv  f.  klin.  Med.,”  1869,  Bd.  VI. 

104.  Kussmaul,  “ Die  peristaltische  Unruhe  des  Magens,”  “ Sammlung  klin. 
Vortrage,”  1880,  Nr.  18 1. 

105.  Kutneff,  “ Neurasthenie,  Herabsinken  von  Bauchorganen  und  gastro- 
intestinale  Atonie,”  Ref.  in  the  “ Jahresberichte,”  1894,  Bd.  11. 

106.  Laffitte,  “ Des  Crises  Gastriques,”  “ Gaz.  des  Hop.,”  Jan.,  1894. 

107.  Landouzy  et  Dejerine,  Societe  de  Biologie,  1884. 

108.  Leo,  “ Ueber  Bulimie,”  “ Deutsche  med.  Wochenschr.,”  1889,  Nr.  29  u. 
30- 

109.  Leube,  “Ueber  nervose  Dyspepsie,”  “ Deutsches  Archiv  f.  klin  Med.,” 
1878,  Bd.  xxiii. 

no.  Leven,  “ Estomac  et  Cerveau,”  Paris,  1884. 

in.  Leven,  “ Phenomenes  Nerveux  lies  a la  Dyspepsie,”  “ Gaz.  des  Hop.,” 
1880,  No.  40. 

1 12.  Leven,  “ Phenomenes  Nerveux  qui  se  Produisent  sous  l’lnfluence  de  la 
Dyspepsie,”  ibid.,  1880,  No.  137. 

1 13.  Leyden,  “Ueber  Anfalle  von  periodischem  Erbrechen,  nebst  Bemerk- 
ungen  fiber  nervose  Magenaffectionen,”  “ Zeitschr.  f.  klin.  Med.,”  Bd.  iv, 
1882. 

1 14.  Liebmann,  G.,  “ Meine  Erfahrungen  mit  Hyperaciditat,”  “New  Yorker 
med.  Monatsschr.,”  1897,  IX,  311-318. 

1 1 5.  Liell,  E.  W.,  “The  Relation  of  the  Pregnant  Uterus  to  the  Reflex 
Nausea  and  Vomiting  Accompanying  Gestation,”  “ Amer.  Medico-Surg.  Bull.,” 
2i,  xi,  1897. 

1 16.  Littig,  L.  W.,  “Gastric  Neuroses,”  Transactions  Iowa  Medical  Society, 
Burlington,  1898. 

1 17.  Loeb,  M.,  “ Tetanie  bei  Magenerweiterung,”  “Deutsches  Archiv  f. 
klin.  Med.,”  1890,  Bd.  lxvi. 

1 18.  Luzzato,  A.  M.,  “ Un  caso  di  mericissmo  connotevoli  alterazioni  del 
chimismo  gastrico,”  “ Riv.  Ven.  di  Scienze  Med.,”  hi,  p.  116. 

1 19.  Lyman,  H.  M.,  “Nervous  Dyspepsia,”  “Jour.  Amer.  Med.  Assoc.,” 
1897,  xxviii,  pp.  959-962. 


LITERATURE  ON  GASTRIC  NEUROSES.  79 1 

120.  Malbranc,  “ Ueber  Behandlung  von  Gastralgieen  mit  der  inneren 
Magendusche,”  etc.,  “ Berl.  klin.  Wochenschr.,”  1878. 

121.  Marcus,  A.,  “ Ein  Fall  von  hysterischer  Magenneurose  (unstillbares 
Erbrechen)  compliciert  mit  Diabetes  insipidus  bei  einem  Manne,”  Dissert., 
Miinchen,  1896-97. 

122.  Mariani,  “ De  1’ Hypersecretion  Gastrique,”  Th&se  de  Montpellier, 

1896. 

123.  Mathieu  et  Milan,  “Etude  sur  le  Pituite  Hemorragique  des  Hyster- 
iques,”  Paris,  1896. 

124.  Maybaum,  J.,  “ Archiv  f.  Verdauungskrankh.,”  Bd.  1,  Heft  4. 

125.  Melzer,  S.  J.,  “Berl.  klin.  Wochenschr.,”  1888,  Nr.  8. 

126.  Mitchell,  Weir,  “ Fat  and  Blood,”  Philadelphia,  1884. 

127.  Mobius,  S.  A.,  “ Ueber  die  schmerzstillende  Wirkung  der  Elektricitat,” 
“ Berl.  klin.  Wochenschr.,”  1880. 

128.  Mongour  et  Lafarelle,  “ Spasme  du  Pylore,”  “Jour,  de  Med.  de  Bor- 
deaux,” 1898,  xxviii,  p.  176. 

129.  Muller,  Fr.,  “ Tetanie  bei  Dilatatio  ventriculi  und  Achsendrehung  des 
Magens,”  “ Charite  Annalen,”  1888,  Bd.  xm. 

130.  Murdoch,  F.  H.,  “The  Absence  of  Hydrochloric  Acid  in  the  Stomach, 
with  Report  of  Cases,”  “ Phila.  Med.  Jour.,”  1898, 1. 

1 3 1 . Murdoch,  F.  H.,  “ Nervous  Dyspepsia,  with  Report  of  Cases,”  “ N.  Y. 
Med.  Jour.,”  1898,  lxviii,  pp.  437-439. 

132.  Muret,  “Hyperemesis  gravidar.  und  Hysterie,”  “Deutsche  med. 
Wochenschr.,”  1893. 

133.  Naunyn,  “ Zur  Lehre  vom  Husten,”  “ Deutsches  Archiv  f.  klin.  Med.,” 

XXIII. 

134.  Neumann,  “ Deutsche  Klinik,”  1861,  Nr.  3. 

135.  Nonne,  “ Beitrage  zur  Kenntniss  der  im  Verlaufe  der  perniciosen  An- 
amie  beobachteten  Spinalerkrankungen,”  “Archiv  f.  Psychiatrie,”  Sep.  H., 
Bd.  xxv. 

136.  v.  Noorden,  “ Klinische  Untersuchungen  iiber  die  Magenverdauung  bei 
Geisteskrankheiten,”  “Archiv  f.  Psychiatrie  und  Nervenkrankheiten,”  Bd.  x. 

137.  v.  Noorden,  “ Pathologie  der  gastrischen  Crisen,”  “Charite  Annalen,” 
1890. 

138.  Oettinger,  W.,  “Idiopathic  Gastric  Crises;  Periodical  Vomiting  of  von 
Leyden,”  “ Med.  Weekly,”  1897,  v,  pp.  374-376. 

139.  Olivetti,  B.,  ed.  Muggia,  A.,  “ Azione  della  pilocarpina  sulla  secrezione 
chlorata  del  ventricolo  nell  ipoedana-chloridria,”  “ Gazz.  med.  di  Torino” 

1897,  xlviii,  661-666. 

140.  Olivetti,  B.,  “ Fleiner’s  Methode  in  der  Behandlung  der  Hyperchlor- 
hydrie,”  “ Therapeutische  Monatshefte,”  Berlin,  1898,  xn. 

141.  Oppenheim,  “Berl.  klin.  Wochenschr.,”  1885. 

142.  Oser,  “Die  Neurosen  des  Magens  und  ihre  Behandlung,”  “Wiener 
Klinik,”  1885,  Heft  5 u.  6. 

143.  Pacanowski,  “ Deutsches  Archiv  f.  klin.  Med.,”  Bd.  XL. 

144.  Panecki,  “ Retroflexio  uteri  und  Magenneurose,”  “ Therapeutische 
Monatshefte,”  1892. 

145.  Petitjean,  “ Contribution  a l’litude  des  Crises  Gastriques  dans  l’Ataxie 
Locomotrice,”  “These  de  Paris,”  1874. 


792 


NEUROSES  OF  THE  STOMACH. 


146.  Pettyjohn,  E.  S.,  “ Functional  Gastric  Diseases  and  their  Treatment,” 
“ Physician  and  Surgeon,”  Detroit  and  Ann  Arbor,  1897,  xix,  pp.  258-262. 

147.  Peyer,  A.,  “ Beitrag  zur  Kenntniss  der  Neurosen  des  Magens  und  des 
Darms,”  “ Correspondenzblatt  f.  Schweizer  Aerzte,”  1888. 

148.  Pick,  A.,  “ Ueber  Hyperasthesie  des  Magens,”  “ Wiener  med.  Wochen- 
schr.”  1898,  xlviii. 

149.  Pidoux,  “Rapport  de  l’Herpetisme  et  des  Dyspepsies,”  “ L’Union 
Med.,”  1866,  p.  235. 

150.  Ponsgen,  “Die  motorischen  Verrichtungen des menschlichen  Magens,” 
Strassburg,  1882,  S.  127. 

1 51.  Potain,  “ Paralysie  Consecutive  a des  Troubles  Digestifs,”  “ Gaz.  des 
Hop.,”  1880. 

152.  Raymond,  “Des  Dyspepsies,”  “These  d’aggreg.,”  1878. 

153.  Reed,  B.,  “The  Excessive  Secretion  of  Hydrochloric  Acid  by  the 
Stomach,  and  its  Possible  Serious  Consequences,”  “ Internat.  Clin.,”  1897. 

154.  Reed,  B.,  “ A New  Intragastric  Electrode  for  the  Treatment  of  Gas- 
tralgia  and  Deficient  Gastric  Motility  with  or  without  Dilation,”  “ Phila. 
Med.  Jour.,”  1898,  1. 

155.  Remond  (de  Metz),  “ Des  Crises  Gastriques  Essentielles,”  “ Arch.  Gen. 
de  Med.,”  1889,  Tome  11. 

156.  Renvers,  “ Berl.  klin.  Wochenschr.,”  1888,  No.  53. 

157.  Richet,  Ch.,  “Du  Sue.  Gastrique  chez  1’Homme  et  les  Animaux,”  Paris, 
1878. 

158.  Richter,  “ Ueber  nervose  Dyspepsie  und  nervose  Enteropathie,”  “Berl. 
klin.  Wochenschr.,”  1882. 

159.  Riegel,  F.,  “ Zur  Lehre  von  der  Tetanie,”  “Deutsches  Archiv  f.  klin. 
Med.,”  1873,  Bd.  Xil. 

160.  Riesmann,  D.,  “ Stomach  from  a Case  of  Rumination,”  “ Tr.  Path. 
Soc.,”  Philadelphia,  1898,  xviii,  p.  120. 

161.  Robin,  A.,  “ Gastro-succhoree  et  Stenose  Pylorique,”  “ Courier  med.,” 
Paris,  1897,  XLVii,  p.  169. 

162.  Rockwell,  A.  D.,  “Atonic  or  Nervous  Dyspepsia  and  its  Treatment  by 
Intragastric  Electrization,”  “ Internat.  Clin.,”  1898. 

163.  Rosenberg,  O.,  “Beitrag  zur  Lehre  von  den  Krankheiten  des  Verdau- 
ungsapparates,”  “ Deutsche  med.  Wochenschr.,”  1879  (Vagusneurose). 

164.  Rosenbach,  O.,  “Die  Emotionsdyspepsie,”  “Berl.  klin.  Wochen- 
schr.,” 1897. 

165.  Rosenheim,  Th.,  “ Berl.  klin.  Wochenschr.,”  1890. 

166.  Rosenheim,  Th.,  “Ueber  nervose  Dyspepsie,”  “Berl.  klin.  Wochen- 
schr.,” 1897,  Nr.  34. 

167.  Rosenstein,  “ Berl.  klin.  Wochenschr.,”  1890,  No.  13. 

168.  Rosenthal,  “ Magenneurosen  und  Magenkatarrh,”  Wien  und  Leipzig, 
1886. 

169.  Rossbach,  “ Nervose  Gastroxynsis  als  eine  eigene  characterisirbare 
Form  der  nervosen  Dyspepsie,”  “ Deutsches  Archiv  f.  klin.  Med.,”  Bd.  xxiv. 

170.  Sansom,  A.  E.,  “ A Note  on  Neuropathic  Dyspepsia  and  its  Correlations 
with  Disturbances  of  the  Rhythm  of  the  Heart,”  “Lancet,”  London,  1897,  11. 

17 1 . Sansom,  L.,  “Sulla  pathogenesi  dell  iperchloridria  primitiva,”  “Ref- 
orma med.  Napoli,”  1897,  xm. 


LITERATURE  ON  GASTRIC  NEUROSES. 


793 


172.  Schetty,  F.,  “ Deutsches  Archiv  f.  klin.  Med.,”  lid.  xliv,  S.  219. 

173.  Schnitzler,  J.,  “ Ueber  einen  Krampftumor  des  Magens,  nebst  Bemerk- 
ungen  zum  sog.  Spasmus  pylori,”  “ Wiener  med.  Wochenschr.,”  1898,  xlviii. 

174.  Schuchardt,  “ Epileptiforme  Anfalle  bei  Magenerkrankungen,”  “ All- 
gem. Zeitschr.  f.  Psychiatrie,”  1882,  Bd.  xxxvm. 

175.  Schiile,  A.,  “ Einige  Bemerkungen  iiber  die  Hyperaciditat ; die  Diat 
bei  derselben,”  “Archiv  f.  Verdauungskrankh.,”  1897,  Heft  in. 

176.  Schiitz,  “ Prager  med.  Wochenschr.,”  1882,  Nr.  II. 

177.  See,  G.,  “ Anwendung  der  Cannabis  indica  in  der  Behandlung  der 
Neurosen  und  gastrischen  Dyspepsien,”  “ Deutsche  med.  Wochenschr.,”  1890. 

178.  Singer,  “ Die  Rumination  beim  Menschen  und  ihre  Beziehung  zum 
Brechact,”  “ Deutsches  Archiv  f.  klin.  Med.,”  1893,  Bd.  Li. 

179.  Sinkler,  W.,  “ Rumination  in  Man,”  “Jour.  Amer.  Med.  Assoc.,”  April 
9,  1898. 

180.  Smith,  D.  E.,  “ Hyperchlorhydria,”  “ Northwest  Lancet,”  St.  Paul, 
XVII. 

181.  v.  Sohlern,  “ Zur  Behandlung  der  nervosen  Magenkrankheiten,” 
“ Berl.  klin.  Wochenschr.,”  1891. 

182.  Sollier,  “ Revue  de  Medecine,”  Aout,  1891. 

183.  Somers,  L.  S.,  “ Merycism,”  “Medical  Record,”  17,  iv,  1897. 

184.  Sorens,  O.,  und  Metzger,  L.,  “Ueber  die  Diat  bei  Superaciditat,” 
“ Miinch.  med.  Wochenschr.,”  1898,  xlv. 

185.  Stiller,  “ Die  nervosen  Magenkrankheiten,”  Stuttgart,  1884. 

186.  Stockton,  “ Medical  Record,”  1894. 

187.  Strauss,  “ Des  £cchymoses  Fabetiques  a la  Suite  des  Crises  Doulour- 
euses,”  “Arch,  de  Neur.,”  i88o-’8i. 

188.  Strauss,  “ Ueber  das  Vorkommen  von  Ammoniak  im  Mageninhalt,” 
etc.,  “ Berl.  klin.  Wochenschr.,”  1893. 

189.  Talma,  “ Zur  Kenntniss  des  Leidens  der  Bauchsympathicus,” 
“ Deutsches  Archiv  f.  klin.  Med.,”  1892,  Bd.  xlix  ; “ Zeitschr.  f.  klin.  Med.,” 
1884,  Bd.  viii,  S.  407. 

190.  Tere,  “ Note  pour  Servis  a l’Histoire  des  Troubles  Gastrique  de  l’Epi- 
lepsie  et  de  l’Heredite  Morbide  Progressive,”  “Journal  de  Neurologie,”  5,  in, 
1896. 

191.  Tournier,  C.,  “ Ouelques  cas  de  Vomissements  Nevrosques,”  “ Province 
Med.,”  Lyon,  1897,  xi. 

192.  Trousseau,  “ Med.  Klinik  des  Hotel  Dieu”  in  Paris,  Bd.  in,  1868,  Cap. 
67. 

193.  Upshur,  J.  N.,  “ Gastralgia,  with  Report  of  a Case,”  “Medical  Reg- 
ister,” Richmond,  1897,  1,  31. 

194.  Wagner,  G.,  “ Zur  Behandlung  der  Superaciditat  des  Magens  mit 
Bergmann’schen  Magenkautabletten,”  “ Therap.  Monatshefte,”  Berlin,  1897, 
XI. 

195.  Westfallen,  “ Kopfschmerzen  gastrischen  Ursprungs,”  “ Berl.  klin. 
Wochenschr.,”  1891. 

196.  Westphal,  C.,  “ Ueber  Agarophobie,  eine  neuropathische  Erscheinung,” 
“ Archiv  f.  Psychiatrie,”  1872,  Bd.  ill. 

197.  Whitney,  H.  B.,  “ Cyclic  Vomiting:  A Brief  Review  of  this  Affection 
as  Illustrated  by  a Typical  Case,”  “ Arch.  Pediat.,”  1898,  xv. 


794 


SENSORY  NEUROSES. 


198.  Hemmeter,  J.  C.,  “ Experimental  Basis  of  the  Treatment  of  Hyper- 
acidity,” etc.,  “ Journ.  Am.  Med.  Assoc.,”  Oct.  9,  1897. 

199.  Hemmeter,  J.  C.,  “ Histologie  d.  Magendriisen  bei  Hyperaciditat,” 
“Archiv  f.  Verdauungskrankh.,”  Bd.  iv,  98,  S.  23. 


CHAPTER  XI. 

SENSORY  NEUROSES. 

HYPERESTHESIA. 

Hyperesthesia  depends  upon  a morbid  increase  in  the  irritability 
of  the  sensory  nerves  of  the  stomach.  It  is  probably  a neurosis 
of  the  vagus,  and  a mild  form  of  gastralgia.  Clinically,  the  two 
forms  of  gastric  sensibility — viz.,  gastralgia  and  hyperesthesia — 
are  differentiated  by  the  following  facts : The  unpleasant  sensation 
of  pressure,  fullness,  and  pain  in  the  epigastrium,  with  eructations, 
nausea,  and  vomiting,  occur  in  hyperesthesia  only  after  the  inges- 
tion of  food : that  is,  there  must  be  a digestive  stimulation  of  the 
mucosa.  The  distress  occurs  only  after  meals,  very  rarely  with  an 
empty  stomach ; but  in  gastralgia  the  pains  and  other  distress 
occur  with  equal  intensity  in  the  full  as  well  as  in  the  empty 
stomach ; digestive  irritation  is  not  necessary  to  cause  gastralgia. 
Hyperesthesia  lasts  several  days,  weeks,  or  even  months,  with 
uniform  or  gradually  increasing  intensity,  and  during  this  time 
dyspeptic  symptoms  occur  daily  after  every  meal  ; in  gastralgia, 
however,  the  pains  last  during  the  attacks,  generally  for  a few 
hours  only.  In  the  intervals  between  the  attacks  the  excitability 
of  the  nerves  is  so  completely  arrested  that  even  strong  irritation — 
like  the  overloading  of  the  stomach  with  food — does  not  cause  a 
return  of  the  pain.  The  various  acts  constituting  normal  diges- 
tion, the  movements  of  the  gastric  wall  and  of  the  contents  of  the 
digestive  tract,  are  phenomena  of  which  a healthy  person  is  not 
conscious,  but  they  may  be  perceived  by  patients  with  increased 
sensitiveness  of  the  gastric  nerve-endings.  As  a result  of  this 
nervous  state  sensations  reach  consciousness  from  these  localities 
which  in  the  normal  being  would  not  pass  the  threshold  of  con- 
sciousness. The  disturbance  of  the  nerves  need  not  necessarily  be  in 
the  end  distributions  of  the  stomach  ; they  may  be  in  the  nerve  itself 


GASTRIC  HYPERESTHESIA. 


795 


or  in  the  central  organ.  Most  frequently  the  seat  may  be  in  the  per- 
ipheral nervous  end  organs  in  the  stomach  ; these  are  the  cases  that 
have  been  caused  by  improper  mode  of  life  and  various  insults  to 
the  mucosa.  In  other  rare  cases  the  gastric  hyperesthesia  may  be 
a perception  due  to  increased  excitability  of  the  nervous  centers. 
In  order  to  intelligently  appreciate  the  sufferings  of  patients  with 
increased  sensibility  it  is  necessary  to  bear  in  mind  that  the 
increased  irritability  brings  about  the  perception  of  transactions 
into  the  digestive  tract  which  in  themselves  are  not  pathological, 
and  if  present  to  the  same  degree  in  a healthy  individual,  would  not 
be  perceived.  The  natural  process  of  digestion  and  absorption  in 
such  patients  is  a train  of  uninterrupted  distressing  sensations. 
The  patients  themselves  generally  misinterpret  their  condition 
or  exaggerate  it,  and  as  a consequence  of  the  various  impressions 
that  they  perceive,  assume  that  they  suffer  from  severe  organic 
disease.  They  often  become  hypochondriacal.  Hyperesthesia 
may  be  an  independent,  idiopathic  or  secondary,  symptomatic 
neurosis. 

Causation. — The  primary  idiopathic  form  occurs  very  frequently 
as  an  accompaniment  to  chlorosis  and  anemia,  particularly  with 
women  and  young  girls.  Also  after  repeated  overloading  of  the 
stomach  with  indigestible  food.  Long-continued  use  of  very  salty 
or  acid  or  spiced  foods,  and  the  ingestion  of  very  hot  or  very  cold 
drinks  after  long  fasting,  and  in  debilitated  states  following  excesses 
in  Venere  et  Baccho.  It  has  been  observed  to  occur  also  after 
chloroform  narcosis.  Secondary  hyperesthesia  occurs  with  hy- 
peracidity and  supersecretion  in  hysterical  patients,  also  in  neu- 
rasthenia and  tabes.  Gastralgia  may  follow  hyperesthesia,  and 
there  are  cases  in  which  both  neuroses  may  exist  simultaneously. 

Symptomatology. — Patients  with  this  neurosis  frequently  feel 
the  pulsations  of  the  abdominal  aorta,  and  complain  of  beating  and 
pulsating  in  the  stomach.  Then,  again,  they  have  a feeling  of  heat 
or  cold,  or  a gnawing,  burning  sensation,  and  an  impression  of  rest- 
lessness through  the  entire  stomach.  The  ingestion  of  food,  no 
matter  of  what  consistency,  causes  a sensation  of  discomfort,  full- 
ness, nausea,  and  even  vomiting.  These  sensations  may  increase  to 
a typical  gastralgia,  and  are  felt  only  during  the  first  period  of 
digestion,  or  they  may  last  as  long  as  food  is  contained  in  the 
stomach.  Some  patients  complain  for  a while  even  after  food 
has  left  the  stomach.  The  pains  are  absent  in  the  morning,  when 
the  stomach  is  entirely  empty.  If  the  hyperesthesia  depend  upon 


796 


SENSORY  NEUROSES. 


hyperchylia,  the  pains  do  not  become  pronounced  until  the  second 
period  of  gastric  digestion,  when  the  acidity  of  the  gastric  chyme 
reaches  its  highest  degree.  In  some  cases  of  hyperesthesia  it  may 
happen  that  the  distress  is  temporarily  relieved  by  the  ingestion  of 
albuminous  food  or  the  taking  of  alkalies.  The  burning,  sticking, 
and  beating  in  the  stomach  may  be  accompanied  by  bulimia. 
These  gastric  symptoms  are  generally  accompanied  by  other  ner- 
vous phenomena  which  are  probably  symptoms  of  the  fundamental 
etiological  disease ; thus  we  meet  with  migraine,  cephalalgia,  and 
neuralgia  in  other  parts  of  the  body,  etc.  The  emesis  which 
occurs  in  hyperesthesia  induces  the  patients  to  restrict  their  diet 
more  and  more,  whereby  the  general  nutrition  and  bodily  resist- 
ance become  very  much  reduced.  Concerning  the  appetite  and 
the  foods  which  are  best  digested,  the  patients  show  the  most 
manifold  contrasts.  Some  of  them  feel  more  distress  after  liquids 
than  after  solids.  The  appetite  does  not  seem  much  affected ; 
some  patients  have  an  intense  feeling  of  hunger.  There  are  no 
very  constant  anomalies  of  motility  or  secretion.  The  bowels  are 
generally  constipated. 

Prognosis. — The  prognosis  is  favorable,  as  the  hyperesthesia 
ceases  when  the  detrimental  and  irritating  conditions  which  excite 
the  sensibility  of  the  stomach  can  be  kept  away,  and  when  the 
fundamental  disease  can  be  removed. 

Diagnosis. — The  affection  may  be  confounded  with  gastralgia, 
and  with  the  painful  symptoms  of  organic  gastric  diseases.  From 
gastralgia  it  can  be  distinguished  by  the  fact  that  the  symptoms 
occur  daily  for  a long  time,  regularly  after  each  meal,  and  that  they 
are  absent  when  the  stomach  is  empty.  Gastralgia  occurs  only 
spasmodically,  rarely  lasts  longer  than  several  hours,  and  is  of 
equal  severity  in  an  empty  as  in  a full  stomach.  The  intervals 
between  the  attacks  are  perfectly  free  from  gastric  distress. 
Concerning  the  differential  diagnosis  between  hyperesthesia  and 
the  distress  of  diseases  of  the  stomach  connected  with  anatomical 
alterations,  we  refer  to  the  differential  points  stated  in  the  diagnosis 
of  gastralgia.  We  might  emphasize  here  that,  in  the  organic  dis- 
eases, the  pains  are  entirely  absent  when  the  stomach  is  empty. 
Atrophic  gastritis  forms  an  exception  to  this  rule.  The  intensity 
of  the  pains  is  influenced  by  the  quality  of  the  food,  which  is  not 
the  case  in  hyperesthesia,  and  that  organic  diseases  are  mostly 
associated  with  tolerably  constant  disturbances  of  secretion  and 
motility. 


GASTRIC  IDIOSYNCRASIES. 


797 


Treatment. — The  treatment  will  be  directed  in  the  first  place  to 
the  correction  of  the  underlying  fundamental  disease.  Wherever 
this  is  not  possible,  or  wherever  an  idiopathic  form  of  hyperesthesia 
is  present,  all  irritants  which  can  exert  detrimental  influence  upon 
the  stomach  must  be  excluded.  All  bodily  and  mental  exertion 
must  be  avoided.  In  severe  cases  the  Weir  Mitchell  rest-cure,  to- 
gether with  a Leube  ulcer  cure,  has,  in  our  experience,  been  very 
efficacious.  Hot,  moist  applications  to  the  stomach  are  very  sooth- 
ing. In  a very  pronounced  case  of  gastric  hyperesthesia  in  a col- 
league, which  returned  regularly  whenever  he  was  under  great 
mental  strain,  the  symptoms  disappeared  entirely  after  a sojourn  at 
the  seashore  for  one  month.  Galvanization  is  a capital  method  of 
treating  this  affection.  The  intragastric  method  may  be  used,  but 
when  the  patient  is  not  accustomed  to  the  swallowing  of  the  elec- 
trode, we  have  obtained  good  results  from  the  external  application 
of  the  large  abdominal  plates.  Use  of  tea,  coffee,  tobacco,  and 
alcohol  must  be  avoided,  as  these  things  have  been  known  to  keep 
up  a hyperesthesia.  Rosenheim  has  suggested  the  following  treat- 
ment (“  Berlin,  klin.  Wochenschr.,”  1890)  internally  : 

R.  Argenti  nitras, 0.2  gr.  iij 

Aquae  menthse  pip., 100.0  ^ iij.  M. 

SlG. — Two  teaspoonfuls  in  a wineglassful  of  water,  on  an  empty  stomach,  in  the 
morning,  and  a half-hour  before  each  meal. 

The  patient  must  be  kept  in  bed,  and  warm  cataplasms  applied 
to  the  epigastrium.  The  diet  consists  of  milk  taken  by  table- 
spoonful doses,  later  on  soft  eggs,  and  scraped  beef  and  dipped  toast. 
When  the  stomach  becomes  more  resistant,  the  patient  may  return 
to  solid  food.  To  remove  the  cause,  Rosenheim  advises  treat- 
ment of  the  general  underlying  affection,  bodily  and  mental  rest, 
and  hydrotherapeutic  measures.  Severe  hyperesthesia  is  some- 
times relieved  by  bromid  of  strontium  and  codein.  We  have  also 
obtained  very  good  results  from  spraying  the  stomach  with  a solu- 
tion of  morphin,  cocain,  and  menthol.  In  doing  this,  a spray  must 
be  used  by  which  we  can  tell  the  exact  amount  of  cocain  and 
morphin  which  reaches  the  stomach  with  the  spraying  liquid.  It 
is  well  not  to  put  more  into  the  spray  than  we  wish  to  put  into 
the  stomach,  otherwise  the  patient  may  absorb  too  much  cocain 
and  morphin. 

Gastric  idiosyncrasies  are  those  peculiar  forms  of  hyperesthe- 
sia in  which  neuropathic  and  sometimes  perfectly  healthy  persons 


79B 


SENSORY  NEUROSES. 


have  morbid  sensations  only  after  ingesting  certain  foods.  These 
sensations  consist  of  headache,  light  fever,  skin  erythema,  and 
urticaria.  The  author  has  observed  persons  who  developed  urti- 
caria after  eating  crabs,  potatoes,  cheese,  or  strawberries.  One  of  our 
patients  regularly  develops  an  acute  acne  whenever  she  eats  cheese. 
Another  patient  regularly  develops  fever,  eructations,  nausea,  and 
vomiting  whenever  he  partakes  of  crabs.  Although  a heightened 
irritability  of  the  sensory  nerves  may  be  instrumental  in  the  devel- 
opment of  these  idiosyncrasies,  it  is  very  plausible  that  autointox- 
ication plays  a very  important  role  in  them.  It  is  probable  that  in 
individuals  who  develop  urticaria  after  eating  certain  foods,  there 
must  be  microorganisms  that  develop  toxins  from  these  foods 
which,  in  turn,  act  in  the  manner  indicated.  Pick  states  that  his 
cases  suffered  also  from  constipation,  which  naturally  favors  the 
putrefaction  of  the  ingesta.  Acting  upon  the  theory  of  autointox- 
ication caused  by  intestinal  putrefaction,  Pick  very  strongly  recom- 
mends the  internal  use  of  creasote  (see  “Albu.  Autointoxica- 
tionen  des  Intestinaltractus,”  part  on  The  Skin,  p.  88 ; also  p.  396 
of  this  volume),  which  in  my  experience  has  proved  useless.  The 
correct  course  to  follow  is  to  avoid  all  foods  entirely  that  are 
known  to  cause  such  distress. 

GASTRALGIA  (Cardialgia  ; Gastrodynia). 

Gastralgia,  or  neuralgia  of  the  stomach,  occurs  in  periodical  and 
spasmodical  attacks  of  severe  gastric  pain,  alternating  with  inter- 
vals of  freedom  from  pain.  Pains  of  greater  or  less  intensity  occur 
with  all  gastric  diseases,  particularly  with  ulcer,  carcinoma,  gas- 
tritis atrophicans,  and  toxic  gastritis.  These  pains  are  a consequence 
of  the  anatomical  alterations  which  these  organic  diseases  effect  in 
the  gastric  wall,  brought  about  most  probably  by  exposure,  dis- 
tortion, and  compression  or  inflammation  of  the  sensory  gastric 
nerves.  Such  pains  have  been  described  in  the  chapter  on  various 
Organic  Diseases  of  the  Stomach.  Gastralgic  pain  results  from  func- 
tional, not  from  structural,  disturbances  of  the  sensory  nerves.  Gas- 
tralgia is  characterized  by  the  irregular  intervals  in  which  it  occurs, 
and  its  independence  of  the  quality  and  quantity  of  the  ingesta. 
The  attacks  come  on  either  suddenly,  or  there  may  be  such  pre- 
monitory symptoms  as  feeling  of  pressure  and  fullness  in  the  stom- 
ach, eructation,  nausea,  vomiting,  headache,  and  salivation.  The 
pains  have  a gnawing,  boring,  burning,  tearing,  or  cramp-like  char- 
acter. They  are  felt  principally  in  the  epigastric  region.  In  some 


GASTKALGI  A. 


799 


cases  the  pain  radiates  to  the  hypochondriac  regions,  the  entire 
abdomen  and  back,  and  may  be  accompanied  by  unmistakable 
signs  of  collapse  and  the  feeling  of  impending  dissolution.  The 
pains  occur  as  well  after  food  that  is  easily  digestible  as  after  indi- 
gestible food. 

In  some  hysterical  patients  the  so-called  “ clavus  hystericus,”  a 
sharply  localized  pain,  as  if  a nail  were  driven  into  apart,  is  well 
described  by  the  sufferer.  There  is  also,  in  some  of  these  cases,  a 
sudden  and  transient  sensation  as  if  a tremendous  ball  were  rising 
in  the  throat  (globus  hystericus).  Nausea  and  vomiting,  as  well  as 
bulimia  and  an  urgent  desire  to  urinate,  are  occasional  symptoms. 
The  paroxysms  may  last  a few  minutes  or  several  hours,  and 
extend  through  the  entire  night;  they  may  begin  at  any  hour  of 
the  day  or  night.  The  intervals  of  relief  may  amount  to  days, 
weeks,  or  months. 

Malaria. — We  have  observed  a number  of  cases  of  malarial  gas- 
tralgia  in  which  the  attacks  occurred  at  regular  intervals,  and  could 
be  distinctly  associated  with  an  evolution  of  the  characteristic 
malarial  parasite  in  the  blood.  These  malarial  gastralgias  are  not 
infrequent  in  fishermen,  and  even  in  sportsmen  who  sojourn  for 
weeks  along  the  shores  of  the  Chesapeake  Bay  in  Maryland.  In  a 
patient  of  this  city  the  gastralgic  attacks  persisted,  notwithstanding 
the  most  careful  treatment,  until  the  patient  could  be  persuaded  to 
give  up  his  ducking  sport  on  the  Chesapeake  Bay,  for  the  relief 
afforded  by  quinin  was  not  permanent.  The  attacks  occur  gener- 
ally without  any  demonstrable  cause.  As  a rule,  only  one  attack 
occurs  in  the  day,  but  there  may  be  as  many  as  four  in  one  day. 
The  end  of  the  attack  may  culminate  in  very  profuse  vomiting, 
which  brings  a great  relief,  the  pains  ceasing  thereafter  as  rapidly 
and  suddenly  as  they  came  on.  Gastralgia  maybe  a primary  idio- 
pathic and  independent  disease  or  a secondary  reflex  neurosis. 

Causation. — The  gastralgia  is  frequently  a result  of  motor  or 
secretory  neuroses — of  gastrospasm,  pylorospasm,  and  cardio- 
spasm, hyperacidity,  and  supersecretion.  The  root  of  the  vagus 
nerve  maybe  irritated  by  functional  and  anatomical  diseases  of  the 
medulla  and  adjacent  portions  of  the  central  nervous  system. 
Boas  (/.  c.,  ii,  S.  214)  enumerates  the  following  causes  of  gastral- 
gia: (1)  Those  that  attack  the  stomach  itself  and  its  immediate 
surroundings.  (2)  Central  causes.  (3)  Infections  and  intoxications. 
(4)  Reflex  causes  emanating  from  other  organs.  (5)  Neurasthenia 
and  hysteria,  (a)  The  causes  that  emanate  from  the  stomach  and 


8oo 


SENSORY  NEUROSES. 


its  immediate  surroundings  are  gastric  ulcer,  gastric  carcinoma,  gas- 
tritis acida  and  atrophicans,  various  forms  of  perigastritis,  and  peri- 
tonitic  adhesion  with  the  pancreas,  liver,  gall-bladder,  spleen,  and 
transverse  colon,  and  other  portions  of  the  intestines.  Furthermore, 
hypersecretion  andgastroxynsis,  tumors  of  neighboring  organs,  and 
pancreatic  cysts.  ( b ) Of  the  central  causes,  he  mentions  the  attacks 
occurring  with  tabes  (“  crises  gastriques  ”).  In  myelitis  and  brain 
tumors,  gastralgic  pains  have  been  observed.  ( c ) Infections  and 
intoxicants  may  cause  gastralgia.  Of  the  first,  a prominent  cause 
of  infection  in  our  latitude  is  malaria,  either  in  its  outspoken 
form  or  in  its  masked  and  latent  type.  Of  intoxicants,  nicotin 
poisoning  and  the  autointoxication  associated  with  uric  acid  and 
gout  are  well-known  causative  factors.  ( d ) Among  the  reflex 

causes  emanating  from  other  organs,  diseases  of  the  genito-urinary 
organs  occupy  the  first  place  in  both  sexes.  Prominent  among 
these  are  displacements  of  the  uterus,  inflammations  of  the  ovaries 
and  tubes,  and  uterine  and  ovarian  neoplasms.  (Panecki,“  Retro- 
flexio  uteri  und  Magenneurosis,”  “ Therapeut.  Monatsheft,”  1892, 
S.  79.)  Independent  organic  gastric  diseases  that  occur  simultane- 
ously must  be  carefully  differentiated  from  the  typical  gastralgia. 
Gastralgias  may  be  associated  with  genito-urinary  diseases  in  the 
male.  (Peyer,  “ Ueber  Magenaffectionen  b.  mannlichen  Genitallei- 
den,”  “ Volkmann’s  Samml.  klin.  Vortr.,”  No.  356.)  The  gastralgias 
that  occur  as  a consequence  of  enteroptosis  have  been  fully  con- 
sidered in  the  chapter  on  Gastroptosis.  ( e ) Stomach  neuralgia  which 
occurs  in  hysterical  and  neurasthenic  persons  without  any  apparent 
cause,  and  those  which  occur  in  anemic  patients,  should  prompt  a 
very  careful  examination  before  we  decide  that  there  is  no  real 
organic  trouble  at  the  foundation  of  the  gastralgia.  Occasionally  we 
may  find  that  gastralgias  occur  with  small  median  herniae  of  the 
linea  alba.  Whenever  motor  insufficiency  exists  with  these  herniae, 
we  presume  that  the  omentum  is  fixed  in  the  hernial  sac.  Such 
cases  have  been  recently  reported  by  Charles  D.  Aaron  and  Rosen- 
heim (“  Berlin,  klin.  Wochenschr.,”  1897,  No.  1 1).  Horner  (“  Ueber 
Cardialgia,  Verursacht  d.  praeperitoneale  Lipome,”  “ Prag.  med. 
Wochenschr.,”  1892,  S.  310)  reports  a case  of  severe  gastralgia 
caused  by  preperitoneal  lipomata.  These  herniae  of  the  linea  alba 
can  be  treated  successfully  only  by  an  operative  or  orthopedic 
method  (bandages). 

F.  Bardenhauer  (“  Ueber  den  epigastrischen  medianen  Bauch- 
bruch,”  in  “ Gesammelte  Beitrage  a.  d.  Gebiete  d.  Chir.  u.  Medi- 


GASTRALGl  A. 


801  ' 

zin,”  etc.,  Wiesbaden,  1893,  S.  35),  Vulpius  (“  Beitr.  z.  klin.  Chirurg.,” 
Bd.  vii,  H.  1),  and  Roth  (“  Archiv  f.  klin.  Chirurg.,”  Bd.  xlii,  H. 
1,  S.  1)  consider  this  subject  from  the  surgical  side.  It  is  possible 
that  in  some  cases  of  gastralgia  in  which  we  can  not  find  other 
diseased  conditions  that  may  have  caused  the  affections,  second- 
ary anatomical  changes  in  the  stomach  may  exist.  Among  these 
are  erosions  without  hemorrhage,  follicular  inflammation,  adhe- 
sions with  neighboring  organs,  and  cicatrices.*  These  conditions 
can  not  be  excluded  with  certainty,  because  they  may  not  cause 
symptoms  for  a long  time.  Every  caution  should  be  exercised  in 
the  diagnosis  of  idiopathic  gastralgia,  as  many  a case  that  is  diag- 
nosed as  a genuine  form  of  gastralgia  of  this  character  is  found, 
after  a very  thorough  examination,  to  be  a result  of  some  ana- 
tomical change,  or  a motor  or  secretory  neurosis  of  the  stomach, 
or  of  a disease  of  some  other  organ.  Idiopathic  gastralgia  should 
be  diagnosed  only  when  symptoms  and  indications  of  other  dis- 
eases can  not  be  discovered  after  an  exhaustive  anamnesis,  and 
repeated  thorough  examinations,  and  instituted  during  the  intervals 
between  the  attacks  when  the  patient  is  free  from  suffering.  The 
author  has  rarely  made  the  diagnosis  of  idiopathic  gastralgia. 

Idiopathic  gastralgia  may  occur  in  connection  with  chlorosis, 
anemia,  chronic  nicotin  poisoning,  nephritis,  incipient  tuberculosis, 
and  convalescence  from  continued  fevers,  and  also  as  a result  of 
alcoholic  and  sexual  excesses.  The  gastralgias  which  occur  with 
arthritis,  malaria,  and  chronic  rheumatism  are  particularly  inter- 
esting from  an  etiological  point  of  view.  We  have  repeatedly 
observed  that  gastralgic  attacks  in  gout  may  take  the  place  of  an 
expected  acute  attack  of  the  joints.  The  association  of  malaria 
with  gastralgia  can  be  established  beyond  a doubt  by  the  blood 
examination  for  the  malarial  parasite,  and  this  kind  of  gastralgia 
can  be  cured  by  the  administration  of  quinin  and  sometimes  of 
arsenic,  and  ceases  entirely  if  the  patient  removes  to  an  environ- 
ment that  is  free  from  malaria.  The  occurrence  of  gastralgia 
during  gout  has  been  explained  by  some  by  assuming  that  the 
deposits  of  uric  acid  and  uric  acid  salts  actually  occur  in  the  walls 
of  the  stomach  and  thereby  irritate  the  endings  of  the  sensory 


* A negro  suffering  from  the  most  intense  gastralgia  with  hyperacidity  was  operated 
on  at  the  Maryland  General  Hospital  by  Dr.  John  D.  Blake,  upon  the  author’s  advice. 
The  stomach  was  bound  to  the  liver,  diaphragm,  and  transverse  colon  by  numerous  adhe- 
sions, those  going  to  the  liver  being  inseparable. 


802 


SENSORY  NEUROSES. 


nerves.  This  theory  explains  how  gastralgia  may  occur  vicariously 
in  place  of  expected  attacks  of  gout. 

Secondary  Gastralgia. — Cases  of  this  type  have  been  reported 
which  were  very  severe  and  obstinate  during  life,  and  in  which 
tumors  were  found  at  the  autopsy  drawing  upon  or  compressing  the 
fibers  of  the  vagus  and  sympathetic.  It  has  been  observed,  also,  in 
Basedow’s  disease,  but  is  more  frequently  the  result  of  direct  or  indi- 
rect irritation  of  the  roots  of  the  vagus  nerve  in  consequence  of 
organic  or  functional  disease  of  the  spinal  cord  or  brain.  We  have 
already  referred  to  the  frequent  attacks  of  gastralgia  occurring  in 
tabes,  which  have  recently  been  explained  by  a sclerotic  degenera- 
tion of  the  nucleus  and  of  the  main  stem  of  the  vagus  (Kahler, 
Oppenheim,  Demange,  Dejerine).  The  gastric  crisis,  which  we 
have  described  elsewhere,  demands  a greater  interest  because  it 
may  occur  in  tabes  as  an  initial  symptom  when  the  other  char- 
acteristic signs,  such  as  absence  of  the  tendon  reflexes,  rigidity  of 
the  pupils,  and  Romberg’s  symptom,  are  not  yet  present,  and  in 
some  cases  the  typical  ataxia  has  not  been  known  to  occur  for  from 
six  months  to  a year  after  critical  gastralgias  of  this  kind.  Erb 
has  established  a very  probable  causal  relation  between  syphilis  and 
tabes,  and  the  hope  has  been  expressed  that  these  early  gastric  crises 
should  stimulate  exhaustive  clinical  examinations  of  the  patients 
with  a view  to  combating  the  disease  by  mercury  and  iodids  at  a 
time  when  the  spinal  changes  are  not  far  progressed.  Leyden  has 
described  gastralgia  with  subacute  myelitis,  and  Oser  with  myelitis 
due  to  compression. 

Symptomatology. — The  symptoms  of  the  attacks  are  generally 
quite  characteristic,  and  the  course  so  typical  that  they  can  not  be 
misinterpreted.  Prodromal  symptoms,  such  as  depressed  spirits, 
headache,  salivation,  nausea,  pressure,  and  fullness  in  the  stomach 
may  occur,  but,  as  a rule,  are  not  observed  and  have  no  diagnostic 
value.  Generally,  the  cases  begin  very  suddenly  with  severe  gas- 
tric pains,  which  are  sometimes  so  intense  as  to  baffle  description. 
Strong  pressure  upon  the  stomach  sometimes  relieves  the  pain — 
in  fact,  the  patients  are  often  found  doubled  up  in  bed,  pressing 
both  hands  upon  the  epigastrium.  If  the  pain  has  been  caused  by 
hyperchylia,  it  is  relieved  by  alkalies  or  albuminous  food.  The 
bowels  are  constipated  and  the  urine  is  suppressed.  The  forehead 
is  covered  with  large  drops  of  cold  perspiration,  the  pulse  is  small, 
occasionally  irregular  and  accelerated.  In  rare  cases  it  has  been 
reported  to  have  been  much  retarded.  Great  prostration  and 


DIAGNOSIS  OF  GASTRALGIA. 


803 


muscular  cramps,  and  even  general  convulsions,  have  been 
known  to  follow.  At  the  end  of  the  attack  the  patients  usually 
indulge  in  repeated  yawning,  eructation,  and  sometimes  vomit- 
ing, and  in  hysterical  patients  a copious  dilute  urine  is  sometimes 
voided. 

Diagnosis. — As  idiopathic  gastralgia  can  rarely  be  logically 
diagnosed,  it  will  be  more  correct  to  consider  gastralgia  as  a symp- 
tom, not  as  a disease  perse;  although  the  fundamental  disease 
causing  it  may  remain  obscure  or  be  missed  entirely  in  the  begin- 
ning of  the  disease,  it  may  become  pronounced  eventually.  Gas- 
tralgias  may  have  to  be  differentiated  from  the  pain  of  ulcer,  acute 
and  chronic  gastritis,  toxic  gastritis,  carcinoma,  from  rheumatism  of 
the  abdominal  muscles,  myalgia,  intercostal  neuralgia,  nephrolithi- 
asis, cholelithiasis,  and  intestinal  colic.  The  differential  diagnosis 
from  ulcer  of  the  stomach  has  been  stated  in  the  chapter  on  Ulcer. 
The  ulcer  pain  is  sharply  circumscribed  in  the  epigastrium  and 
in  the  dorsal  regions.  It  is  directly  dependent  upon  the  quantity 
and  quality  of  the  food.  Pains  from  gastric  ulcer  are  relieved  by 
rest  in  bed,  and  made  worse  by  movement.  This  pain  does  not 
occur  in  paroxysms — it  is  usually  a lasting  discomfort.  There  may 
be  atypical  cases  of  ulcer  in  which  the  diagnosis  becomes  much 
involved.  Boas  (/.  c.y  S.  38)  emphasizes  the  diagnostic  value  of  the 
painful  point  situated  at  the  left  of  the  spinal  column  between  the 
tenth  and  twelfth  thoracic  vertebrae  in  cases  of  gastric  ulcer. 

Von  Leube  advises,  when  other  symptoms  are  missing,  to  treat 
the  disease  as  if  it  were  ulcer,  and  Boas  recommends  the  internal 
administration  of  nitrate  of  silver  for  three  or  four  weeks.  The 
good  result  of  both  of  these  treatments  would  speak  for  gastric 
ulcer.  The  acute  and  chronic  gastritis  are  rarely  so  painful  as 
to  be  confounded  with  gastralgia.  The  pains  of  chronic  atrophic 
gastritis  occur  only  at  a time  when  complete  atrophy  of  the  mucosa 
has  supervened;  and,  inasmuch  as  the  secretion  in  gastralgia  is,  as  a 
rule,  not  suppressed  or  lost,  this  factor  will  constitute  an  important 
diagnostic  feature,  since  HC1  is,  in  a great  majority  of  cases,  absent 
in  gastritis.  From  toxic  gastritis  the  diagnosis  is  made  by  help 
of  the  clinical  history;  from  carcinoma,  by  means  of  ascertaining 
the  state  of  the  motility  and  secretion,  which  is,  as  a rule,  lost  in 
carcinoma,  and  normal  in  gastralgia.  The  pains  of  carcinoma  as 
well  as  of  ulcer  increase  on  pressure ; in  gastralgia  they  diminish 
on  pressure,  and  in  carcinoma  we  have  anemia  and  cachexia  as 
prominent  signs.  It  has  been  said  that  the  galvanic  current,  with 


804 


SENSORY  NEUROSES. 


the  anode  on  the  epigastrium  and  the  cathode  on  the  spinal  column, 
relieves  the  pain.  These  signs  are  not  reliable,  and  as  there  is 
nothing  typical  about  gastralgic  attacks  which  should  distinguish 
them  from  painful  paroxysms  issuing  from  other  abdominal  organs, 
we  may  say  that,  up  to  the  present  time,  no  pathognomonic  sign  or 
symptom  of  gastralgia  exists.  There  are  attacks  of  rheumatism 
and  myalgia  of  the  abdominal  muscles  which  seem  to  become 
focused  in  the  upper  part  of  the  abdomen,  so  that  they  may  be 
confounded  with  gastralgic  pains.  Myalgic  pains  may  occur  from 
severe  exertion  of  the  abdominal  musculature.  These  pains  are 
increased  by  pressing  or  pinching  the  sore  muscles  ; they  are  not 
accompanied  by  any  gastralgic  symptoms  whatever,  are  very  much 
improved  by  rest,  and,  if  they  are  rheumatic,  by  salol  and  salicy- 
late of  soda.  Intercostal  neuralgias  can  be  distinguished  by  the 
excessive  and  permanent  sensitiveness  to  pressure  which  the 
affected  nerves  exhibit  all  along  their  course  from  the  spinal 
column  to  the  sternum.  Cholelithiasis  or  the  pains  of  an  incar- 
cerated or  passing  gall-stone  frequently  irradiate  so  prominently 
to  the  epigastric  region  that  they  are  more  marked  there  than  over 
the  liver,  but  whenever  the  stone  obstructs  the  ductus  choledochus 
temporarily,  the  gall-bladder  may  be  palpable  by  its  dilation,  and 
icterus  and  clay-colored  stools  are  evident  signs  ; but  in  those 
patients  in  which  the  stone  is  impacted  in  the  cystic  duct  and  does 
not  completely  obstruct  it,  or  rapidly  passes  through  it,  a differen- 
tial diagnosis  is  difficult,  because  the  symptoms  before  mentioned 
are  absent.  But  even  in  these  cases  great  sensibility  of  the  liver 
to  pressure,  anteriorly  and  posteriorly,  is,  as  a rule,  present.  The 
liver  is  usually  enlarged,  and  there  is  a painful  point  in  cholelithia- 
sis at  the  twelfth  dorsal  vertebra,  a few  centimeters  to  the  right  of 
the  spinal  column.  A careful  search  for  gall-stone  particles  must 
be  made  in  the  passages.  Gall-stones,  as  a rule,  cause  vomiting, 
while  gastralgia  rarely  does  so.  The  differential  diagnosis  between 
hepatalgia  and  gastralgia  presents  great  difficulties.  In  nephritic 
colic  the  dyspeptic  symptoms  may  be  exactly  like  those  of  gastral- 
gia. The  diagnosis  between  the  two  affections  can  be  made  with 
certainty  by  careful  urinary  examination  for  fragments  of  calculi 
and  traces  of  blood,  or  by  catheterization  of  the  ureters  in  the  inter- 
vals, and  occasionally  by  localizing  the  renal  calculus  by  the  Ront- 
gen  rays.  (See  Leonard,  Chas.  L.,  “ The  X-ray  Diagnosis,  of 
Nephrolithiasis,”  “ Phila.  Med.  Jour.,”  vol.  v,  No.  I,  p.  50,  Jan., 
1900.)  In  intestinal  colic  the  pains  may  be  located  in  the  upper 


TREATMENT  OF  GASTRALGI A. 


805 


part  of  the  abdomen.  They  are  mostly  due  to  excessive  gaseous 
distention  of  the  intestinal  loops,  and  are  associated  with  consti- 
pation, and  cease  after  the  copious  discharge  of  gas. 

Treatment. — In  the  treatment  of  gastralgia  the  fundamental 
cause  must,  if  possible,  be  discovered  and  removed.  In  malarial 
districts  the  treatment  by  quinin  and  tonics  is  the  most  effective, 
if  the  causal  relation  can  be  established.  Chlorosis  and  anemia 
should  be  treated  by  albuminate  or  peptonate  of  iron,  ferratin, 
bone-marrow,  arsenic,  and  highly  nutritious  diet.  In  some  cases 
there  is  no  better  remedy  than  the  tincture  of  the  chlorid  of  iron. 
If  the  patient  is  an  inveterate  smoker,  he  must  be  cautioned  to 
cease  his  habit.  Enteroptosis,  gout,  and  rheumatism  must  have 
suitable  therapeutic  attention.  Disturbances  of  the  genito-urinary 
organs,  particularly  of  the  female  sexual  organs,  will  command  the 
attention  of  the  specialist.  Wherever  we  can  find  no  cause  for 
gastralgia,  the  only  thing  that  can  be  done  is  to  treat  it  sympto- 
matically. The  most  effective  agent  in  our  experience  for  this 
purpose  has  been  the  galvanic  current.  Large,  felt-covered,  copper 
plates  are  dipped  in  water  as  hot  as  the  patient  can  bear  it,  the 
anode  placed  on  the  epigastrium  and  the  cathode  on  the  spinal 
column,  extending  from  the  cervical  region  downward  between  the 
scapulae.  For  this  purpose  we  use  very  strong  currents — not  less 
than  twenty-five  milliamperes.  Oser  (“  Die  Neurosen  des  Magens,” 
etc.,  Vienna  and  Leipsic,  1885)  claims  to  have  observed  cessation 
of  the  pains  after  application  of  the  faradic  current.  When  the 
pains  are  not  too  intense,  the  internal  administration  of  phosphate 
of  codein,  ^ of  a grain  every  three  hours,  chloral  hydrate,  fifteen 
grains  every  two  hours,  Dover’s  powder,  tincture  or  extract  of 
hyoscyamus,  extract  of  belladonna,  and  camphorated  tincture  of 
opium  are  available  remedies.  Compound  spirits  of  ether  and  the 
ethereal  tincture  of  valerian,  twenty  drops  every  two  hours,  are 
useful  when  collapse  is  associated  with  the  pain.  Exalgin,  antipyrin, 
and  antifebrin  have  been  recommended  by  Penzoldt.  If  the  col- 
lapse is  marked,  wine,  whisky,  ether,  and  ammonia  should  be  given 
until  it  has  passed  over.  In  pains  of  great  intensity,  the  sovereign 
remedy  is  a hypodermic  injection  of  ^ of  a grain  of  morphin  sul- 
phate, together  with  yq-q-  of  a grain  of  atropin  sulphate  injected 
directly  into  the  epigastric  region.  Boas  recommends  suppositories 
of  extract  of  opium  and  extract  of  belladonna.  All  of  these  agents 
are  useful  for  the  immediate  treatment  of  a paroxysm  ; they  prob- 
ably have  no  curative  effect  on  the  underlying  etiological  trouble. 

53 


8o6 


SENSORY  NEUROSES. 


The  irritability  of  the  mucosa  can  be  effectively  reduced  and  gas- 
tralgic  attacks  sometimes  altogether  prevented  from  recurring  by 
intragastric  irrigation  with  lukewarm  carbonated  water  (Malbranc, 
Kussmaul),  or  by  treating  the  mucosa  according  to  Fleiner’s 
method — with  suspensions  of  bismuth  subnitrate.  We  have  seen 
excellent  results  from  irrigations  containing  bismuth  subnitrate 
(o i j ) , bismuth  subgallate,  5ss  in  one  pint  of  camphor  water.  The 
outflowing  camphor  water  must  be  measured  so  as  to  ascertain  that 
not  over  §j  remains  in  the  stomach.  Although  the  pains  of  gas- 
tralgia  are  not  influenced  directly  by  the  character  of  the  food,  the 
diet  should  be  very  bland  and  unirritating,  and  should  not  be  taken 
in  large  quantities. 

Gastralgokenosis. — Under  this  name  Boas  describes  a painful 
emptiness  of  the  stomach  which  occurs  one  to  two  hours  after 
meals,  and  may  be  so  severe  as  to  embarrass  the  respiration  of  the 
patient.  The  paroxysms  last  but  one-quarter  to  one-half  an  hour, 
and  are  not  connected  with  bulimia.  These  attacks  are  said  to  be 
relieved  by  the  ingestion  of  milk,  bread,  etc.  One  of  the  cases  of 
Boas  developed  into  an  attack  every  time  he  drank  wine  or  cham- 
pagne or  ate  cake.  We  have  never  seen  a case  that  corresponds 
to  Boas’  description  of  this  malady,  and  would  suggest  that  it  is 
probably  a gastric  hyperesthesia  associated  with  hyperperistalsis 
and  a strong  secretion  of  HC1,  particularly  as  the  cases  reported  by 
Boas  show  that  the  reactions  for  HC1  were  quite  marked. 


ANOMALIES  OF  THE  SENSATIONS  OF  HUNGER  AND 
APPETITE . 

BULIMIA,  OR  HYPEROREXIA. 

Morbid  increase  of  the  sensation  of  hunger  may  occur  as  an 
independent  idiopathic  neurosis,  as  a result  of  abnormal  irritability 
of  the  center  controlling  the  sensation  of  hunger,  or  as  a symptom 
of  organic  diseases.  An  intelligent  insight  into  the  pathogenesis  of 
bulimia  is  possible  only  with  a knowledge  of  the  origin  of  the 
sensation  of  hunger.  A modern  physiological  theory  suggests 
that  the  hunger  center  in  the  medulla  oblongata  is  stimulated  nor- 
mally by  the  blood  as  soon  as  it  has  become  impoverished  in 
nutritive  substances,  and  that  the  sensation  of  hunger  ceases  when 
the  blood  is  saturated  with  nutritive  substances.  Stiller  and 
others  assert  that  the  sensation  of  hunger  results  from  excitation 


BULIMIA  OR  HYPEROREXI A. 


807 


of  specific  hunger  nerves  in  the  stomach,  and  that  from  here  the 
sensation  is  conducted  centripetally  to  the  hunger  center,  and 
that,  therefore,  the  normal  sensation,  as  a rule,  is  brought  to  con- 
sciousness indirectly.  Neither  of  these  theories  is  supported 
by  satisfactory  clinical  and  experimental  evidence.  The  appetite 
ceases  when  the  stomach  is  filled  with  food,  but  that  does  not 
imply  that  the  nutritive  materials  are  already  absorbed  into  the 
blood.  This  may  require  from  three  to  four  hours.  In  many 
gastric  diseases  the  feeling  of  hunger  is  indirectly  affected  by  the 
local  disease,  either  increased  or  diminished.  There  are  also 
general  (metabolic)  diseases  which  directly  or  indirectly  increase 
or  diminish  the  sensation  of  hunger.  In  some  persons,  even 
in  the  normal  condition,  vehement  emotional  excitations  may 
cause  a loss  of  hunger  and  appetite,  although  the  blood  is  un- 
doubtedly impoverished  in  nutritive  substances,  so  that  we  have 
clinical  evidence  sufficient  to  demonstrate  a local,  gastric,  and 
a.  remote  or  central  nervous  excitation  of  hunger.  According  to 
one  hypothesis,  hunger  results  every  time  the  stomach  becomes 
entirely  empty,  and  Leo  (“  Ueber  Bulimia,”  “ Deutsche  med.  Woch- 
enschr.,”  1889,  Nr.  29  und  30)  has  asserted,  in  a most  comprehen- 
sive report  on  this  affection,  that  the  abnormally  rapid  evacuation 
of  the  stomach  is  the  cause  of  bulimia.  This  would  naturally 
include  that  bulimia  is  very  frequent  with  pyloric  insufficiency,  in 
which,  as  we  know,  the  ingesta  at  once  enter  the  intestine  from 
the  stomach.  Bulimia  should  also  then  be  frequent  in  cases  where 
a gastroenterostomy  has  been  executed  for  benign  stenosis  of  the 
pylorus ; this  is  not  the  experience  of  the  author  with  his  cases  of 
this  class.  Ewald  and  Fleischer  have  reported  cases  of  bulimia  in 
which  there  was  no  hypermotility.  The  combination  of  bulimia 
with  hypermotility  may  possibly  be  explained  by  the  fact  that 
intense  excitation  of  the  hunger  center  may  extend  to  neighboring 
centers  in  the  medulla,  and  involve  even  the  vagus  center,  which 
responds  by  affecting  a more  rapid  evacuation  of  the  gastric  con- 
tents into  the  intestines.  Some  of  the  accompanying  symptoms  of 
bulimia  (tinnitus  and  roaring  in  the  ears,  palpitation  of  the  heart, 
and  fainting)  are  attributed  by  R.  Ewald  (the  physiologist)  to  sec- 
ondary irritation  of  nervous  centers  lying  in  close  proximity  to  the 
hunger  center.  The  affection  expresses  itself  by  violent  sensa- 
tions of  hunger  coming  on  suddenly,  even  shortly  after  the  com- 
pletion of  a full  meal,  and  if  the  desire  for  food  is  not  immediately 
gratified,  the  patients  exhibit  signs  of  weakness,  headache,  pal- 


8o8 


SENSORY  NEUROSES. 


lor  of  the  face,  palpitation  of  the  heart,  roaring  noises  in  the  ears, 
and  gastric  distress.  The  attacks  may  sometimes  occur  periodic- 
ally, but,  as  a rule,  occur  irregularly.  In  the  intervals  between  the 
attacks  hunger  and  appetite  are  normal,  but  there  are  cases  in 
which  bulimia  may  alternate  with  anorexia. 

Causation. — Bulimia  may  be  an  idiopathic,  central  neurosis  con- 
nected with  abnormal  irritability  of  the  hunger  center,  or  a symp- 
tomatic affection  which  Leo  (/.  c.)  has  observed  in  exophthalmic 
goiter,  with  gastric  ulcer  and  hyperacidity,  chronic  gastritis,  tape- 
worm, diarrhea,  and  menorrhagia.  It  has  been  observed  even  with 
carcinoma  and  dilation.  Fleischer  states,  without  reserve,  that  the 
hyperexcitability  of  the  hunger  center  is  not  caused  by  sudden 
and  excessive  impoverishment  of  the  blood  in  nutritive  substances, 
because  the  attacks  may  occur  immediately  after  an  abundantly 
nutritious  meal  which  has  brought  about  a feeling  of  satiety,  and 
because,  in  other  cases,  the  morbid  sensation  may  be  relieved  by  a 
mouthful  of  bread  or  a swallow  of  beer  or  wine.  The  fact  that 
the  sensations  of  hunger  and  thirst  are  normal  in  the  intervals 
between  the  attacks,  or  even  at  times  entirely  absent,  argues 
against  the  assumption  that  bulimia  is  always  caused  by  a con- 
dition of  the  blood  acting  upon  the  central  nervous  system.  The 
following  are  morbid  conditions  in  which  bulimia  has  been 
observed  to  occur  : Cerebral  tumors,  epilepsy,  psychoses,  hysteria 
and  neurasthenia,  focal  diseases  of  the  brain,  cerebral  concussion, 
Basedow’s  disease,  Addison’s  disease,  tuberculosis,  syphilis  (accord- 
ing to  Fournier,  “Gazette  Hebdom.,”  1871,  No.  1—3,  it  occurs 
between  the  third  and  sixth  month  of  this  disease),  diabetes 
mellitus,  uterine  disease,  chronic  gastritis,  ulcer,  dilation,  car- 
cinoma, enteritis,  and  intestinal  parasites.  Bulimia  has  also  been 
observed  during  the  puerperium.  Some  authors  classify  the 
ravenous  appetite  following  exhaustive  continued  fevers,  as  well  as 
that  following  abundant  loss  of  blood,  with  bulimia.  This,  in  our 
opinion,  is  not  a justifiable  classification,  because  the  increase  of 
hunger  in  these  cases  can  be  explained  in  a simple  and  natural  way 
without  assuming  a hypothetical  excitability  of  the  hunger  center. 
In  diabetes  mellitus  we  may  assume  the  existence  of  an  abnormal 
irritability  of  the  hunger  center  because  these  patients  are  not 
satisfied  even  shortly  after  large  meals.  It  has  been  supposed  that 
the  glucose  circulating  in  the  blood  is  the  agent  that  causes  this 
irritation  of  the  hunger  center.  In  diabetic  patients  in  which  the 
sugar  in  the  blood  and  urine  has  been  reduced  by  a diet  limited 


SYMPTOMS  OF  BULIMIA. 


809 


exclusively  to  fat  and  albuminous  food,  the  torturing  feelings  of 
hunger  disappear,  to  return  again  if  the  mellituria  is  allowed  to 
increase  on  other  diet.  According  to  Pettenkofer  and  Voit,  the 
metabolism  of  diabetic  patients  is  much  increased  ; which,  of  course, 
means  a more  rapid  consumption  of  the  nutritive  elements  of  the 
blood.  The  impoverishment  of  the  blood  is  further  augmented  by 
the  fact  that  the  sugar  which  is  formed  from  the  amylaceous 
substances  of  the  food  is  only  partially  or  not  at  all  utilized  in  the 
economy.  The  diagnosis  of  bulimia  should  only  be  made  in 
diabetes  if  the  violent  sensations  of  hunger  continue  notwith- 
standing very  rich  and  very  abundant  meals,  or  if  it  recurs  very 
soon  after  such  meals,  by  which  the  blood  must  have  been  charged 
with  nutritive  substances  for  a l.onger  time.  Ewald  and  Boas  have 
observed  that  the  attacks  become  less  frequent  after  bodily  exer- 
cise in  the  open  air.  According  to  Rosenthal,  the  affection  is  more 
frequent  in  women  than  in  men,  and  occurs  most  often  between  the 
twentieth  and  fortieth  years. 

Symptomatology. — The  main  and  most  characteristic  symptom 
is  the  impulsive  sensation  of  hunger,  which  by  any  and  every 
means  commands  the  ingestion  of  food.  The  pallor,  weakness, 
and  terror,  with  attacks  of  fainting  and  roaring  in  the  ears,  we  have 
already  described.  This  sensation  comes  on  generally  within  one 
to  two  hours  after  meals,  but  it  may  occur  within  ten  minutes  after 
meals.  We  have  known  three  old  gentlemen  who  were  for  a long 
time  aroused  in  the  middle  of  the  night  by  this  torturing  sensation 
of  hunger.  Some  patients  complain  of  gnawing  and  boring  pain 
if  the  hunger  is  not  gratified.  Very  small  quantities  of  milk,  beer, 
or  wine,  or  only  a few  mouthfuls  of  cracker  or  bread,  will  cause 
the  entire  train  of  symptoms  to  disappear.  Peyer  (“  Correspon- 
denzbl.  Schweitzer  Aerzte,”  1888,  Nr.  20)  reports  a case  of  a parox- 
ysm of  bulimia  occurring  in  a female  patient  when  she  was  away 
from  home  visiting  a friend.  The  weakness  ensuing  is  described 
as  having  been  so  great  that  she  could  not  return  home.  Peyer 
asserts  that  in  three-quarters  of  an  hour  she  consumed  three  pints 
of  milk,  twenty-three  eggs,  and  two  pints  of  strong  wine  before 
the  bulimia  and  pain  in  the  stomach  ceased.  The  patient  then  fell 
asleep,  and  on  awakening  returned  home  perfectly  well.  Potton  re- 
ports the  case  of  a young,  hysterical  girl  who  was  obliged  to  take 
eleven  or  twelve  meals  a day,  and  even  eat  during  the  night;  she 
is  claimed  to  have  ingested  between  ten  and  twelve  kilograms  of 
food  per  diem,  and  was  finally  cured  by  gradually  increasing  doses 


8io 


SENSORY  NEUROSES. 


of  morphin.  This  was  a case  of  so-called  continued  bulimia.  We 
have  made  studies  of  the  dietary  in  two  of  our  cases,  a male  and  a 
female  patient,  and  controlled  the  metabolism  by  determinations 
of  the  total  nitrogen  output  in  the  urine  and  feces.  The  man  took 
in  food  amounting  to  7368  calories  on  an  average,  daily  ; the  woman 
consumed  food  to  the  value  of  8131  calories.  The  curious  obser- 
vation made  was  that  both  patients  lost  weight,  and  the  stools  con- 
tained from  y to  y?  of  the  ingested  food-stuffs  in  an  undigested 
form.  The  female  was  not  cured,  but  the  man  gave  himself 
up  to  strict  sanatorium  management — his  diet  was  gradually 
reduced  to  2400  calories;  under  this  food  value  he  gained  weight, 
and  the  urine  contained  less  of  toxic  products  than  on  his  old 
bulimic  food  supply.  Medicines  were  not  used  ; he  was  simply 
put  under  constant  guard,  day  and  night,  by  reliable  nurses,  and 
no  more  food  allowed  than  was  ordered  by  the  physician. 

Diagnosis. — Wherever  the  abnormal  sensation  of  hunger  oc- 
curs shortly  after  abundant  food  has  been  taken,  the  diagnosis  is 
not  difficult ; at  other  times  it  may  be  confounded  with  polyphagia 
and  acoria.  In  polyphagia  the  desire  for  eating  is  very  much  in- 
creased, but  it  does  not  occur  until  some  time  after  the  meals,  and 
occurs  gradually,  not  developing  the  intense  hunger  suddenly. 
So,  polyphagia  is  simple  increase  of  the  normal  sensation  of  appe- 
tite, such  as  we  find  in  diabetes  mellitus.  It  is  impossible  strictly  to 
separate  polyphagia  from  bulimia — both  occur  under  similar  con- 
ditions and  as  primary  or  secondary  neuroses.  Bouveret  (“  Traite 
des  Maladies  de  1’Estomac,”  Paris,  1893,  page  654)  refers  to  a case 
in  which  a patient  seventeen  years  old  could  devour  100  pounds  of 
meat  in  twenty-four  hours,  and  Rosenthal  reports  an  instance  of  a 
woman,  aged  twenty-eight  years,  who  ate  at  one  meal  a whole 
roast  of  goose  and  a large  portion  of  bread.  There  is  a so-called 
continued  form  of  bulimia  which  alternates  with  acoria,  or  the 
absence  of  the  feeling  of  gratification  or  satisfaction  after  meals. 
If  it  can  be  found  that  the  feeling  of  hunger  is  very  great,  and 
even  continues  or  returns  after  abundant  meals,  then  we  are  dealing 
with  bulimia;  but  if  the  sensation  of  hunger  is  normal  or  reduced, 
and  ceases  after  larger  meals,  but  without  causing  the  feeling  of 
satiety,  we  are  dealing  with  acoria.  The  continued  form  of  bulimia 
has  hitherto  been  found  only  with  diabetes  mellitus  and  hysteria. 
We  have  had  two  cases  in  hospital  practice  which  illustrate  that 
bulimia  and  polyphagia  may  be  developed  by  practice.  Both  cases 
occurred  in  negroes  who  had,  as  a result  of  a number  of  wagers. 


ACORIA. 


8 1 1 

eaten  large  quantities  of  food.  One  colored  man  was  a waiter  at  a 
hotel  at  Cape  May,  N.  J.,and  made  a practice  of  exhibiting  himself  by 
eating  a huge  watermelon  together  with  eight  pies.  The  other  negro, 
who  was  a patient  at  Baltimore,  gradually  developed  his  polyphagia 
from  participating  in  rival  encounters  with  other  individuals  of  his 
race  to  see  who  could  eat  the  most  oysters.  It  is  claimed  that  this 
man  could  eat  three  quarts  of  oysters,  with  a large  amount  of 
crackers  and  beer.  Both  negroes  found  later  that  the  habit  had 
developed  into  a disease,  the  tremendous  appetite  developing  very 
often  within  a half  hour  after  the  big  meals  of  bread,  fish,  and  egg 
had  been  taken.  One  of  them  has  been  cured  by  dram  doses  of 
bromid  of  ammonia  four  times  daily.  The  diagnosis  of  an  affec- 
tion of  this  character  can  not  be  stated  in  such  exact  terms  as  that 
of  an  organic  disease,  as  individual  opinions  of  specialists  as  to 
what  really  constitutes  bulimia  will  probably  vary  greatly.  (The 
treatment  will  be  considered  together  with  that  of  acoria.) 


ACORIA. 

This  word  is  derived  from  « and  %opiwufu,  I become  satiated. 

“Acoria  ” denotes  the  absence  of  the  normal  feeling  of  satiation, 
even  after  very  abundant  meals,  without  increase  of  hunger  or 
appetite. 

Acoria  is  not  identical  with  bulimia  or  polyphagia,  for  in  both 
of  these  there  is  a very  strong  feeling  of  hunger,  while  in  acoria 
we  may  have  absence  of  appetite.  Even  in  polyphagic  gluttons 
the  feeling  of  satiation  will  eventually  supervene,  but  not  in  acoria. 
The  disease  is  generally  secondary  to  neurasthenia,  hysteria,  and 
certain  psychoses.  It  is  occasionally  met  with  in  sexual  neuras- 
thenics. The  feeling  of  satiation  is  no  positive  sensation ; it  occurs 
when  hunger  and  appetite  have  been  appeased,  and  is  therefore 
a negative  sensation.  Hunger  and  appetite  cease  normally  when 
the  hunger  center  passes  from  a sensation  of  excitation  to  that 
of  rest.  The  amount  of  food  required  to  accomplish  this  varies 
greatly  in  different  persons,  and  even  in  the  same  person  at  different 
times.  One  hypothesis  has  attempted  to  explain  acoria  on  the 
basis  of  overexcitation  of  the  hunger  center.  If  this  were  the 
case,  we  would  find,  periodically  at  least,  an  increased  sensation  of 
hunger  after  large  meals,  which  is  never  observed  in  acoria,  for 
hunger  and  appetite  are  normal,  or  even  subnormal,  in  acoria. 
Some  patients  even  state  that  after  meals  hunger  ceases,  but  they 


SENSORY  NEUROSES. 


have  no  feeling  of  satiation ; in  fact,  no  impression  whatever  from 
the  stomach  informing  them  that  they  have  eaten  enough.  It  is 
well  known  that  many  people  are  not  satisfied  to  introduce  food 
until  the  appetite  has  been  appeased,  but  they  continue  long 
enough  to  perceive  a feeling  of  pressure  and  slight  fullness  in  the 
stomach,  which  is  a result  of  a moderate  distention  of  the  gastric 
walls  by  ingesta.  While  moderate  eaters  perceive  this  sensation  as 
uncomfortable  and  indicating  supersatiation,  gormandizers  gradu- 
ally become  accustomed  to  this  feeling  of  pressure  and  fullness, 
sometimes  from  early  childhood,  so  that  eventually  they  do  not 
believe  themselves  satiated  before  this  distention  occurs,  and  this 
fullness  and  distention  are  finally  confounded  with  the  normal  sen- 
sation of  satiety. 

The  next  step  in  the  development  of  this  nervous  anomaly  is 
that  the  feeling  of  pressure  and  fullness  may  mimic  a temporary 
normal  feeling  of  satiation,  while  at  the  same  time  the  excitation 
of  the  hunger  center  continues.  The  sensation  of  hunger,  when 
it  is  not  very  strong,  may  be  in  some  cases  removed  by  filling  the 
stomach  with  perfectly  indigestible  material,  such  as  leaves  and 
sawdust.  In  the  voyage  of  the  Jeanette  (Journal  of  Lieutenant 
de  Long,  commanding  the  expedition,  1883)  the  crew  of  the  sur- 
viving members  subsisted  upon  scraps  of  deer  skin,  which,  from  its 
bulk  in  the  stomach,  seemed  to  afford  relief  from  hunger.  After 
everything  was  exhausted  they  lived  upon  an  infusion  made  from 
arctic  willow,  containing  really  no  nourishment,  and  ate  two  old 
boots.  As  the  feeling  of  satiation  is  absent  after  copious  filling  of 
the  stomach  with  food,  and  as  it  can  not  be  disguised  by  an 
abnormal  feeling  of  hunger,  because  hunger  is  normal  or  sub- 
normal in  acoria,  another  explanation  that  has  been  offered  for 
this  nervous  affliction  is  that  it  is  due  to  loss  of  sensibility,  or 
anesthesia,  of  the  gastric  sensory  nerves.  This  seems  to  be  a very 
probable  explanation,  since  we  have  personally  had  at  least  one 
experience  that  would  suggest  a local  gastric  anesthesia  as  an  ex- 
planation of  acoria.  The  case  we  have  in  mind  is  that  of  a young 
woman  whose  stomach  we  had  sprayed  with  a three  per  cent,  solu- 
tion of  cocain  and  menthol.  She  returned  on  the  same  day,  stating 
that,  although  she  had  taken  a long  bicycle  ride  after  the  spraying, 
and  returned  home  feeling  quite  hungry,  she  had  the  impression 
that  the  food  she  ate  never  reached  the  stomach.  She  had  no  feel- 
ing in  her  stomach  that  the  meal  effected  satiation.  At  first  we 
overlooked  the  causal  relation  between  the  spraying  with  menthol 


NERVOUS  ANOREXIA. 


813 


and  cocain  for  this  temporary  acoria,  and  our  attention  was  attracted 
to  it  after  the  same  symptoms  were  complained  of  each  time  the 
menthol  and  cocain  were  used.  These  agents  had  been  employed 
for  the  relief  of  gastralgic  pains  resulting  from  erosions.  The 
case  ultimately  recovered  by  treating  it  with  suspensions  of  sub- 
nitrate of  bismuth.  It  is  conceivable  that  anesthesia  of  the  stom- 
ach nerves  may  occur  from  repeated  overdistention,  as  occurs 
in  bulimia,  polyphagia,  diabetes  mellitus,  and  dilation  of  the 
stomach. 

Symptomatology. — As  the  only  symptom  is  the  absence  of 
satiation,  the  clinical  picture  is  not  very  manifold.  The  complaints 
of  the  patients  are  limited  to  the  statement  that  large  meals  cause 
no  sensation  of  having  had  enough  to  eat,  and  that  they  do  not 
know  when  to  cease  eating;  that  they  have  to  measure  out  their 
food  previous  to  beginning  to  eat,  in  order  to  know  when  they 
have  had  sufficient.  Some  of  these  patients  try  to  compel  a feeling 
of  satiation  by  the  ingestion  of  enormous  quantities  of  food  and 
drink.  This  has  been  reported  as  a cause  of  gastritis,  atony,  and 
dilation.  The  prognosis  varies  according  to  the  fundamental 
disease.  The  diagnosis  is  made  from  the  single  important  symptom 
and  the  exclusion  of  bulimia  and  polyphagia.  Sometimes  we  find 
transitions  from  acoria  to  bulimia,  which  Boas  explains  by  a reac- 
tive hyperesthesia  following  an  anesthesia  of  the  gastric  nerves. 
Acoria  is  distinguished  from  polyphagia  by  the  increased  desire  for 
food,  which  is  marked  in  the  latter, very  likely  as  a result  of  increased 
oxidation,  while  the  diagnosis  from  bulimia  hinges  upon  the  raven- 
ous desire  for  food  in  the  latter;  in  both  the  feeling  of  satiation  will 
eventually  supervene. 

Treatment. — The  treatment  of  bulimia  when  it  is  a secondary 
disease  must  have  regard  for  removal  of  the  primary  cause,  such  as 
intestinal  parasites,  genito-urinary  diseases,  hyperacidity,  or  ulcer, 
and  any  existing  neurasthenia,  hysteria,  or  psychosis.  The 
bromids  are  very  valuable  remedies  to  reduce  the  irritability  of  the 
hunger  center ; they  should  be  given  in  the  form  of  bromid  of 
ammonia  or  strontium,  thirty  grains  of  either  four  times  a day, 
preferably  in  peppermint  water.  The  following  formula  will  be 
found  useful  in  bulimia: 


B.  Tinct.  opii  camph., 81.0  f^iij 

Tinct.  belladonna, 1.0  gtt.  xl 

Elix.  simplic., q.  s.  180.0  f^vj.  M. 


Sig. — One-half  of  a fluidounce  three  times  a day. 


814 


SENSORY  NEUROSES. 


Arsenic,  in  form  of  Fowler’s  solution,  beginning  with  three  to 
five  drops,  and  gradually  increasing  the  dose  to  ten  to  fifteen  drops, 
is  highly  recommended  by  Boas.  Rosenthal  recommends  subcu- 
taneous injections  of  extract  of  opium,  and  has  seen  good  results 
in  bulimia  from  cocain  hydrochlorate.  Morphin  is  a remedy  that 
has  been  followed  by  good  results  in  this  affection.  An  attempt 
should  be  made  with  the  use  of  electricity  in  the  treatment.  In  one 
of  the  colored  patients  to  whom  we  referred  as  champion  gluttons, 
and  who  had  subsequently  developed  bulimia,  the  symptoms  im- 
proved very  much  under  the  intragastric  use  of  the  constant  current. 
The  treatment  of  acoria  should  be  mainly  that  of  neurasthenia ; 
climatic  changes  and  electrical  hydropathic  cures  are  most  effec- 
tive. Intragastric  douches,  with  alternating  warm  and  cold  water, 
have  been  recommended.  It  is  very  important  that  these  patients 
should  be  watched  by  healthy  friends  during  their  eating ; thorough 
mastication  and  insalivation  should  be  insisted  upon.  Strychnin 
and  massage  of  the  stomach  suggest  themselves  as  rational  means 
of  treatment. 


NERVOUS  ANOREXIA. 

By  anorexia  is  meant  an  entire  absence  of  appetite  and  loss  of 
the  sensation  of  hunger.  The  superlative  degree  of  this  sensation 
is  expressed  in  the  disgust  and  repugnance  toward  all  food.  There 
are  probably  no  pathological  conditions,  neither  of  the  stomach  nor 
of  any  other  organ  of  the  body,  in  which  anorexia  is  not  occasionally 
met  with.  In  most  anatomical  diseases  of  the  stomach  anorexia  is 
a regular  accompaniment.  The  separation  of  appetite  and  hunger 
is  not  so  clear  as  one  might  suppose ; the  two  are  not  necessarily 
synonymous,  nor  does  one  include  the  other.  Penzoldt  defines 
hunger  as  the  warning  or  admonition,  and  appetite  as  the  pleasure 
of  eating  (“  Bibliothek  der  ges.  medizin.  Wissenschaften,  heraus- 
gegeben  von  Drasche,”  article  on  “ Anorexia ”).  There  may  even  be 
appetite  when  there  can  not  possibly  be  hunger.  We  have  already 
spoken  of  the  various  forms  of  anorexia  that  may  accompany  the 
organic  and  functional  diseases  of  the  stomach.  By  nervous  ano- 
rexia we  mean  loss  of  appetite,  and  even  repugnance  to  food,  that 
may  extend  over  weeks  and  months,  with  a perfectly  intact  diges- 
tive apparatus;  this  affection  is  found  principally  in  women,  and  is 
based  upon  neurasthenia,  hysteria,  anemia,  chlorosis,  and  certain 
neuroses  of  the  stomach.  It  is  found  in  those  addicted  to  the 
excessive  use  of  alcohol  and  tobacco,  and  as  a symptom  of  the 


TREATMENT  OF  ANOREXIA. 


815 


morphin  habit.  It  is,  therefore,  not  a disease  peculiar  to  itself, 
not  a typical  morbid  entity,  but  rather  a sequence.  Whether  or 
not  nervous  anorexia  may  be  an  independent  disease  of  central 
origin,  a neurosis  connected  with  a reduced  irritability  of  the  hun- 
ger center,  has,  up  to  the  present  time,  not  been  satisfactorily 
investigated.  The  course  and  the  prognosis  depend  upon  the 
degree  of  the  repugnance  for  food.  Among  the  insane  and  very 
neurasthenic  patients  fatal  cases  have  been  reported. 

Symptomatology. — The  patients  who,  from  loss  of  appetite  or 
distress,  can  not  take  food,  grow  anemic  and  weak,  appear  very 
emaciated,  have  a slow,  feeble  pulse,  cold  hands  and  feet,  and  may 
even  give  the  impression  of  tuberculous  patients.  Rosenthal 
(“  Magenneurosen,”  etc.,  Vienna  and  Leipzig,  1886),  Gull  (“The 
Lancet,”  1868),  and  Charcot  (“Oeuvres  Completes,”  tome  ill,  p. 
240)  have  reported  fatal  cases  of  nervous  anorexia.  Insomnia  is 
a frequent  symptom  of  this  affection.  Very  slight  anatomical 
changes  in  the  stomach  may  cause  anorexia ; it  is,  therefore,  almost 
impossible  to  make  the  diagnosis  of  secondary  or  primary  anorexia 
with  precision. 

Diagnosis. — There  is  no  difficulty  about  the  diagnosis  of 
anorexia,  but  it  is  not  always  easy  to  discover  the  real  cause  of  it. 
We  will  find  under  the  consideration  of  enteroptosis  that  almost 
any  abdominal  organ  when  dislocated  may  produce  this  symptom. 
Organic  affections  of  the  stomach  must  be  excluded  before  we  can 
make  the  diagnosis  of  nervous  anorexia.  Very  frequently  chronic 
gastritis,  incipient  tuberculosis,  and  carcinoma  begin  with  this 
symptom  before  any  other  signs  or  symptoms  are  manifest. 

Treatment. — The  primary  object  of  the  treatment  must  be 
to  improve  the  general  nervous  condition,  to  correct  any  exist- 
ing fundamental  disease,  to  act  upon  the  psychical  sphere  by  per- 
suasion, suggestion,  and  firm  but  kind  argument,  and,  finally,  to 
combat  the  anorexia  itself  directly.  Any  existing  neurasthenia 
and  hysteria  should  be  treated  by  methods  that  have  been  spoken 
of  repeatedly  for  these  affections.  Dujardin-Beaumetz  (“Traite- 
ment  des  Maladies  de  l’Estomac,”  1891,  p.  326)  speaks  very  highly 
of  arsenic  in  the  treatment  of  nervous  anorexia.  In  anemia  mild 
preparations  of  iron  (see  ferratin)  are  almost  indispensable.  The 
tincture  of  the  chlorid  of  iron  and  the  Blaud  pill  will  rarely  disagree, 
and  in  those  cases  in  which  these  forms  produce  gastric  distress  I 
found  that  organic  mixtures  of  iron  did  so  likewise.  (See  Hem- 
meter,  “Absorption  of  Iron  from  the  Gastro-intestinal  Tract,”  etc., 


8i6 


NEUROSES  OF  SECRETION. 


“ Phila.  Med.  Jour.,”  January  13,  1900.)  It  has  been  found  that 
iron  injected  subcutaneously  will  produce  dyspeptic  distress 
(Glaevecke,  “Arch.  f.  experim.  Path.  u.  Pharm.,”  1883,  Bd.  xvn). 
This  effect  of  iron  in  rare  cases  is  unavoidable  and  not  well  under- 
stood. In  order  to  improve  the  general  nutrition,  the  Weir 
Mitchell  rest-cure, — which  consists  in  isolating  the  patient  from 
his  family  and  placing  him  under  the  supervision  of  a trained 
nurse  and  an  experienced  physician,  and  feeding  him  so  abundantly 
that  gradually  a gain  of  weight  is  accomplished, — together  with 
the  use  of  baths,  massage,  and  electricity,  has,  in  many  cases  in 
our  experience,  produced  happy  results  when  other  means  have 
failed.  When  there  is  an  absolute  repugnance  for  food,  or  when 
the  patient  is  insane,  artificial  compulsory  alimentation  by  gavage 
should  not  be  postponed  too  long.  We  have  considered  this  fully 
on  page  190.  In  the  beginning  of  the  trouble  the  bitter  tonics  are 
available  to  stimulate  the  appetite.  The  basic  orexin,  five  to  ten 
grains  three  times  a day,  in  a cup  of  hot  bouillon,  produces  some- 
times excellent  results  in  these  cases  of  nervous  loss  of  appetite. 

Boas  speaks  very  highly  of  the  cinchona  bark.  It  may  be  pre- 
scribed in  the  following  formula : 


R.  Tinct.  cinchonse  comp. 40.0  f!|iss 

Acid,  sulphuric,  dil. , io.o  f^ij 

Syr.  zingiber., q.  s.  240.0  f|jvj.  M. 


SlG. — One-half  of  a fluidounce  in  two  ounces  of  water,  through  a glass  tube, 
three  times  a day. 


In  some  cases  in  which  the  anorexia  was  due  to  a feeling  of 
pressure  and  discomfort  after  eating,  Rosenthal  reports  good  results 
from  ten  to  fifteen  grains  of  bromid  of  sodium  given  before  meals. 
Boas  cautions  against  the  use  of  mineral  waters  in  the  treatment  of 
this  neurosis.  One  most  approved  combination  for  anorexia  is 
given  on  page  571  ; it  contains  dilute  HC1,  because  I have  found, 
in  a very  large  number  of  cases  of  intense  nervous  anorexia,  that 
the  gastric  secretion  is  very  much  deduced  or  entirely  lost,  and 
I have  rarely  observed  persistent  anorexia  together  with  normal 
HC1  secretion. 


SUPEKACI DITY. 


Si/ 


CHAPTER  XII. 

NEUROSES  OF  SECRETION. 

HYPERCHYLIA  (Hyper-  or  Superacidity;  Hyperciilorhydria). 

Most  diagnosticians  whose  clinical  and  laboratory  experience 
renders  them  competent  to  judge,  consider  hyperacidity  and  hyper- 
secretion of  the  gastric  juice  to  be  neuroses  of  the  secretory  func- 
tion. They  are  regarded  as  functional  disturbances  of  the  nerves 
of  the  stomach,  which  may  occur  as  individual  diseases  or  as  part 
of  other  neurotic  conditions.  This  view  no  doubt  is  correct  in  a 
large  number  of  the  cases.  It  includes  the  opinion  that  in  this  dis- 
ease no  characteristic  changes  in  the  structure  of  the  gastric 
mucous  membrane  are  demonstrable.  Judging  from  the  results  of 
Hayem,  Cohnheim,  and  Einhorn,  and  the  author,*  it  is  beyond  a 
doubt  that  in  more  than  one-half  the  cases  of  hyperacidity  ex- 
amined, proliferation  of  the  glandular  elements  is  present. 

I have  not  only  examined  fragments  of  mucosa  that  were  accident- 
ally found  in  the  wash-water,  but  have  had  opportunities  of  making 
autopsies  on  cases  of  pronounced  and  prolonged  hyperacidity  that 
died  of  intercurrent  diseases.  In  serial  sections  of  these  stomachs 
it  was  found  that  the  prevailing  state  of  the  mucosa  in  the  inter- 
mediate zone  and  fundus  was  that  of  glandular  proliferation,  with 
increase  in  the  number  of  oxyntic  cells.  Such  stomachs  do  not 
show  the  same  conditions  throughout.  On  making  serial  sections 
of  large  pieces  of  the  secretory  portion,  one  occasionally  meets  with 
areas  in  which  the  glandular  structure  is  apparently  normal.  At 
very  rare  intervals  and  in  rare  cases  one  can  even  find  sections 
showing  partial  glandular  atrophy.  This  is  so  rare  as  to  be 
insignificant.  Even  in  normal  stomachs  one  sometimes  finds  indi- 
cations of  atrophy  in  serial  sections,  and  we  consider  that  these 
changes  are  very  limited,  and,  perhaps,  may  be  considered  as  pro- 
cesses of  reconstruction  and  transition,  where  accidentally  injured 
or  exhausted  glands  break  down  in  minute  foci  and  are  replaced 
gradually  by  newly  formed  gland-cells.  The  prevailing  condition, 


* Hemmeter,  “ Z.  Histologie  d.  Magendriisen  b.  Hyperaciditat,”  “ Archiv  f.  Ver- 
dauungskrankheiten,”  Bd.  IV,  S.  23. 


8 1 8 


NEUROSES  OF  SECRETION. 


then,  in  hyperacidity,  according  to  our  opinion,  is  proliferation  of 
the  glandular  elements  and  increase  of  oxyntic  or  border  cells. 

A large  number  of  microscopical  investigations  will  be  neces- 
sary to  confirm  this  opinion.  I have  thus  far  examined  the 
entire  stomach  of  four  cases  that  gave  the  clinical  picture  of  hyper- 
acidity before  death.  In  all  four  of  these  cases  the  proliferation  of 
the  glandular  elements  was  uniformly  present.  Strauss  has  de- 
scribed conditions  in  the  gastric  glandular  layer  which  are  con- 
firmatory of  my  own  results  (“  Virchow’s  Archiv,”  1898,  Bd.  cliv). 

Sir  William  Roberts  (“  Digestion  and  Diet,”  p.  240)  holds  that 
the  acid  in  what  he  calls  acid  dyspepsia  (which  seems  to  me  an  objec- 
tionable term,  since  it  does  not  define  which  of  the  diseases  that 
are  connected  with  excess  of  acidity  he  refers  to)  is  not  unmixed 
HC1,  but  that  lactic,  butyric,  tartaric,  and  malic  acids  are  present. 
These  are  probably  derived  from  salts  of  the  organic  acids  present 
in  articles  of  food  which  are  decomposed  by  the  HC1  of  the  gas- 
tric juice.  There  may,  of  course,  be  a hyperacidity  due  to  excess 
of  organic  acids,  which  may  present  all  the  symptoms  of  hyper- 
chlorhydria;  in  such  cases  there  is,  in  my  experience,  no  HC1 
secreted  at  all.  What  I refer  to  clinically  as  hyperacidity,  how- 
ever, is  an  excessive  formation  of  hydrochloric  acid  from  the  gas- 
tric glands.  Concerning  the  nature  and  origin  of  this  acid  we 
have  nothing  but  theories. 

It  has  been  suggested  that  the  hyperchlorhydria  is  due  to  an 
excess  of  chlorids  in  the  organism,  from  which  it  liberates  itself  by 
excretion  into  an  organ  where  the  freeing  of  the  system  from 
chlorids  could  at  the  same  time  become  of  utility  as  a digestive 
secretion  in  the  form  of  HC1.  The  author  has  made  a number  of 
experiments  by  feeding  carnivorous  animals  with  food  from  which 
the  chlorids  had  been  removed  so  far  as  was  possible.  The  acidity 
of  the  gastric  juice  of  the  dog  will  become  very  much  reduced  if 
the  chlorids  are  withdrawn  from  the  food.  This,  however,  is  no 
proof  of  the  supposition  that  the  reduction  of  chlorids  is  the  cause  of 
the  diminished  secretion  of  HC1,  because  foods  containing  consider- 
able of  chlorids  are  a healthy  stimulant  to  the  normal  secretion  of 
HC1,  and  food  deprived  of  chlorids  can  not  exert  this  stimulation 
upon  the  mucosa.  Personally,  the  author  considers  it  very  probable 
that  hyperacidity  is  frequently  an  adaptive  process : that  is  to  say, 
the  glandular  layer  gradually  develops  greater  secretory  powers, 
because  more  secretion  of  HC1  is  required  by  the  nature  of  the 
ingested  food.  We  have  been  told  by  two  physicians  practising  in 


RELATION  OF  ACIDITY  OF  URINE  AND  GASTRIC  ACIDITY.  8 19 

Japan  that  hyperacidity,  as  well  as  gastric  ulcer,  are  practically 
unknown  in  that  country,  which  may  be  partially  explained  by  the 
exclusive  carbohydrate  diet  upon  which  the  middle  and  lower 
classes  of  that  nation  exist. 

It  is  a well-known  fact  that  the  gastric  juice  of  carnivora  contains 
relatively  more  HC1  than  that  of  the  herbivora.  It  may  not  be  so  well 
known  that  the  gastric  juice  of  a carnivorous  animal  can  be  made 
to  contain  a less  amount  of  HC1  by  being  fed  upon  a carbohydrate 
diet  for  a long  time.  Two  dogs  of  the  same  litter,  (a),  fed  exclusively 
on  milk,  potatoes,  and  rye  bread,  and  (£),  fed  exclusively  on  beef, 
mutton,  pork,  fish,  and  water:  At  the  end  of  one  year  dog  (a),  fed 
upon  carbohydrates,  had  a gastric  juice  one  hour  after  a roll  and  a 
half  pint  of  water,  containing  3 per  1000  of  HC1 ; dog  ( b ),  who  was 
fed  upon  a meat  diet,  had  a gastric  juice  containing  6.540  per  1000 
HC1  after  the  same  test-meal.  The  figures  are  the  results  of  the  aver- 
age of  ten  different  analyses  on  each  dog.  These  two  dogs  were 
raised  in  two  entirely  different  families.  Dog  (a)  was  raised  by  a 
gentleman  living  in  a country  district  where  meat  was  not  easily  ob- 
tained and  milk  was  very  abundant ; dog  ( b ) was  raised  in  the  city, 
and  lived  upon  the  refuse  meats  from  the  table.  Since  the  publica- 
tion of  the  first  edition  these  two  fox  terriers  have  been  kept  in  the 
same  families  and  two  other  terriers  have  been  raised  in  the  same 
way.  The  results  of  test-meals  showing  that  the  gastric  juice  of 
the  dogs  raised  on  meat  contains  twice  as  much  HC1  on  the  aver- 
age (6.6320  per  1000)  as  that  of  the  dogs  fed  on  milk,  bread,  and 
potatoes.  Unless  conducted  in  this  manner,  and  watched  by  com- 
petent observers  for  a long  time, — at  least  one  year, — the  experi- 
ment is  of  no  practical  utility.  It  is  conceivable  that  we  do  not  as 
yet  know  all  of  the  constituents  of  the  gastric  juice  ; clinically,  it 
has  been  very  frequently  observed  that  the  secretions  of  the  intes- 
tines may  contain  traces  of  products  of  metabolism  and  other 
toxins  when  the  function  of  the  kidney  is  suppressed  or  lost.  The 
gastric  j uice  of  epileptics  may  contain  toxic  substances.  Augustini, 
who  recently  investigated  this  subject,  found  that  the  gastric  juice 
of  an  epileptic,  when  injected  into  the  abdomen  of  a rabbit,  proved 
fatal,  with  general  toxic  symptoms  and  clonic  convulsions.  This 
was  especially  true  when  the  gastric  juice  was  obtained  immediately 
before  or  after  an  attack.  Normal  gastric  juice  was  found  to  pro- 
duce no  such  evil  effects.  The  probable  action  of  bacteria  can 
not  be  excluded  from  these  experiments.  Augustini  concludes 
from  these  experiments  that  systematic  lavage  and  disinfection  of 


820 


NEUROSES  OF  SECRETION. 


the  stomach  and  intestines  are  indicated  in  all  cases  of  epilepsy. 
What  we  wish  to  emphasize  in  this  introduction  to  the  considera- 
tion of  hyperacidity  is  that  hyperchlorhydria,  although  frequently 
a neurosis,  is,  in  our  opinion,  very  often  a process  of  adaptation  of 
the  mucosa  to  the  demand  for  increased  work. 

Acidity  of  the  Urine  and  Gastric  Contents  in  the  Healthy 
and  in  the  Dyspeptic. — Mathieu  and  Treheux  (“  Arch.  Gen.  de 
Med.,”  November,  1895)  have  made  researches  on  this  subject. 
They  examined  the  urine  hourly  during  the  afternoon,  after  the 
midday  meal,  carrying  out  their  investigations  on  twelve  persons, 
after  eighty-four  different  meals,  thus  making  over  400  estimates 
of  the  degree  of  acidity  of  the  gastric  contents  and  urine.  The 
individuals  examined  were  the  subjects  of  hyperchlorhydria,  with 
and  without  symptoms  of  gastric  dilation,  carcinoma,  etc.  The 
authors  conclude  that : (1)  There  is  a relation  between  the  acidity  of 
the  gastric  contents  and  the  urine.  (2)  The  greater  the  production 
of  acid,  whether  by  secretion  or  fermentation,  the  greater  the 
amount  of  acid  excretion  in  the  urine.  (3)  Normally,  the  acidity 
of  the  urine  falls  during  the  first  three  to  five  hours  after  eating; 
thereafter  it  increases.  (4)  Most  often  there  is  an  almost  absolute 
parallelism  between  the  two  curves  of  gastric  and  urinary  acidity, 
but  this  is  destroyed  after  a repast  by  the  presence  of  polyuria. 
(5)  If  the  acid  is  withdrawn  by  any  means  from  the  stomach,  the 
amount  in  the  urine  falls  also,  and  the  latter  may  even  become 
alkaline.  (6)  The  average  quantity  eliminated  by  the  urine  hourly 
is  greater  in  hypochlorhydria  (subacidity)  than  in  hyperchlorhy- 
dria (superacidity).  (7)  Milk  increases  the  acid  in  the  urine, 
owing  to  its  giving  rise  to  lactic  acid  in  the  stomach.  (8)  It  is  not 
possible,  at  any  rate  at  present,  to  trace  the  curves  of  urinary 
acidity  so  as  to  bear  indirectly  on  the  question  of  the  chemical 
variety  of  the  dyspepsia.  (9)  Milk  must  be  excluded  from  test- 
meals  when  these  curves  are  to  be  studied.  (10)  Patients  should 
be  subjected  to  a constant  regimen  for  some  time  before  the  in- 
vestigations. 

Nature  and  Concept. — As  the  name  implies,  the  factor  with 
which  we  are  most  particularly  concerned  in  this  neurosis  is  the 
HC1.  With  superacidity,  a gastric  juice  unusually  rich  in  HC1  and 
pepsin  is  secreted  in  very  large  quantities  during  digestion,  as  a 
result  of  the  stimulation  of  the  foods.  On  this  account  free  HC1 
may  be  proved  in  the  stomach  after  test-meals  much  earlier  than 
under  normal  circumstances,  and  the  acidity  of  the  digestive 


HISTORY  OF  SUPERACIDITY. 


821 


mixture  is  further  increased  as  digestion  proceeds.  Superacidity 
may  be  an  independent  disease  confined  to  the  stomach  alone, 
or  a partial  symptom  of  hysteria,  neurasthenia,  and  melancholia. 
It  may  also  be  noticed  as  a reflex  neurosis  with  renal  calculus  and 
hepatic  colic,  and  as  the  companion  of  organic  changes  of  the 
stomach  (ulcus  ventriculi,  gastritis  acida). 

Historical. — Even  if  superacidity,  like  supersecretion,  has  been 
demonstrated  with  certainty  only  in  the  last  twelve  years,  through 
the  researches  of  Reichmann,  Jaworski,  van  den  Velden,  Riegel, 
the  latter’s  pupils,  and  others,  and  the  aspect  of  the  disease  has 
been  precisely  defined  by  them,  nevertheless,  as  Ewald  justly  em- 
phasizes, it  would  be  an  error  to  believe  that  we  have  to  do  with 
an  entirely  new  discovery,  since  both  these  anomalies  of  secretion, 
as  also  their  nervous  origin,  were  known  to  older  physicians  in  the 
beginning  and  middle  of  this  century — men  celebrated  in  England, 
France,  and  Germany  (Trousseau,  Todd,  Budd,  Copland,  Pem- 
berton, Hiibner,  and  others).  By  some  of  these,  the  most  impor- 
tant symptoms  were  also  correctly  stated.  It  is  not  intended  that 
the  merit  of  the  previously  mentioned  investigators  of  these  neu- 
roses of  secretion  shall  be  in  any  way  diminished  by  this  older 
historical  reminiscence,  for  as  the  older  physicians,  owing  to  the 
lack  of  exact  methods,  could  not  recognize  those  anomalies  of 
secretion  with  certainty,  their  results  were  soon  forgotten ; Reich- 
mann was  the  first  who,  by  a thorough  examination  of  the  contents 
of  the  stomach,  with  the  help  of  newer  and  constantly  improving 
methods,  furnished  certain  proof  of  the  existence  of  secretory  dis- 
orders which  had  previously  been  only  suspected,  while  it  was 
Ewald  especially  who  emphasized  particularly  the  nervous  origin 
of  supersecretion  and  superacidity,  so  that  soon  they  were  generally 
recognized  as  neuroses.  The  observations  of  Reichmann  were 
soon  after  confirmed  by  von  Noorden,  Honigmann,  Riegel,  Ja- 
worski, Saly,  and  others,  and  to-day  there  is  a consensus  of  opinion 
concerning  the  nature  and  consequences  of  both  neuroses.  Jaworski 
designates  both  neuroses  as  very  frequent  disorders,  since  he  could 
prove  them  in  almost  two-thirds  of  his  patients  who  had  diseases 
of  the  stomach,  while  Riegel  also  observed  them  very  frequently  in 
Hessia, — although  not  quite  so  frequently  as  Jaworski, — Ewald, 
with  whom  the  author  can  agree,  states  that  they,  especially  super- 
secretion, occurred  only  in  a fraction  of  his  patients  with  diseases 
of  the  stomach,  so  that  supersecretion  should  be  called  rare,  rather 
than  frequent. 

54 


822 


NEUROSES  OF  SECRETION. 


Etiology. — The  fundamental  causes  of  superacidity  are  still 
unknown.  The  little  that  has  up  to  date  become  known  con- 
cerning the  etiology  of  the  disease  is  confined  to  the  knowledge  of 
a few  predisposing  factors.  Very  excitable  people,  predisposed  to 
nervous  disorders,  more  frequently  become  affected  with  super- 
acidity than  those  of  calm  temperament,  who  do  not  lose  their 
equanimity  so  easily,  although  it  is  not  found  entirely  wanting 
in  the  latter.  Jaworski  found  hyperacidity  very  frequently  in 
the  excitable  Jewish  population  of  Galicia,  preeminently  disposed 
to  nervous  disorders.  With  hysterical  patients  superacidity  was 
noticed  by  Jolly,  and  in  melancholic  subjects  by  von  Noorden,  and 
it  is  also  a frequent  companion  to  neurasthenia.  The  disease  is 
more  common  in  men  than  in  women.  The  educated,  and  particu- 
larly the  learned,  classes  furnish  the  main  body  of  patients  suffering 
from  superacidity,  though  it  is  not  infrequent  in  the  laboring 
classes.  Local  causes  seem  to  play  an  important  role  in  the  etiology 
of  superacidity,  and  this  is  vouched  for  by  the  frequent  occurrence 
of  the  disease  in  Galicia  and  Hessia  (Riegel),  while  it  is  much  rarer 
in  other  districts.  It  would  be  a valuable  contribution  by  various 
gastro-enterologists  of  the  United  States  if  they  collected  and  re- 
ported the  frequency  of  hyperacidity  and  other  gastric  diseases 
occurring  in  their  localities,  so  as  to  throw  light  on  the  influences 
of  race,  climate,  geographical  distribution,  etc.  It  is  my  opinion 
that  a diet  rich  in  fish,  meats,  and  proteids  in  general  predispose  to 
hyperacidity.  That  the  frequent  occurrence  of  superacidity  with 
cholelithiasis  and  nephrolithiasis  is  a causal  relation  and  not  a mere 
accidental  coincidence  is  shown  by  the  fact  that  the  stomach  com- 
plaints dependent  on  superacidity  generally  disappear  quickly  after 
the  passage  of  the  calculi  into  the  intestines  and  bladder  respectively. 
The  relation  between  superacidity  and  peptic  ulcer  has  been  suffi- 
ciently dwelt  upon  in  the  discussion  of  the  pathogenesis  of  the  latter ; 
whether  superacidity  is  a cause  or  result  of  the  ulcer,  it  has,  up  to 
date,  been  impossible  to  decide  with  certainty.  In  the  first  half  of 
this  work  the  author  has  laid  down  reasons  why  hyperacidity  may 
in  some  instances  be  sufficiently  explained  by  the  proliferation  of 
glandular  elements  observed  in  fragments  of  mucosa  found  in  the 
wash-water  in  one-half  to  two-thirds  of  the  cases  of  hyperacidity 
examined  (Hemmeter,  “ Experimental  Basis  of  the  Dietetic  and 
Medicinal  Treatment  of  Hyperacidity,”  etc.,  “ Jour.  Amer.  Med. 
Asso.,”  Oct.  9,  1897).  Whether  this  condition  is  the  cause  or  the 


SYMPTOMATOLOGY  OF  SUPERACI DITY.  823 

result  of  the  neurasthenia  is  difficult  to  determine,  though  we  ob- 
served it  when  no  neurasthenia  could  be  detected. 

Symptomatology. — Disturbances  of  Sensibility. — The  subjective 
complaints  consist  chiefly  in  contracting,  boring,  burning,  or 
gnawing  pains  in  the  entire  region  of  the  stomach,  which  generally 
radiate  forward  or  toward  the  back.  As  they  are  the  consequences 
of  a strong  irritation  of  the  mucous  membrane  of  the  stomach  by 
its  superacid  contents,  they  are  generally  noticed  only  during 
digestion,  appearing  some  time  after  eating,  and  generally  increasing 
perceptibly  with  the  progress  of  digestion.  They  are  much  influ- 
enced by  the  quantity  and  composition  of  the  food;  with  meats 
they  are  in  some  patients  less  perceptible  than  with  an  amylaceous 
diet.  After  the  introduction  of  food  very  rich  in  albumin  they  ap- 
pear later  than  with  a diet  poor  in  albuminates,  mainly  because 
in  the  former  case  the  appearance  of  free  HC1  in  the  contents  of 
the  stomach  is  postponed  because  the  first  HC1  that  is  secreted 
combines  with  the  albumen.  At  the  height  of  digestion  the  symp- 
toms are  generally  most  severe.  Temporary,  strong,  cramp-like 
pains  in  the  region  of  the  pylorus  are  generally  the  result  of  a spasm 
of  the  muscular  sphincter  of  the  pylorus.  By  alkalies,  as  also  by 
the  renewed  taking  of  milk,  eggs,  or  meat,  the  painful  sensations  are 
generally  soon  alleviated  or  temporarily  done  away  with,  so  long  as 
the  acid  is  held  in  combination  by  the  alkalies  or  albuminates.  If 
a strong  generation  and  collection  of  gases  occur,  the  region  of 
the  stomach  is  swollen,  and  in  some  degree  sensitive  to  touch. 
If  the  escape  of  the  gases  upward  or  downward  is  temporarily 
prevented  by  simultaneous  cramp  of  the  cardia  and  pylorus,  the 
complaints  are  considerably  increased,  owing  to  the  strong  expan- 
sion of  the  walls  of  the  stomach.  Other  gastric  symptoms,  such  as 
nausea,  belching,  and  vomiting  of  very  acid  masses  accompany 
hyperchylia  very  frequently.  Belching  effects  slight,  passing 
relief,  while  copious  vomiting  brings  greater  and  more  lasting  relief. 
If  small  quantities  of  the  very  acid  contents  of  the  stomach  are 
brought  up  through  the  eructations,  and  if  the  mucous  membrane 
of  the  esophagus  is  subjected  to  caustic  action  by  the  latter,  heart- 
burn develops,  which  may  increase  to  a severe  contracting  pain 
under  the  sternum,  which  extends  to  the  pharynx  (pyrosis  hydro- 
chlorica,  Sticker).  The  same  complaints,  naturally,  may  also 
appear  after  the  vomiting  of  the  contents  of  a very  acid  stomach. 
The  manifold  subjective  symptoms  previously  stated  are  sometimes 
also  observed  with  neurasthenic  patients  in  whom  the  acidity  of 


824 


NEUROSES  OF  SECRETION. 


the  gastric  juice  is  normal.  An  abnormal  sensibility  of  the  gastric 
nerves  to  hydrochloric  acid  must  be  supposed  in  these  cases 
(Talma).  The  appetite  is  generally  undisturbed  in  patients  afflicted 
with  superacidity;  occasionally,  it  is  even  increased.  Thirst  is 
often  much  increased. 

The  Influence  of  Hyperchylia  upon  the  Transformation  of  the  Foods 
in  the  Stomach. — As  is  well  known,  with  increasing  acidity  of  the 
gastric  juice  (at  least,  up  to  a certain  limit)  its  digestive  power 
for  albuminous  foods  is  increased,  and  peptonization  proceeds 
more  quickly  and  freely  the  sooner  free  hydrochloric  acid  is 
present  in  the  contents  of  the  stomach.  Both  conditions  are 
given  with  patients  suffering  from  hyperacidity.  The  acidity  of 
the  gastric  juice  is  much  greater  than  that  of  the  normal  secretion, 
which  amounts  to  0.15  to  0.2  per  cent.  It  varies  between  0.3  and 
0.6  per  cent,  in  hyperchylia;  in  severe  cases  between  0.4  and  0.6 
per  cent.,  so  that  in  these  80  to  120  c.c.  of  a decinormal  solution 
of  sodium  hydroxid  are  necessary  to  neutralize  100  c.c.  of  the  gas- 
tric contents  drawn  at  the  height  of  the  digestion  of  a test-meal. 
Free  HC1  may  be  shown  in  the  contents  of  the  stomach  in  ten 
minutes  after  a test-breakfast,  instead  of  in  an  hour,  and  in  one 
hour,  instead  of  in  three  to  four  hours,  after  the  full  test-dinner ; 
therefore,  the  peptonization  of  albumin  proceeds  in  a very  prompt 
and  free  manner.  On  the  other  hand,  gastric  amylolysis  is  some- 
what retarded,  as  the  effectiveness  of  the  ptyalin  is  interrupted  very 
early  by  the  appearance  of  free  HC1.  On  this  account  one  finds,  in 
three  to  four  hours  after  an  experimental  meal,  no  undigested  mus- 
cular fibers  and  albuminous  particles  in  the  contents  of  the  stom- 
ach ; but  many  unchanged  amylaceous  particles  may  still  be  found 
in  the  residue  on  the  filter.  (This  is  best  studied  with  the  double 
test-meal,  as  recommended  on  pp.  120,  121.) 

If  the  acidity  of  the  gastric  juice  exceeds  a certain  maximum 
(0.6  to  0.7  per  cent,  and  over),  even  the  digestion  of  the  albumin 
is  in  some  way  retarded  (Schwann),  due,  in  my  opinion,  to  an 
unusually  large  amount  of  peptone  present.  Ferments  do  not 
act  readily  in  the  presence  of  an  excess  of  their  products.  But  up 
to  the  present  time  such  great  quantities  of  free  HC1  have  not  been 
met  with  in  the  contents  of  the  stomachs  of  patients  suffering  from 
hyperacidity. 

A copious  formation  and  collection  of  gases  may  occur  in  this 
neurosis  of  secretion. 

The  Effect  on  the  Motor  Function. — With  very  severe  irritation 


THE  EFFECT  ON  THE  MOTOR  FUNCTION.  825 

of  the  mucous  membrane  of  the  stomach  by  the  overacid  contents, 
abnormally  severe  contractions  of  the  musculature  are  produced 
reflexly,  by  which  a quicker  flow  of  blood  to  and  from  the  gastric 
walls  is  effected.  A more  intimate  contact  of  the  ingesta  with  the 
mucous  membrane  of  stomach  hastens  secretion  as  well  as  the 
digestion  and  resorption  of  the  albuminates,  and  also  the  passing 
over  of  the  chyme  into  the  intestines.  Therefore,  one  should  ex- 
pect a quickened  emptying  of  the  stomach  in  patients  with  hyper- 
acidity; but  in  many  cases  exactly  the  opposite  is  noted — namely, 
a retarded  passage  of  the  contents  of  the  stomach  into  the  intestines. 
It  is  generally  caused  by  a stubborn,  often-recurring  cramp  of 
the  pylorus,  brought  about  by  the  strong  irritation  of  the  mucous 
membrane  of  the  pylorus  by  HC1,  which  even  the  most  extreme 
contractions  of  the  rest  of  the  musculature  can  not  overcome. 
These  overexertions  of  the  latter  may  lead  to  fatigue  and  to 
atony,  and  the  appearance  of  this  state  is  furthered  by  the  fact 
that  the  coats  of  the  stomach  are  burdened  and  distended  by  the 
ingesta  more  than  under  normal  circumstances.  Since,  however, 
the  musculature  can  rest  and  recuperate  with  an  empty  stomach, 
the  atony  does  not  very  frequently  pass  over  into  a chronic  state 
of  dilation  of  the  stomach.  The  formation  of  the  dilation  is,  how- 
ever, to  be  feared  when  the  cramp  of  the  pylorus  brings  about  a 
hypertrophy  of  its  ring  muscles,  and  with  it  a stenosis  of  its 
lumen.  The  disturbances  of  circulation  in  the  coats  of  the  stom- 
ach, caused  by  the  cramp  of  the  pylorus,  in  the  presence  of  a very 
acid  and  potent  gastric  juice  may  favor  the  formation  of  peptic 
ulcer.  The  troublesome  thirst  so  often  complained  of  by  patients 
was  formerly  explained  by  a reduction  of  the  power  of  resorption 
of  the  mucous  membrane,  caused  by  the  strong  irritation  of  the 
same  (HC1)  and  spasm  of  the  smaller  vessels.  The  quick  cessa- 
tion of  thirst  after  copious  drafts  of  water  has  been  explained  by 
the  dilution  of  the  acid  chyme  and  a decrease  of  the  irritation  of 
the  mucous  membrane. 

That  superacidity  may  cause  disturbance  of  resorption  is  not 
to  be  denied.  Since  it  is  known,  however,  that  the  greater  part 
of  the  water  introduced  is  absorbed  only  in  the  intestine,  and  that 
the  resorption  of  water  in  the  normal  stomach  is  only  very  slight, 
it  might  be  more  correct  to  trace  back  the  thirst  with  superacidity 
to  the  cramp  of  the  pylorus  and  the  longer  retention  of  the  water 
in  the  stomach.  After  copious  drinking  of  water,  with  dilution  of 
the  contents  of  the  stomach,  the  irritation  of  the  mucous  mem- 


826 


NEUROSES  OF  SECRETION. 


brane  of  the  pylorus  decreases,  the  cramp  is  lessened,  and  the 
water,  passing  into  the  small  intestine,  is  then  quickly  absorbed  in 
the  latter.  That,  indeed,  a cramp  of  the  pylorus  with  hyperacidity 
often  causes  retention  of  the  contents  of  the  stomach  may  be 
proved  by  the  introduction  of  the  tube  before  and  after  taking  the 
water — especially  when  it  contains  alkalies  (Saratoga  Vichy). 
Before  the  taking  of  water  the  contents  of  the  stomach  still  show 
abundance  of  food  ; while  some  time  after,  the  stomach  is  generally 
found  to  be  entirely  empty. 

Urine. — After  copious  vomiting,  by  which  a part  of  the  HC1  is 
permanently  removed  from  the  organism,  the  urine  has  an  alkaline 
or  neutral  reaction  (Sticker,  Gluzinski,  Jaworski,  and  Hiibner);  but 
this  may  be  observed  during  the  digestion  in  the  stomach  without 
vomiting.  Since  the  phosphates  more  easily  separate  out  of  the 
alkaline  urine,  it  may  happen  that  the  urine  is  turbid  or  milk- 
like when  voided,  a circumstance  sometimes  unnecessarily  alarm- 
ing the  patient ; or,  after  standing  a while,  the  urine  may  show  a 
very  plentiful  sediment.  The  chlorids  are  sometimes  decreased. 

The  state  of  nutrition  generally  remains  good,  especially  at  first. 
If  considerable  disturbance  of  the  motility  appears,  the  nutrition 
becomes  impaired. 

The  Digestion  of  the  Foods  in  the  Intestine. — If  the  contents  of 
the  stomach  enter  the  intestine  in  an  overacid  condition,  it  requires 
much  more  than  the  usual  time  to  attain  the  alkaline  reaction  in 
the  contents  of  the  intestines  with  the  help  of  the  mixed  alkaline 
intestinal  juices.  An  alkaline  medium  is  the  most  favorable  for  the 
digestion  of  fats  and  carbohydrates. 

In  the  period  immediately  succeeding  the  passage  of  the  chyme 
into  the  small  intestine,  so  long  as  there  is  still  free  HC1  present, 
a small  part  of  the  undigested  albumin  is  peptonized  by  the  pepsin 
which  has  passed  over  along  with  it,  while,  on  the  other  hand,  the 
transformation  of  the  carbohydrates  and  fats  is  arrested  in  this 
time.  Consequently,  the  digestion  and  assimilation  of  the  foods 
in  the  intestine  are  much  retarded  in  severe  cases  of  hyperacidity, 
and  the  evacuation  of  the  bowels  is  correspondingly  delayed.  The 
very  acid  chyme  occasionally  produces  an  abnormally  intense 
peristalsis  of  the  intestine,  so  that  in  exceptional  cases  the  evacu- 
ation of  the  intestines  may  be  diarrheic  in  character. 

Prognosis. — This  is  favorable  if  the  disease  is  of  recent  origin  ; 
older  cases,  however,  are  often  stubborn.  The  ever- recurring  pains 
and  disturbances  of  digestion  may,  in  the  course  of  time,  exhaust 


DIFFERENTIATION  OF  HYPERACIDITY  FROM  ULCER.  827 

the  patient.  With  symptomatic  superacidity  the  prognosis  must 
be  made  in  accordance  with  that  of  the  primary  complaints.  If 
these — e.  g .,  hysteria,  neurasthenia,  melancholia,  peptic  ulcer,  or 
cholelithiasis  and  nephrolithiasis — are  successfully  relieved,  the 
superacidity  will  quickly  disappear.  In  the  author’s  experience  per- 
manent relief  may  follow  persistent  treatment,  even  in  chronic  cases. 

Diagnosis. — In  this  disease  our  double  test-meal  (see  p.  1 2 1 ) is 
a special  diagnostic  aid.  If  a strong  reaction  for  HCl  is  shown  in  the 
contents  of  the  stomach  after  ten  to  twenty  minutes  succeeding  the 
test-breakfast,  or  in  one  to  one  and  one-half  hours  after  the  test- 
dinner,  and  if  the  macroscopic  and  microscopic  examinations  in  the 
residue  on  the  filter  still  show  abundant  remnants  of  carbohydrates, 
with  complete  absence  of  muscular  fibers  and  particles  of  albumin, 
then  the  diagnosis  of  hyperacidity  is  established,  even  though  the 
other  previously  mentioned  symptoms  may  be  absent.  In  order 
to  prove  or  disprove  a coexistent  supersecretion,  we  recommend  to 
let  the  patient  take  the  test-meal  at  night,  and  the  next  morning 
introduce  the  tube  before  breakfast.  If  it  contains  large  quantities 
(over  ioo  c.c.)  of  a potent  secretion,  then  supersecretion  exists  side 
by  side  with  superacidity;  and  if  the  stomach  be  empty,  or  if 
only  a small  quantity  of  gastric  juice  be  found  in  it,  then  superse- 
cretion is  not  present.  The  result  is  still  more  certain  if  a few 
hours  after  the  last  evening  meal  the  stomach  is  thoroughly 
washed  out  and  the  tube  is  introduced  into  the  jejune  stomach 
the  next  morning.  Schreiber  asserts  that  supersecretion  is  found 
only  in  atonic  stomachs. 

The  differential  diagnosis  between  the  ulcer  and  hyperacidity  is 
of  practical  importance  on  account  of  the  therapeutics  to  be  fol- 
lowed. With  both  diseases  the  manifold  subjective  complaints 
appear  usually  after  eating  ; with  peptic  ulcer  patients,  generally 
very  soon  after  eating  ; with  those  suffering  from  hyperacidity,  later 
on  at  the  height  of  digestion,  though  the  onset  varies  considerably 
according  to  the  quantity  and  character  of  the  foods. 

In  gastric  ulcer  the  pains  are  generally  confined  to  one  region, — 
namely,  the  epigastrium  (circumscribed  pain  caused  by  pressure), — 
and  they  very  often  radiate  forward,  laterally,  toward  the  loins  and 
shoulder-blades  (dorsal  pain-points),  while  in  the  case  of  super- 
acidity a diffused  sensation  of  pain  exists  in  the  whole  region  of 
the  stomach  and  the  radiating  pains  are  wanting,  and  also  the 
dorsal  pain-points,  which,  in  the  case  of  ulcer,  will  be  present  in 
about  one-third  of  the  cases. 


828 


NEUROSES  OF  SECRETION. 


In  the  case  of  ulcer  the  pains  are  generally  strongest  when  food 
in  itself  difficult  of  digestion  has  been  introduced  in  large  quanti- 
ties, and  it  is  irrelevant  in  this  case  if  the  food  consisted  mainly 
of  carbohydrates  or  meats ; in  the  case  of  hyperacidity  the  pains 
are  generally  less  severe  after  abundant  meals,  even  if  the  latter 
consisted  of  foods  in  themselves  difficult  of  digestion,  provided 
only  that  they  are  rich  in  albumin ; after  smaller  meals  with  little 
albumin  the  pains  are  not  relieved,  for  it  is  the  albumin  or  proteid 
of  the  food  which  alone  has  binding  affinity  for  the  excess  of  HC1. 

If  the  symptoms  observed  in  the  patient  do  not  suffice  to  estab- 
lish a positive  differential  diagnosis  between  ulcer  and  hyperacidity, 
it  is  safer  to  treat  the  patient  for  ulcer — this  may  be  the  case  when 
it  is  impossible  to  pass  the  tube  on  account  of  suspected  ulcer. 
If  the  pains  become  less  or  cease  entirely  soon  after  beginning  this 
treatment,  it  is  probably  a case  of  ulcer,  while  if  they  remain  the 
same  or  increase,  it  is  a case  of  hyperacidity.  If  the  hyperacidity 
is  removed  by  this  treatment  at  the  same  time  as  the  ulcer,  this 
fact  suggests  that  the  hyperchylia  was  not  the  cause,  but  the  result, 
of  ulcer.  On  the  other  hand,  if,  after  curing  the  ulcer,  the  hyper- 
chylia continues,  we  may  presume  either  an  accidental  coincidence 
of  the  two,  or  else  the  hyperacidity  has  caused  the  ulcer.  In  the 
latter  case  the  breaking  out  of  the  ulcer  or  the  formation  of  new 
ulcers  is  to  be  feared  in  the  future  should  the  hyperacidity  continue. 

Concerning  the  terminology  of  this  and  allied  diseases  it  is 
necessary  to  emphasize  that  the  term  “ chylia  ” refers  to  the  gastric 
juice  as  a whole, — i.  e .,  including  HC1,  pepsin,  and  chymosin, — but 
the  word  “ acidity,”  of  course,  can  not  include  these  ferments.  As 
the  HC1  is  the  principal  constituent  which  is  increased,  and  though 
the  ferments  are  more  active,  there  is  no  evidence  proving  that 
they  are  proportionately  increased  with  the  acid  HC1  in  simple 
hyperacidity  or,  as  it  is  also  called,  superacidity — I consider  the 
latter  term  preferable  to  the  word  “ hyperchyliaP 

Therapeutics. — ( a ) Diet. — The  selection  of  proper  diet  for  these 
cases  is  one  of  the  most  important  duties  of  the  general  practi- 
tioner and  specialist.  There  are  two  systems  of  dietetic  treatment 
for  hyperacidity.  One  favors  the  use  of  amylaceous  diet  and  the 
restriction  of  proteids,  because  the  latter  are  powerful  stimulants 
to  HC1  secretion.  The  advocates  of  the  other  argue  that,  since 
the  manifold  complaints  with  hyperchylia  are  a result  of  the 
irritation  of  the  nerves  of  the  stomach  by  free  HC1,  therefore,  in 
the  fixing  of  a rational  diet  such  foods  must  be  chosen  which 


DIET  IN  HYPERACIDITY. 


829 


combine  with  the  greatest  quantity  of  MCI — that  is,  in  the  first 
place,  meats ; in  the  second,  vegetables  especially  rich  in  proteid. 
All  the  stimulants  which  might  further  increase  the  irritation  of 
the  nerves  of  the  stomach  must  be  avoided — viz.,  pungent  spices, 
tapioca,  pepper,  also  mustard,  horseradish,  ginger,  organic  acids, 
such  as  lactic,  acetic,  citric,  and  tartaric  acids,  fatty  acids  (rancid 
fat);  table  salt  must,  so  far  as  possible,  be  kept  out  of  the 
stomach  ; drinks  rich  in  alcohol  are  injurious — strong  beer,  heavy 
wines,  but  especially  whisky  and  cognac.  Food  and  drink  must 
not  be  taken  too  cold  (not  under  8°  to  io°  R. — io°  to  12. 50  C.)  and 
not  too  hot  (not  over  45  0 R.  or  56°  C.).  After  foods  in  themselves 
difficult  of  digestion,  the  complaints  are  not  increased,  provided  they 
contain  much  albumin,  than  after  easily  digestible  ones ; nevertheless 
the  latter  are  to  be  preferred,  and  careful  preparation  is  requisite  in 
order  to  avoid  a mechanical  irritation  of  the  nerves  of  secretion. 
A diet  consisting  only  of  carbohydrates  is,  in  our  experience,  not 
injurious.  I have  exhaustively  stated  the  advisability  of  amy- 
laceous diet  in  hyperacidity  on  pages  195  to  197.  Pure  fats  are 
allowed  in  the  same  quantities  as  in  the  case  of  healthy  people. 
H.  Strauss  and  L.  Aldor  have  given  the  experimental  evidence 
that  fats  are  digested  as  well  in  hyperacidity  as  in  subacidity 
(“  Zeitschr.  f.  diat.  u.  physik.  Therap.,”  Bd.  1,  S.  134).  Fats  and 
oils  have  a tendency  to  diminish  the  HC1  secretion  (Pawlow,  /.  c.)} 
and  therefore  have  a therapeutic  value.  As  sugar  does  no  harm 
in  the  case  of  most  patients,  such  baked  foods  (cakes)  are  to  be 
permitted  in  which,  by  a long  process  of  baking  or  roasting,  a part 
of  the  starch  has  been  dextrinized  : that  is,  well-toasted  bread, 
cakes,  breadcrust  soaked  in  milk,  and  also  certain  dextrinized 
flours  (Horlick’s  food,  Kufeke’s  flour,  and  others).*  On  account  of 
frequent  disturbance  of  the  motility  large  quantities  of  water,  by 
which  the  muscularis  of  the  stomach  is  unusually  distended,  must 
not  be  introduced  at  one  time;  it  is  much  better  to  give  small 
quantities  frequently,  by  which  at  the  same  time  the  acid  contents 
of  the  stomach  are  diluted.  Burning  thirst  is  best  quenched  by 
frequent  imbibing  of  small  quantities  of  alkaline  mineral  waters 


* Since  the  first  edition  of  this  work  my  experimental  results  and  practical  recom- 
mendations of  an  amylaceous  diet  for  hyperacidity  have  been  confirmed  by  Wold  Bach- 
mann  (“Archiv  f.  Verdauungslcrank.,”  Bd.  v,  S.  336),  by  Chr.  Jiirgensen,  and  J. 
Justesen  (“  Zeitschr.  f.  diat.  u.  physikal.  Therap.,”  Bd.  Ill,  S.  541) — and  the  histological 
observations  have  been  confirmed  by  H.  Strauss  and  J.  S.  Myer  (“  Virchow’s  Archiv,” 
Bd:  cliv). 


830 


NEUROSES  OF  SECRETION. 


(Saratoga  Vichy,  Geyser,  Capon  Springs,  Apollinaris  water,  Selt- 
ers,  Geisshubler,  Fachinger  water),  which  are  rich  in  alkalies  and 
carbonic  acid  gas.  The  latter  is  not  only  soothing,  but  also  favors 
resorption. 

Since  the  percentage  of  albumin  of  the  various  foods,  and  hence 
also  their  valence  toward  HC1,  vary  remarkably,  a table  of  all 
these  foods  is  given  on  page  248,  showing  how  much  hydrochloric 
acid  they  may  hold  in  combination  until  the  appearance  of  a weak 
but  distinct  reaction  with  the  Baeyer-Gunzburg  reagent. 

In  the  two  columns  those  foods  occupy  the  first  places  which 
combine  with  the  least  amount  of  HC1 ; those  which  combine  with 
the  greatest  amount  of  hydrochloric  acid  (meat,  poultry,  game, 
fish,  vegetables,  etc.)  stand  at  the  end  of  the  column. 

From  this  survey  it  appears  that  for  patients  with  hyperchylia, 
veal,  beef,  mutton,  and  raw  ham  (which  hold  in  combination  two 
or  three  times  as  much  HC1  as  the  same  quantities  of  sweetbread, 
liver  pudding,  and  calf’s  brain)  are  to  be  recommended  if  the 
second  system  on  the  preceding  page  is  selected.  For  the  same 
reason  the  Leube-Rosenthal  meat  solution,  which  in  itself  is  easily 
digestible,  can  be  recommended.  Cooked  ham  and  finely  minced 
pork  are  also  suitable  meats.  Of  the  other  foods,  Swiss  cheese, 
Roquefort,  pea  sausage,  brick  cheese,  and  of  the  various  kinds  of 
bread,  especially  pumpernickel  and  rye  bread  are  recommended  by 
Fleischer — I have  no  personal  experience  with  this  form  of  diet. 
Wheat  bread  is  not  so  suitable,  as  700  gm.  of  it  are  necessary  to 
combine  with  the  same  quantity  of  HC1,  which  is  held  in  com- 
bination by  300  gm.  of  pumpernickel  or  100  gm.  of  veal.  Beer  is 
not  suitable.  Milk  is  to  be  recommended,  both  on  account  of  its 
digestibility  and  composition.  If,  on  account  of  muscular  disturb- 
ances, it  is  desired  to  avoid  large  quantities  of  liquids,  condensed 
milk  should  be  advised ; 600  gm.  milk,  condensed  to  one-fourth 
of  its  volume,  combines  with  as  much  HC1  as  100  gm.  veal.  Cocoa 
is  also  to  be  recommended. 

If  gastric  distress  and  pain  appear  after  supper  before  bedtime, 
the  patient  should  drink  a cup  of  lukewarm  milk,  bouillon  with 
egg,  and  meat  solution,  or  eat  raw  ham  scraped  fine,  or  one  egg, 
which  also  combines  with  a great  deal  of  HC1  (see  p.  248). 

This  large  ingestion  of  proteid  and  albuminous  food,  espe- 
cially advocated  by  Fleischer  for  hyperacidity,  does  not  lead  to 
permanent  relief,  in  the  author’s  experience.  According  to  care- 
fully conducted  experiments  and  analyses,  he  is  of  the  opinion 


MEDICINAL  TREATMENT  OF  HYPERACIDITY.  83 1 

that  a proteid  diet  may  keep  up  a hyperacidity  because  it  is  a 
stronger  stimulation  to  HC1  secretion  (see  pp.  195-19 7). 

( b ) Medicinal  Treatment. — We  refer  to  pages  334  to  336  in  ex- 
planation of  the  use  of  alkalies  in  hyperacidity.  Magnesia  is 
preferable  to  the  carbonates  because  it  can  not  form  chlorids, 
which  may  irritate  the  mucosa.  As  may  be  seen  from  the  table 
(p.  248),  the  albuminates  of  the  foods  may  take  up  considerable 
quantities  of  HC1,  and  after  their  transformation  into  peptone  hydro- 
chlorate they  aid  the  nutrition  of  the  body,  which  is  not  the  case 
with  the  chlorids.  The  digestive  products  of  albumin,  hemi- 
albuminose,  and  peptone,  combine  with  more  HC1  in  the  formation 
of  their  hydrochlorate  compounds  than  albumin  itself  (peptone 
almost  twice  the  amount),  and  the  peptonizing  as  well  as  fte 
decomposition  of  the  peptone  hydrochlorate  in  the  blood  require 
some  time,  so  that  the  HC1  combined  with  it  does  not  readily 
become  free  again. 

Some  of  the  alkalies  may  be  taken  in  the  form  of  alkaline  mineral 
water  — Saratoga  Vichy,  St.  Louis  Spring  (Mich.),  Apollinaris, 
Biliner  water,  Fachinger,  Selters,  and  French  Vichy.  Magnesia 
usta,  bicarbonate  of  soda,  sodium  biborate  (Jaworski,  L.  Wolff), 
are  best  prescribed  as  indicated  on  pages  334  to  336.  If  there 
is  an  inclination  to  the  formation  of  gases,  the  bicarbonate  of 
soda  is  to  be  replaced  by  magnesia  usta  in  order  not  to  increase 
the  amount  of  gas  by  the  C02  which  is  set  free  from  the  former. 
Magnesia  usta  has  also  the  advantage  of  forming  a chlorid  which 
has  a mild  aperient  effect.  The  following  are  the  author’s  favorite 
formulae  : 


R.  Magnes.  ustae,  io.o 

Sodii  bicarb., 

Pulv.  rad.  rhei, aa  5.0 

Ext.  belladonnae, . 0.3  M. 


SiG. — One-half  of  a teaspoonful  three-quarters  of  an  hour  after  meals. 

Or— 

R.  Sodii  bicarb., 

Potass,  carbonat., 


Magnes.  ustae, aa  5.0 

Ext  belladonnae, 0*25 

Sacchar.  lactis, 20.0  M. 


SiG. — One-half  of  a teaspoonful  one  hour  after  each  meal. 

(See  also  formulae  on  p.  338.) 

Extract  of  belladonna  or  atropin  has  a decided  effect  in  check 


832 


NEUROSES  OF  SECRETION. 


ing  the  secretion  of  gastric  juice;  in  some  experiments  the 
amount  of  HC1  was  reduced  to  one-third  or  one-half  the  normal 
amount  (Riegel,  “Verhandl.  d.  Congress,  f.  innere  Medicin,”  1899, 
S.  328). 

According  to  Jaworski’s  experiments,  the  continued  use  of  large 
quantities  of  Carlsbad  salt  and  the  thermal  waters  of  Carlsbad 
reduce  the  secretion  of  the  acids  of  the  stomach ; this  might  ex- 
plain the  beneficial  influence  of  a protracted  stay  at  Carlsbad  (see  p. 
336).  We  are  assured  that  the  Bedford  and  the  Saratoga  Carlsbad 
mineral  waters  in  our  country  have  an  equally  beneficial  effect. 
If  the  pains  in  the  region  of  the  stomach  continue  in  spite  of  the 
remedies  discussed  thus  far,  narcotics  are  prescribed,  especially  ex- 
trftt  of  belladonna  (0.03  gm.  daily)  and  atropin  sulphate  (0.0005  to 
0.001  gm.,  or  yjTo  °f  a gra-in)>  given  with  advantage,  together  with 
magnesia  usta  or  ammoniomagnesium  phosphate — substances  which 
not  only  only  have  the  effect  of  reducing  pain,  but  also  inhibit  the 
secretion  of  the  glands  ; codein  phosphate  (0.03  gm.  % to  % daily) 
is  a reliable  drug  for  this  purpose.  Cocain  muriate  is  not  suitable 
on  account  of  the  fact  that  its  effect  passes  away  rapidly,  but  bro- 
mid  of  sodium  and  bromid  of  ammonium  (2.5  to  4.0  in  twenty-four 
hours),  when  taken  for  some  time,  often  do  good  service.  Strontium 
bromid  is  even  better  tolerated  than  the  sodium  or  ammonium  salt. 

On  the  other  hand,  the  use  of  morphin  muriate  must  be  as  lim- 
ited as  possible.  According  to  Hitzig  and  Alt,  morphin  muriate 
is,  to  a great  extent,  excreted  in  the  gastric  juice  and  also  with  the 
saliva,  and  therefore  reaches  the  stomach  again  after  absorption. 
Small  quantities  of  morphin,  however,  excite  the  nerves  more  than 
they  calm  them. 

If  the  patients  complain  of  severe  pains  even  on  an  empty 
stomach  (without  being  able  to  prove  supersecretion  or  hyperesthe- 
sia), then  lavage  of  the  stomach,  irrigation  of  the  mucous  membrane, 
and  internal  douches,  which  were  first  recommended  by  Malbranc, 
will  give  more  permanent  relief. 

With  very  stubborn  cramp-like  pains  in  the  region  of  the  pylorus 
(pylorospasm)  there  is  nothing  to  be  done  but  to  remove  the 
strongly  acid  contents  of  the  stomach  with  the  tube  and  to  wash 
out  the  stomach,  first  with  lukewarm  water,  then  with  bicarbonate 
of  sodium,  and  to  leave  a small  part  of  the  latter  in  the  organ. 

Jaworski’s  treatment  by  stronger  or  weaker  effervescent  alkaline 
waters  has  proved  useful  in  our  experience.  The  following  are  the 
formulae : 


MEDICINAL  TREATMENT  OF  HYPERACIDITY 


«33 


Alkaline  Effervescent  Solution. 

i.  II. 

Strong.  Whak. 

Sodium  bicarbonate 8.0  5.0 

Sodium  salicyl. , . . 2.5  20 

Sodium  biborat 2.0  1.0 

Add  above  to  one  liter  (one  quart)  of  carbonated  water. 

Directions. — On  an  empty  stomach  take  x/z  of  a tumblerful  of  the  stronger  solution, 
No.  I,  in  the  morning.  After  each  meal  drink  ]/3  to  '/2  of  a tumblerful  of  the  milder 
solution,  No.  II. 

These  solutions  are  markedly  efficacious  if  the  hyperacidity  is 
associated  with  uric  acid  diathesis. 

The  electrical  treatment  has  been  used  successfully  by  Einhorn 
for  this  purpose,  and  he  especially  favors  the  internal  galvanization 
of  the  stomach.  Since  the  anode  has  a calming  effect  upon  the 
irritated  nerves  (Heidenhain),  it  is  perhaps  best  to  introduce  the 
anode  with  the  intragastric  electrode  into  the  stomach  filled  with 
moderate  quantities  of  lukewarm  water,  and  to  apply  the  cathode 
to  the  sternum,  epigastrium,  or  spine. 

Constipation  will,  as  a rule,  be  relieved  by  neutralization  of  the 
excess  of  HC1,  but  in  the  rare  cases  in  which  it  is  not,  it  is  to  be 
fought  with  rhubarb  preparations  (pulv.  rad.  rhei,  40.0;  natr. 
sulph.,  20.0),  Carlsbad  Sprudel  salts,  by  injections,  massage  of  the 
intestines,  and  glycerin  suppositories.  Injections  of  eight  ounces 
of  olive  oil  into  the  colon,  according  to  Fleiner’s  method,  is  effica- 
cious in  many  cases.  Since  superacidity  is  frequently  a neurosis, 
we  must,  in  general,  influence  the  nervous  system  favorably  by 
a sojourn  in  the  country,  in  the  mountains,  at  the  seashore,  by  cold 
rubbings,  gymnastics,  and  abstention  from  severe  mental  labor. 
A treatment  recommended  by  Biedert  and  Langermann  (/.  c.)  has 
been  found  serviceable  by  the  author.  The  stomach  is  first  washed 
out  by  a solution  of  sodium  bicarbonate.  When  the  water  returns 
clean,  we  pour  in  a one  per  cent,  suspension  of  magnesia  usta ; 
when  this  has  run  out,  it  is  followed  by  a one-half  per  cent,  solu- 
tion of  tannin.  In  the  place  of  the  latter,  particularly  when  it  is 
not  well  tolerated,  we  often  use  a suspension  of  bismuth  subnitrate  ; 
when  the  pains  are  severe,  the  author  prefers  lavage,  with  a suspen- 
sion of  one  dram  each  of  bismuth  subgallate  and  bismuth  subni- 
trate in  one  quart  of  warm  water. 


834 


NEUROSES  OF  SECRETION. 


PERIODICAL  ATYPICAL  FLOW  OF  GASTRIC  JUICE  (Gastroxynsis 
( Rossbach ),  Gastroxie  (. Lepine ),  Gastrosuccorrhea  Periodica 
( Reichmann )). 

Gastroxynsis,  or  periodical  flow  of  gastric  juice,  is  an  atypical 
secretion  of  the  peptic  glands — atypical  because  it  does  not  occur 
after  a normal  digestive  stimulation,  but  rather  when  the  stomach 
is  empty.  The  attacks  are  associated  with  intense  gastric  distress, 
severe  spasmodic  pain,  and  vomiting  of  considerable  quantities  of 
very  acid  gastric  juice.  This  peculiar  neurosis  is  found  almost  ex- 
clusively among  the  educated  classes,  and  particularly  among  those 
individuals  who  are  subjected  to  unremitting  mental  exertion.  In 
exceptional  cases  persons  belonging  to  the  laboring  classes  are 
attacked  by  it.  The  malady  occurs  in  attacks  which  last  from  one 
to  three  days,  returning  in  some  instances  every  week,  and  in 
others  at  intervals  of  months.  The  attacks  are  more  frequent  when 
the  mental  exertion  is  severest,  and  become  rare  as  soon  as 
pauses  of  mental  rest  intervene.  During  vacation  of  these  brain- 
workers, or  sojourn  at  the  seashore  or  in  the  mountains,  the  attacks 
disappear  entirely,  to  return  again  when  the  sufferer  applies  him- 
self to  his  profession.  The  pains,  which  are  most  probably  caused 
by  irritation  of  the  mucosa,  by  the  intensely  acid  secretion,  are 
generally  preceded  by  nausea,  eructation,  and  pyrosis.  Eventually 
the  emesis  of  large  quantities  of  acid  liquids  supervenes,  and,  as  a 
rule,  terminates  the  attack.  The  sufferers  generally  recuperate 
quickly.  Jiirgensen  and  Ewald  have  reported  cases  of  typical 
migraine  that  were  also  associated  with  superacidity.  Rossbach 
(“  Deutsch.  Archiv  f.  klin.  Med.,”  Bd.  xxxv,  1885)  and  Rosenthal 
(/.  c.)  have  suggested  hypotheses  attempting  to  explain  the 
pathogenesis  of  periodic  flow  of  gastric  juice;  their  theories  are 
not  supported  by  experimental  evidence,  and  have  not  cleared 
up  the  subject. 

Etiology. — Among  the  incidental  causes  we  meet  with  exces- 
sive and  exhausting  mental  exertion,  intense  emotional  excitement, 
anger,  nicotin  poisoning,  and  occasionally  dietetic  errors.  The 
so-called  periodic  flow  of  gastric  juice,  as  first  described  by  Reich- 
mann (“  Berlin,  klin.  Wochenschr.,”  1882,  Nr.  40),  and  the  gas- 
troxynsis of  Rossbach,  are,  in  our  opinion,  simply  phases  of  the 
same  neurosis,  not  different  diseases. 

Symptomatology. — The  attacks  occur  very  acutely,  more  fre- 
quently on  an  empty  stomach,  and  with  a feeling  of  pressure  in 


SYMPTOMATOLOGY  OF  GASTROXYNSIS. 


835 


the  head  increasing  to  intense  headache,  pain  in  and  over  the  eyes, 
distress,  pressure,  and  fullness  in  the  stomach,  increasing  to  gas- 
tralgia.  Eructation,  pyrosis,  and  nausea  usher  in  abundant  vomit- 
ing of  highly  acid  mucous  masses  ; the  quantity  of  HC1  in  the  vomit 
may  be  fifty  per  cent,  and  even  exceed  this.  Repeated  vomiting 
will  bring  up  mucus  and  bile.  When  the  vomit  occurs  while  the 
stomach  still  contains  ingesta,  this  will  show  the  same  chemical 
reactions  as  are  found  in  hyperacidity.  The  drinking  of  water 
relieves  the  gastric  distress  by  diluting  the  acid,  but  generally  in- 
creases the  vomiting.  In  our  experience  the  attacks  occur,  as  a 
rule,  in  the  middle  of  the  night,  or  in  the  early  hours  of  the  morn- 
ing. The  patient  has  a very  pale  appearance,  and  the  extremities 
are  frequently  cold.  A few  hours  after  the  first  vomiting  of  gastric 
juice  the  attack  may  be  repeated,  and  again  an  equally  large  quan- 
tity of  gastric  secretion  containing  no  food  particles  whatever  may 
be  vomited.  In  a case  which  the  author  saw  in  consultation  with 
Dr.  J.  B.  Schwatka,  of  Baltimore,  the  patient  vomited  surprisingly 
large  quantities  of  pure  straw-colored  gastric  juice.  The  amount 
was  between  5 10  and  600  c.c.  every  time  he  vomited,  which  usually 
was  three  or  four  times  in  twenty-four  hours.  The  patient  retained 
no  food  for  eight  days,  was  fed  by  nutritive  enemata,  and  finally 
recovered  under  lavage  with  bicarbonate  of  sodium  and  spraying  the 
stomach  with  nitrate  of  silver  1 : 1000.  At  night  a hypodermic  of 
morphin,  gr.,  and  atropin,  gr.,  was  given.  The  acidity  of  vomit 
was  3.5  per  thousand  (free  HC1).  Occasionally,  the  gastric  pains 
are  the  only  symptom,  and  headache  follows  later  on  ; in  fact,  the 
symptoms  might  be  differentiated  into  gastric  and  cerebral  symp- 
toms— at  times  the  former  prevail,  and  at  others,  the  latter.  The 
highly  acid  liquids  in  the  stomach  very  likely  cause  a reflex  spas- 
modic pylorospasm.  Eructation,  insufficiency  of  the  cardia,  and 
pneumatosis  are  frequent  accompaniments.  Periodical  atypical  flow 
of  gastric  juice  may  be  an  independent  neurosis  of  secretion,  or 
reflexly  caused  by  diseases  of  the  central  nervous  system.  The 
gastric  crises  occurring  in  tabes  have  been  classed  with  periodical 
secretion  by  some  authors,  but  according  to  von  Noorden  (“Charite 
Annalen,”  1890),  Bouveret  (/.  c.,  p.  680),  and  Boas  (“  Deutsch.  med. 
Wochenschr.,”  1889,  Nr.  42)  the  liquids  vomited  in  gastric  crises 
are  not  always  acid,  and  frequently  may  be  found  alkaline.  They 
are  not  associated  with  the  very  severe  phenomena  of  highly 
increased  acidity  of  gastric  juice;  namely,  the  strong  pyrosis,  and 
the  feeling  of  a corrosive  substance  in  the  stomach.  Bouveret  has 


NEUROSES  OF  SECRETION. 


836 

expressed  his  doubt  concerning  the  existence  of  a central  form  of 
periodical  gastrosuccorrhea. 

Diagnosis. — Gastroxynsis  maybe  confounded  with  the  migraine 
associated  with  gastric  symptoms,  with  intermittent  forms  of  severe 
hyperchylia,  and  with  the  gastric  crises.  The  diagnosis  can  be 
made  by  chemical  analysis  of  the  vomited  matter.  The  attacks 
usually  occur  in  the  midst  of  good  health,  and  the  severe  thirst, 
loss  of  appetite,  cephalalgia,  and  great  prostration  are  characteristic 
symptoms.  Rossbach  found  an  acidity  of  four  per  thousand  (HC1) 
in  one  of  his  cases,  and  Boas  found  that  there  was  a hyperacidity 
even  in  the  intervals  between  the  attacks,  and  that  the  amount  of 
gastric  juice  during  the  attacks  was  not  much  increased  as  com- 
pared to  that  found  in  the  intervals. 

Example  I. — Miss  M.  G.,  age  twenty-four,  of  neuropathic  extraction,  has 
frequently  had  attacks  of  vomiting  and  gastric  pain  during  childhood.  For 
about  six  years  she  has  suffered  from  intense  pyrosis,  which  was  relieved  by 
bicarbonate  of  sodium  tablets.  Sometimes  the  heartburn  ceased  after  the  in- 
gestion of  food.  She  is  a music  teacher,  and  frequently  spends  eight  to  ten 
hours  a day  teaching  pupils  and  giving  singing  lessons.  The  appetite  is  at  all 
times  very  good,  bowels  slightly  constipated.  The  acidity  after  our  double 
test-meal  taken  in  the  interval  between  the  attacks  is  equal  to  0.3  per  cent.  HC1. 
About  once  a week  she  has  distressing  attacks  of  gastralgia,  associated  with 
severe  headache  and  vomiting  of  very  acid  liquid  masses.  The  attacks  occur 
generally  between  two  and  three  o’clock  in  the  morning,  when  she  has  spent 
a day  at  hard  work  teaching  pupils.  The  patient  awakes  suddenly  with  a feel- 
ing extending  from  her  stomach  to  her  throat,  which  is  described  as  a twisting 
of  the  gullet.  Severe  cephalalgia,  giddiness,  nausea,  and  vomiting  follow. 
Sometimes  she  does  not  vomit,  but  the  attack  is  passed  off  by  rapidly  drinking 
a half-pint  of  water  with  a teaspoonful  of  bicarbonate  of  soda.  Physical  ex- 
amination, entirely  negative.  Urine,  the  indican  is  increased.  Urea,  uric  acid, 
ratio  high.  No  splashing  sound  in  the  stomach  prior  to  ingestion  of  food  or 
drink.  Acidity  of  filtrate  of  vomited  matter,  which  apparently  was  free  from  bile, 
was  equal  to  2.8  per  thousand  (HC1),  or  0.28  per  cent.  The  fact  that  the  acidity 
was  less  during  the  attack  than  during  the  intervals,  suggested  that  the  HC1 
had  been  neutralized  through  bile,  duodenal  secretions,  or  saliva,  but  the  care- 
ful examination  for  these  constituents  was  negative.  During  a summer  vaca- 
tion in  which  the  patient  undertook  a trip  to  Europe,  she  vomited  daily  from 
sea-sickness,  but  in  three  months,  while  she  was  in  Germany,  she  did  not  have 
one  attack.  On  returning,  the  acidity,  after  a similar  test-meal,  as  before  stated, 
was  equal  to  1.5  per  thousand  (HC1).  General  condition  much  improved. 

Example  II. — This  case  is  that  of  a colleague,  a friend  of  the  author’s,  who 
has  described  his  case  with  great  accuracy  on  repeated  occasions.  The  attacks 
usually  occur  at  night,  associated  with  headache  and  gastric  distress,  and  cul- 
minate in  the  vomiting  of  large  masses  of  highly  acid  material.  The  doctor  is 
an  indefatigable  brain-worker,  allowed  himself  very  little,  if  any,  recreation. 


CHRONIC  SUPERSECRETION.  837 

His  general  nutrition  is  good,  and  he  has  found  that  his  attacks  are  rapidly 
relieved  by  the  taking  of  ordinary  cane-sugar  (Ewald). 

Periodical  vomiting,  when  associated  with  hyperacidity,  must  be 
carefully  distinguished  from  gastroxynsis. 

Treatment. — This  includes,  in  the  first  place,  the  avoidance  of 
stimulants  and  narcotics:  alcohol  and  tobacco,  as  well  as  strong 
coffee.  It  is  most  essential  that  the  patients  should  avoid 
mental  overwork.  They  should,  in  fact,  refrain  from  brain-work 
altogether,  and  allow  themselves  three  or  four  months  a year  to 
enjoy  recreation  in  the  mountains  or  at  the  seashore.  Physical 
exercise  should  be  indulged  in  moderately  but  systematically. 
The  bicycle  is  an  excellent  remedy  for  periodical  flow  of  gastric 
juice;  and  also  horseback  riding,  swimming,  rowing,  fencing, 
gymnastic  exercises,  and  outdoor  games.  During  the  attack 
itself,  the  effects  of  the  excess  of  acid  should  be  counterbalanced 
by  copious  drafts  of  suspensions  of  calcined  magnesia,  ammonio- 
magnesium  phosphate,  or  bicarbonate  of  sodium.  When  the 
vomiting  has  occurred  at  short  intervals,  one  should  not  hesitate 
to  pass  the  stomach-tube,  wash  out  the  stomach  with  sodium  bi- 
carbonate, and  afterward  treat  the  mucosa  with  suspensions  of  bis- 
muth subgallate  (Sij  to  Oj)  or  with  argentic  nitrate,  I : 1000.  A 
mustard  plaster  should  be  placed  over  the  epigastrium.  If  this 
can  not  be  conveniently  had,  a hot-water  bag  will  act  similarly. 
The  bromid  of  strontium  and  bromid  of  ammonium,  in  doses  of 
thirty  grains  three  times  a day,  have  an  undeniable  effect  upon  the 
frequency  of  the  attacks.  The  diet  should  be  carefully  adjusted  to 
the  digestive  capacity  of  the  stomach.  We  usually  recommend 
Penzoldt’s  diet  order,  which  is  given  among  the  diet  lists.  In  the 
intervals  between  the  attacks  the  patients  should  undergo  treat- 
ment as  outlined  for  hyperacidity.  Belladonna  or  atropia  are 
often  valuable  aids  to  the  treatment;  their  mode  of  action  has 
been  explained  on  page  830. 


CHRONIC  CONTINUOUS  FLOW  OF  GASTRIC  JUICE  (Chronic 
Hyper-  or  Supersecretion  (Riege/),  Gastrosuccorrhea 
Chronica  ( Reichmann ). 

We  have  our  doubts  whether  such  a condition  of  permanent 
irritation  of  the  gastric  secretory  nerves  and  uninterrupted  secre- 
tion exists  as  a primary  disorder.  Chronic  gastrosuccorrhea,  which 
55 


838 


NEUROSES  OF  SECRETION. 


Reichmann  claimed  to  have  observed  and  first  described  in  1882 
(‘‘Berlin,  klin.  Wochenschr.,”  1882,  Nr.  40;  1884,  Nr.  48;  1887, 
Nr.  12)  as  a disease  peculiar  to  itself,  is  stated  by  him  to  be  a dis- 
order characterized  by  the  chronic  uninterrupted  secretion  of  gastric 
juice  at  all  times,  even  when  there  is  no  food  in  the  stomach.  In 
a fasting  condition  in  the  morning,  Reichmann  and  others  claim 
that  gastric  juice  could  be  drawn  from  the  stomach  in  these  cases. 
As  we  have  seen  in  the  description  of  the  organic  gastric  diseases, 
particularly  in  severe  reflex  neuroses,  in  dilation,  and  gastric 
ulcer,  continued  flow  of  gastric  juice  is  a frequent  symptom,  asso- 
ciating itself  with  alteration  and  loss  of  substance  in  the  mucosa. 
Occurring  as  a secondary  affection,  it  may  still  be  able  to  effect 
severe  damage  to  the  gastric  walls.  The  diagnosis  of  this  hypo- 
thetical disease  hinges  upon  the  presence  of  gastric  juice  contain- 
ing HC1  and  ferments  in  the  jejune  or  fasting  stomach.  This 
question  has  been  very  carefully  investigated  by  Schreiber 
(“  Deutsch.  Archiv  f.  klin.  Medizin,”  Bd.  liii,  S.  90).  He  found,  in 
Konigsberg,  that  in  over  70  per  cent,  of  his  patients  a digestive 
secretion  was  contained  in  the  fasting  stomach. 

Physiologically  speaking,  an  absolutely  clean  and  empty  stomach 
should,  in  the  morning,  contain  no  gastric  juice,  as  the  glandular 
apparatus  is  normally  in  a resting  state,  but  practically  the  human 
stomach  is  very  rarely  in  this  condition.  It  contains  at  all  times 
epithelial  detritus,  dust,  bacteria,  secretions  from  the  mouth,  lar- 
ynx, and  pharynx,  particularly  saliva,  which  at  different  intervals 
are  swallowed  consciously  or  unconsciously.  These  albumin- 
ous, mucous  masses,  which  are  generally  weakly  alkaline,  and 
which  collect  particularly  during  the  night,  incite  the  specific  gas- 
tric glands  to  secrete  their  physiological  product  just  as  any 
weakly  albuminous  food  would  do.  This  is  a kind  of  pseudo  or 
frustrate  digestion,  because,  so  far  as  nutrition  is  concerned,  this 
slow  digestion  going  on  constantly  is  of  no  value.  This  slight 
pseudodigestion,  which,  according  to  Schreiber,  is  present  perhaps 
at  all  times,  is  augmented  and  multiplied  by  the  permanent  pres- 
ence of  actual  food  masses  when  the  stomach  is  dilated.  The 
frustrate  digestion  becomes  a real  one.  In  all  dilations  with  reten- 
tion of  food  we  have  a permanent,  real  digestion,  and  an  augmented 
permanent  secretion  corresponding  to  it. 

This  so-called  continued  hypersecretion  leads  to  the  digestion 
and  assimilation  of  proteids  and  albuminous  bodies  of  the  food, 
while  the  normal  digestion  of  carbohydrates  is  impeded.  The 


NATURE  OK  SUPERS ECKETION. 


839 


phenomena  that  are  claimed  to  be  typical  of  chronic  continued 
hypersecretion  are  unavoidable  consequences  of  dilation.  The 
cardinal  point  of  distinction — namely,  that  digestive  secretions  are 
contained  in  the  stomach  on  the  morning  following  a very  effective 
washing  out  executed  the  evening  before — is  certainly  not  peculiar 
to  chronic  hypersecretion,  but  occurs  also  with  dilation.  Schreiber 
has  called  attention  to  the  fact  that  it  is  exceedingly  difficult,  even 
impossible,  to  completely  evacuate  and  clean  out  a dilated  stomach. 
During  gastrotomies  food  substances  have  been  found  in  the 
stomach,  notwithstanding  very  energetic  efforts  to  free  it  of  all 
remnants  beforehand.  When  a patient  with  a dilated  stomach  is 
to  be  examined  for  the  gastric  contents  prior  to  taking  food  in  the 
morning,  it  is  expedient  not  to  be  satisfied  with  the  simple  expres- 
sion method  of  Ewald,  when  this  is  negative,  but  to  place  the 
patient  in  a horizontal  position,  and,  while  he  makes  efforts  at 
straining  as  if  he  were  bearing  down  for  stool,  the  operator  must 
compress  the  stomach  near  the  fundus,  which,  in  these  cases,  is 
sometimes  found  below  the  umbilicus. 

In  the  reports  of  a number  of  advocates  of  chronic  hypersecre- 
tion as  a primary  disease  per  se , one  frequently  finds  that  the 
authors  state  that  small  quantities  of  food  remnants  were  found  in 
the  fasting  stomach.  The  argument  generally  follows  that  such 
small  quantities  of  food  could  not  be  the  cause  of  the  large 
quantity  of  gastric  juice  secreted,  contending  that  the  latter  must 
have  been  secreted  spontaneously.  At  the  same  time,  an  illogical 
position  is  demonstrated  by  the  assertion  that  the  momentary 
contact  of  a soft  stomach-tube  with  the  mucosa  is  the  cause  of  the 
secretion  of  eighty  to  one  hundred  centimeters  of  gastric  juice. 
This  assertion,  it  should  not  be  forgotten,  is  made  by  a number  of 
those  who  have  found  food  remnants  in  the  stomachs  of  these  cases. 
That  is  to  say,  the  effort  is  made  to  ignore  the  physiological 
stimulus  of  food  which  is  contained  in  the  stomach  for  hours,  and 
emphasize  the  rather  insignificant  momentary  stimulation  caused 
by  the  introduction  of  a tube.  As  Schreiber  correctly  points  out, 
the  freedom  of  the  stomach  contents  from  food  particles  is  very 
often  only  an  apparent,  not  a real,  one.  It  is  caused  by  imperfections 
in  our  methods  of  investigation,  and  when  one  closely  considers  the 
symptoms  of  chronic  hypersecretion,  as  they  are  described  by  the 
adherents  of  Reichmann,  they  seem,  in  many  cases,  to  be  identical 
with  those  of  dilation.  We  have  been  able  to  exclude  the  hypo- 
thetical factor  of  the  stomach-tube  in  causing  a secretion  of  gastric 


840 


NEUROSES  OF  SECRETION. 


juice  in  a normal  fasting  stomach.  In  a number  of  our  students 
who  consented  to  take  a hypodermic  injection  of  apomorphin  before 
they  had  eaten  anything  in  the  morning,  we  demonstrated  the 
presence  of  HC1  in  the  vomited  matter.  There  is,  therefore,  in 
some  persons  and  to  some  degree  a physiological  normal  continued 
secretion  of  gastric  juice,  as  Schreiber  correctly  asserts  (“  Deutsch. 
medizin.  Wochenschr.,”  1894,  Nr.  18-21);  in  these  the  stomach 
secretes  gastric  juice  normally  and  independently  of  the  ingestion 
of  food.  Ewald  and  Boas  cite  a case  which  has  been  quoted  by 
Riegel  (“Deutsch.  med.  Wochenschr.,”  1893,  Nr.  31,  32)  in  oppo- 
sition to  the  views  of  Schreiber.  This  female  patient  had  a pecu- 
liar gastric  neurosis  founded  on  a hysterical  basis.  For  six  years 
the  patient  vomited  everything  that  was  ingested ; fluids  were 
vomited  immediately,  and  solid  food  after  two  to  four  hours.  When 
she  had  taken  100  c.c.  of  water  on  an  empty  stomach  in  the  morn- 
ing, she  vomited  it  very  soon  thereafter,  and  Ewald  and  Boas  could 
not  find  free  HCl  in  it,  and  therefore  concluded  that  the  fasting 
stomach  secretes  no  gastric  juice  under  normal  conditions.  Aside 
from  the  fact  that  this  woman  may  have  had  a spasm  of  the 
esophagus  or  cardia  preventing  the  small  amount  of  water  from 
ever  reaching  the  stomach,  it  is  not  fair  to  decide  a physiological 
question  from  results  obtained  from  a chronic  neurotic  patient ; 
for,  as  we  know,  in  this  class  of  individuals  the  greatest  variation 
in  the  state  of  the  gastric  secretion  exists  (see  Heterochylia).  The 
results  obtained  on  human  beings  with  gastric  fistulae  (see  W.  Beau- 
mont on  his  Canadian  hunter,  Alexis  St.  Martin,  also  the  cases  of 
Kretschy-Richet)  are  inadmissible  to  the  solution  of  this  physio- 
logical question,  because  they  are  made  on  individuals  under  patho- 
logical conditions. 

The  existence  of  HCl  in  normal  stomachs  may  be  demon- 
strated by  giving  healthy  individuals  long  pieces  of  thin  thread, 
which  with  some  practice  they  can  learn  to  swallow  on  an  empty 
stomach  ; this  silk  or  thread  is  so  thin  that  it  does  not  irritate  the 
gastric  wall  to  any  degree,  at  least  not  so  much  as  a stomach-tube ; 
the  thread  is  then  rapidly  withdrawn  and  pressed  between  pieces 
of  Congo  paper,  when  it  can  be  seen  that  the  Congo  paper  turns 
dark  blue.  We  have  also  introduced  the  thread  already  stained 
with  Congo  red,  and  obtained  the  blue  discoloration  from  fasting 
normal  stomachs.  Undoubtedly  there  are  great  individual  varia- 
tions in  the  genuine  as  well  as  in  the  frustrate  digestion,  caused  by 
the  secretive  power  of  the  glands  and  the  character  of  the  food. 


TYPES  OF  CHRONIC  GASTKOSUCCOfcKHKA. 


84  I 


Morbid  conditions  influence  both  of  these  types  of  digestion 
quantitatively  and  qualitatively.  Conditions  which  incite  the  glands 
will  increase  the  HC1,  and  conditions  which  weaken  the  mucosa, 
such  as  gastritis,  diminish  the  HC1  during  real  digestion  after 
meals,  as  well  as  during  the  frustrate  digestion  occurring  during 
the  night  and  on  a fasting  stomach.  These  variations  are  also 
frequently  found  in  dilation.  If  the  gastrectasia  occurred  on  the 
basis  of  an  ulcer,  the  true  secretion,  as  well  as  the  permanent  secre- 
tion of  a frustrate  character,  will  be  increased,  and  reversely,  when 
carcinoma  or  chronic  gastritis  is  present,  together  with  dilation, 
both  kinds  of  secretion  will  be  diminished,  or  they  may  not  contain 
HCl  at  all.  In  diagnosing  a dilated  stomach  it  is  important  to 
bear  in  mind  that  a stomach  may  be  very  much  enlarged  and  still 
its  greater  curvature  may  not  have  descended  to  any  considerable 
extent.  Frequently  the  very  cause  that  has  brought  about  dila- 
tion— for  instance,  perigastritis,  or  adhesions  about  the  stomach — 
makes  a descent  of  the  greater  curvature  impossible,  simply  because 
it  can  not  descend,  being  bound  down  into  this  position  in  the  upper 
part  of  the  abdomen  by  inflammatory  adhesions.  Therefore  it  is 
possible  that  a stomach  may  be  dilated  and  yet  give  no  splashing 
sound  about  the  neighborhood  of  the  umbilicus,  nor  need  it  be 
much  displaced  from  its  normal  position.  The  stomach  may,  in 
fact,  enlarge  in  an  upward  and  backward  or  lateral  direction  when 
its  descent  is  made  impossible  by  adhesions.  The  presence  or 
absence  of  food  particles  in  contents  drawn  from  the  fasting  stomach 
can  not  always  be  recognized  by  the  naked  eye.  What  resembles 
a turbid  liquid  free  from  ingesta  to  the  naked  eye,  will  often 
show  undigested  rice,  bread,  and  other  carbohydrates  under  the 
microscope.  There  is,  however,  a second  class  of  cases  of  chronic 
continuous  flow  of  gastric  juice  in  which  absolutely  no  organic 
disease  of  the  stomach  and  no  dilation  are  demonstrable.  These 
are  the  typical  cases  of  Reichmann  and  Riegel,  and  due  to  exces- 
sive reaction  of  the  gastric  mucosa  to  the  stimulation  of  the 
ingesta.  We  have  personally  seen  cases  which,  according  to 
the  description  of  Reichmann  and  Riegel,  would  have  to  be  classed 
as  typical  chronic  hypersecretion,  in  which  the  stomach  was  appar- 
ently in  its  normal  place,  and  no  organic  gastric  disease  could  be 
determined  with  the  most  exact  methods  of  examination.  In  three 
of  these  cases  we  could  extract  from  100  to  150  c.c.  of  gastric 
juice  from  the  fasting  stomach,  apparently  containing  no  food  con- 
tents but  occasionally  containing  traces  of  bile.  The  acidity  of 


842 


NEUROSES  OF  SECRETION. 


this  secretion  when  filtered  was  equal  to  8o°  HC1  by  decinormal 
solution  of  sodium  hydroxid  and  either  Congo  or  dimethylamido- 
benzol. 

The  total  acidity  was  no  in  one  of  the  cases- — that  of  a young 
bank  clerk  twenty-four  years  of  age.  He  also  suffered  from  con- 
stipation, pyrosis,  increasing  to  pain,  and  vomiting  which  came  on 
very  soon  after  meals.  The  examination  of  the  contents  one  hour 
after  our  complex  test-meal  gave  the  following  results:  Total 
acidity,  108  ; free  HC1,  84;  biuret  reaction,  positive ; patellar  and 
pupillary  reflexes,  normal.  For  eight  consecutive  days  free  HC1 
and  gastric  ferments  could  be  detected  in  the  contents  from  the 
fasting  stomach.  As  his  trouble  was  persistent  and  he  was  deter- 
mined to  get  well,  he  consented  to  a course  of  exclusive  rectal 
feeding.  He  was  nourished  for  ten  days  by  the  rectum,  and  at  the 
same  time  his  stomach  was  washed  out  with  suspensions  of  magnesia 
usta  every  day.  Under  these  conditions,  when  no  food  was  ingested 
per  os,  the  gastrosuccorrhea  rapidly  diminished,  and  disappeared 
entirely  on  the  fourth  day,  so  that  not  even  the  swallowed  masses 
of  mucus  and  saliva  could  sufficiently  stimulate  the  mucosa  to  pro- 
duce a secretion  of  HC1.  This  has  occurred  in  three  of  our  cases 
where  the  amounts  of  gastric  juice  found  on  an  empty  stomach 
exceeded  100  c.c.  A second  one  of  these  cases  was  that  of  a young 
girl  with  chronic  flow  of  gastric  juice,  who  was  operated  on  upon 
our  suggestion  by  Dr.  R.  W.  Johnson  at  the  Maryland  General 
Hospital.  After  the  abdomen  was  opened  and  the  stomach 
incised,  no  anatomical  cause  for  the  persistent  vomiting  and  gas- 
tralgia  could  be  detected.  On  replacing  the  stomach,  however, 
and  inserting  the  finger  into  the  pylorus,  a rather  sharp  bend  in 
the  duodenum  was  evident  to  the  author.  Undoubtedly  this  kink 
became  more  manifest  when  food  was  ingested,  the  stomach 
thereby  dragging  upon  this  acute  angle  in  the  duodenum.  It  was 
one  of  those  cases  of  motor  insufficiency  which  Broadbent  has 
described  (“British  Medical  Jour.,”  vol.  11,  1893,  pp.  1193  and 
1268)  due  to  kinking  of  the  duodenum  by  an  abnormally  short 
duodenohepatic  ligament.  During  the  operation  the  pylorus  was 
also  enlarged  by  sewing  together  the  oblique  incision  which  had 
been  made  (it  is  true  only  for  explorative  reasons),  but  was  in 
closing  up  sutured  in  such  a way  as  to  resemble  a pyloroplastic 
operation.  The  patient  made  a perfect  recovery,  and  there  was  no 
more  gastrosuccorrhea,  vomiting,  or  gastralgia. 

She  remained  in  the  hospital  for  two  months  after  the  operation, 


CONCLUSIONS  REGARDING  CHRONIC  HYPERSECRETION.  843 

and  was  not  supplied  with  specially  prepared  diet,  but  lived  upon 
the  regular  hospital  fare  without  gastric  distress,  and  was  dis- 
charged in  good  condition.  Einhorn  (/.  c.f  p.  313)  agrees  with 
Reichmann  as  to  the  existence  of  a pathological  continuous  gas- 
trosuccorrhea,  although  he  restricts  this  name  to  cases  not  present- 
ing organic  lesions  of  the  stomach.  Whenever  the  latter  exists 
(lesions),  he  looks  upon  the  accompanying  gastrosuccorrhea  as  a 
consequence  of  the  main  trouble,  but  not  as  a cause  of  the  organic 
lesion.  It  is  the  exclusion  of  these  organic  troubles,  particularly 
of  enlargements  of  the  stomach  and  motor  insufficiency,  in  which 
the  greater  curvature  has  not  descended,  which  presents  so  much 
difficulty.  In  all*  the  cases  of  chronic  continued  hypersecretion 
that  we  have  examined  with  regard  to  this  question,  we  were 
enabled  to  discover  some  organic  lesion,  most  frequently  an  atony, 
pyloric  stenosis,  or  dilation  from  some  cause.  After  a careful  in- 
vestigation of  a large  clinical  material  I incline  to  the  opinion  that 
chronic  hypersecretion  is  in  the  majority  of  cases  not  a sponta- 
neous, idiopathic  neurosis,  but  a secondary  symptomatic  phenom- 
enon. I base  my  conclusion  upon  the  following  facts  : (1)  That 
gastric  juice  in  amounts  varying  between  20  and  30  c.c.  is  con- 
tained normally  in  the  fasting  stomach  in  about  8 per  cent,  of 
cases  examined  by  myself;  the  secretion  of  the  peptic  glands 
being  set  up  by  the  presence  of  mucus,  saliva,  dust,  bacteria, 
epithelial  detritus,  etc.  (2)  That  apparently  clear  gastric  juice 
obtained  from  a fasting  stomach  may  show  presence  of  food  par- 
ticles microscopically.  (3)  That  it  is  not  possible  to  exclude 
dilation  nor  ulcer  in  all  of  these  cases,  particularly  when  the  dila- 
tion is  not  marked  by  the  descent  of  the  greater  curvature.  (4) 
The  liquid  obtained  from  undoubted  dilations  of  the  stomach  may 
contain  absolutely  no  food  particles,  thus  simulating  the  condition 
for  chronic  gastrosuccorrhea.  (5)  Gastric  contents  obtained  from 
dilation  of  the  stomach  do  not  always  show  the  presence  of 
products  of  imperfect  starch  digestion  (erythrodextrin).  This  is 
particularly  the  case  when  we  meet  with  dilation  accompanied  by 
hyperacidity,  but  with  a fair  motility,  or  where  the  peristalsis  is  only 
periodically  lost.  In  any  case  of  hyperacidity  it  is  possible  that 
the  products  of  starch  digestion  may  be  absent  when  very  little 
carbohydrate  food  has  been  ingested.  This  may,  of  course,  also 
happen  with  gastrosuccorrhea.  (6)  In  cases  of  typical,  so-called 
chronic,  continued  supersecretion,  the  symptoms  cease  entirely  and 
the  stomach  contains  no  gastric  juice  in  the  morning  after  the 


844 


NEUROSES  OF  SECRETION. 


patient  has  been  fed  by  the  rectum  for  four  to  eight  days.  (7) 
Diseases  presenting  the  classical  picture  of  Reichmann’s  disease 
have  been  known  to  disappear  entirely  after  a gastro- enterostomy 
or  a pyloroplastic  operation  was  performed. 

Symptomatology. — This  is  essentially  the  same  as  in  motor 
insufficiency  with  hyperacidity.  (See  chapter  on  this  subject.) 

The  periodic  flow  of  gastric  juice,  which  we  have  already 
described  (p.  834),  is  either  a functional  neurosis  or  a reflex  affec- 
tion (tabes  dorsalis),  or  connected  with  an  affection  of  the  sym- 
pathetic. It  is  identical  with  the  gastroxynsis  of  Rossbach. 
Possibly,  also,  the  periodic  vomiting  of  Leyden  belongs  to  this 
group  of  neuroses.  The  chronic  gastrosuccorrhea  is  a symptom , 
and  has  not  the  claim  to  be  considered  a morbid  entity  like  the 
periodic  or  spasmodic  gastrosuccorrhea.  Chronic  flow  of  gastric 
juice  may  be  a complication  of  ulcer  and  motor  insufficiency. 
From  a pathological  standpoint,  it  is  well  established  that  gastritis 
may  accompany  ulcer  as  well  as  dilation  (Rokitansky,  Lebert, 
Orth,  Cruveilhier).  The  gastritis  which  accompanies  these  dis- 
eases, and  which  shows  hyperacidity,  has  been  called  by  Kor- 
czynski  and  Jaworski  (“  Deutsch.  Archiv  f.  klin.  Med.,”  Bd.  xlvij, 
S.  578)  “ catarrhus  acidus,”  and  by  Hayem  (“Gazette  Hebdom.,” 
1892,  Nos.  33  and  34)  it  has  been  designated  as  “ gastrite  hyper- 
peptique.”  These  expressions  signify  the  same  complexity  of 
symptoms  as  those  first  described  by  Reichmann  under  the  name 
of  “ gastrosuccorrhea.”  The  “ gastritis  acida  ” of  Boas  is  quite  a 
different  thing — a characteristic  form  of  chronic  gastritis. 

Diagnosis. — The  main  question  to  decide  is  not  whether  we 
are  dealing  with  chronic  gastrosuccorrhea,  which  is  not  very 
difficult  to  find  out,  but  to  determine  which  disease  it  is  a con- 
sequence of.  The  most  frequent  causes  are  ulcer,  pylorospasm, 
and  mechanical  insufficiency.  For  a fuller  explication  of  these 
subjects  and  their  consequences  we  must  refer  to  the  chapters 
in  which  they  are  considered.  If  150  to  300  c.c.  of  gastric  juice 
can  be  drawn  from  the  stomach  before  taking  food  in  the  morn- 
ing, which  juice  is  free  from  food  remnants,  and  there  are  no 
evidences  of  motor  insufficiency,  the  case  will  be  one  of  primary 
neurotic  chronic  gastrosuccorrhea.  But  if  the  food  remnants  are 
very  evident  and  especially  if  organic  diseases  are  demonstrable, 
the  condition  is  secondary. 

Treatment. — If  ulcer,  pylorospasm,  or  dilation  can  be  demon- 
strated to  exist,  the  treatment  must  be  directed  to  these  fundamental 


LITERATURE  ON  CHRONIC  GASTROSUCCORRHEA.  845 

causes.  (See  Treatment  of  Ulcer  and  Motor  Insufficiency.)  In  the 
absence  of  any  definite  etiological  factor,  the  treatment  is  that  de- 
scribed under  hyperchylia.  Under  all  conditions  massage  of  the 
stomach  and  intestines,  intragastric  application  of  the  galvanic  and 
faradic  currents,  and  washing  out  of  the  stomach  are  very  essential 
adjuncts  to  treatment.  Where  there  is  much  secretion  of  gastric 
juice,  even  on  an  empty  stomach,  the  use  of  a stomach-tube  can  not 
be  consistently  neglected.  It  is  the  only  way  to  remove  the  excess 
of  secretion  directly;  then,  again,  the  best  treatment  of  a hyper- 
chylia is  that  which  is  supplied  directly  to  the  mucosa  in  the  form  of 
irrigations  with  calcined  magnesia,  sodium  bicarbonate,  tannin  ( ]/2 
of  one  per  cent,  solution),  and  suspensions  of  bismuth  subnitrate. 
The  methodical  use  of  alkalies  affords  great  relief  to  the  pyrosis 
and  eructation,  and  facilitates  carbohydrate  digestion.  The  alka- 
lies which  we  recommend  most  strongly  are  the  magnesia  usta 
and  the  ammoniophosphate  of  magnesium.  Einhorn  speaks  very 
favorably  of  spraying  the  stomach  with  a solution  of  nitrate  of 
silver,  I : 1000.  Reichmann  administers  the  nitrate  of  silver  in 
solution  or  in  gelatin  capsules.  The  author  uses  this  salt  in  the 
form  of  lavage  (i : 1000)  and  can  speak  with  favor  of  this  treatment. 

The  diet  will  vary  with  the  underlying  causative  disease.  It  will 
be  either  that  for  ulcer  or  dilation,  or  that  for  hyperchylia.  Where 
the  stomach  is  extremely  sensitive,  the  diet  orders  of  Penzoldt  may 
be  safely  tried,  because  they  are  very  sparing  and  make  little  de- 
mands upon  the  capacity  of  the  stomach.  Exclusive  rectal  feeding 
may  be  necessary ; it  is,  as  a rule,  promptly  followed  by  good 
results. 

Dr.  D.  L.  Edsall  has  given  a lucid  representation  of  recent  litera- 
ture on  this  subject  (“  Amer.  Jour.  Med.  Sciences,”  vol.  cxvii, 
1899,  p.  694). 


LITERATURE 

ON  CHRONIC  GASTROSUCCORRHEA. 

1.  Boas,  “ Specielle  Diagnostik  u.  Therapie  d.  Magenkrankheiten,”  2.  Aufl. 

2.  Bouveret  et  Devic,  “ La  Dyspepsie  par  Hypersecretion  Gastrique  ” (Mala- 
die  de  Reichmann),  Paris,  1892.  (Monograph.) 

3.  Cavazzani,  A.,  “ Della  malattia  di  Reichmann  e della  sua  cura,”  “ Clin. 
Med.  Ital.,”  Milan,  1898,  xxxvn. 

4.  Combemale,  “Maladie  de  Reichmann  un  Dyspepsie  par  Hypersecretion 
Gastrique,”  “ Echo  Med.  du  Nord,”  Lille,  1897,  1. 

5.  Debove  et  Remond,  “ Les  Maladies  de  l’Estomac.” 


846 


NEUROSES  OF  SECRETION. 


6.  Faucher,  “ De  la  Crise  Aigue  dans  la  Maladie  de  Reichmann”  (Gastrite 
Chronique  avec  Hypersecretion),  “Jour,  de  Med.  Prat.,”  25,  vi,  1897. 

7.  Hayem,  “ Resume  de  l’Anatomie  Pathologique  de  la  Gastrite  Chronique,” 
“ Gaz.  Hebdom.,”  1892,  Nos.  33,  34. 

8.  Hayem,  “ Ueber  Gastritis  parenchymatosa,”  “Allgem.  Wien.  med. 
Zeitung,”  1894,  No.  2 ff. 

9.  Hayem,  “ Stenose  incomplete  du  Pylore,  Pretendue  Maladie  de  Reich- 
mann,” “ Presse  Medicale,”  31  mars,  1897. 

10.  Jaworski,  “ Zeitschr.  f.  klin.  Med.,”  Bd.  XI,  Heft  2 u.  3 ; “ Munch,  med. 
Wochenschr.,”  1887,  No.  7 u.  8 ; “Wien.  med.  Presse,”  1886,  No.  52;  “Wien, 
med.  Wochenschr.,”  1887,  No.  49  u.  f. 

11.  Johnson,  E.  E.,  “ Munch,  med.  Wochenschr.,”  1887,  No.  48  u.  f. 

12.  Johnson  und  Behm  (“Zeitschr.  f.  klin.  Med.,”  Bd.  xxn,  S.  478),  “Re- 
port of  106  Cases  of  Supersecretion,”  including  all  cases  where  slight  amounts 
of  gastric  juice  were  found,  and  give  complete  literature. 

13.  v.  Korczynski  und  Jaworski,  “ Deutsches  Archiv  f.  klin.  Med.,”  Bd. 
XLVII,  S.  578. 

14.  Leyden,  “ Zeitschr.  f.  klin.  Med.,”  1882,  Bd.  vi,  S.  605. 

15.  Linossier,  “ Maladie  de  Reichmann  et  Stenose  Pylorique,”  “ Semaine 
Med.,”  Paris,  1898,  xvm. 

16.  Lyon,  G.,  “ L’ Analyse  du  sue  Gastrique,”  Paris,  1890. 

17.  Lyon,  G.,  “ Les  Theories  Nouvelles  sur  la  Gastrosuccorrhee  ou  Maladie 
de  Reichmann  et  sou  Traitement,”  “ Rev.  de  Therap.  Med.  et  Chir.,”  Paris, 
1897,  LXIV. 

18.  Martius,  F.,  “ Ueber  den  Inhalt  des  gesunden,  niichternen  Magens  und 
den  continuirlichen  Magensaftfluss,”  “Deutsche  med.  Wochenschr.,”  1894, 
Nr.  32. 

19.  Morano,  G.,  “ Malattia  di  Reichmann,”  “ Riforma  Med.,”  Napoli,  1898, 
xiv,  pt.  4. 

20.  Reichmann,  “ Berl.  klin.  Wochenschr.,”  1892,  Nr.  40;  1884,  Nr.  48; 
1887,  Nr.  12  u.  f. ; 1887,  Nr.  14. 

21.  Riegel,  “Zeitschr.  f.  klin.  Med.,”  Bd.  xi  u.  XII ; “ Munch,  med.  Woch- 
enschr.,” 1884,  Nr.  45  u.  46;  “Deutsche  med.  Wochenschr.,”  1887,  Nr.  29; 
1892,  No.  21  ; 1893,  Nr.  30  u.  31  ; “ Volkmann’s  Samml.  klin.  Vortrage,”  1886, 
S.  289. 

22.  Rosin,  “ Ueber  das  Secret  des  niichternen  Magens,”  Deutsche  med. 
Wochenschr.,”  1893,  Nr.  30. 

23.  Rossbach,  “ Deutsches  Archiv  f.  klin.  Med.,”  1885,  Bd.  xxxv. 

24.  Roux,  “Le  Syndrome  de  Reichmann,  Expose  Critique  des  Travaux 
Recents  sur  l’Hypersecretion  Chlorhydrique  Continue,”  “ Gaz.  des  Hopit.,” 
No.  61,  1897. 

25.  Saupault,  “ Sur  Un  cas  de  Gastro-succorree,”  “ Gaz.  Hebd.  de  Paris,” 
27  Janvier,  1897. 

26.  Schreiber,  Jul.,  “ Gastrektasie  u.  deren  Verhaltniss  z.  chronischen  Hyper- 
secretion,” “Archiv  f.  Verdauungskrankh.,”  Bd.  11,  S.  423. 

27.  Schreiber,  Jul.,  “Ueber  den  continuirlichen  Magensaftfluss”  (Secretio 
hydrochlorica  continua),  “ Deutsche  med.  Wochenschr.,”  1893,  Nr.  29  u.  30; 
ibid  , “ Ueber  continuirlichen  Magensaftfluss,”  “ Deutsche  med.  Wochenschr.,” 
1894,  Nr.  18,  20,  u.  21. 


SUBACIDITY. 


847 


28.  Sticker,  “ Munch,  med.  Wochenschr.,”  1886,  Nr.  32  u.  33. 

29.  Strubing,  “Zeitschr.  f.  klin.  Med.,”  1885,  Bd.  ix,  S.  381. 

30.  Vente,  A.,  Inaug.-Dissert.,  Giessen,  1890. 

31.  Wolff,  “Zeitschr.  f.  klin.  Med.,”  Bd.  xvi. 

32.  Text-books  of  Leube,  Riegel,  Boas,  Ewald,  Debove  et  Rdmond,  Bou- 
veret,  Penzoldt,  Fleiner,  S.  Martin,  A.  Pick,  Mathieu,  Einhorn. 

33.  Edsall,  D.  L.,  “ Amer.  Jour.  Med.  Sciences,”  vol.  cxvii,  1899,  p.  695. 


SUBACIDITY  (Hypochlorhydria  or  Hypochylia). 

Subacidity,  as  a neurosis,  is  a disease  in  which,  even  during  the 
height  of  digestion,  gastric  juice  is  secreted  in  which  the  HC1,  and 
with  it  the  pepsin  and  rennin,  are  present  in  smaller  amounts  than 
normal.  We  will  not  consider  under  this  head  those  secretory 
anomalies  in  which  the  secretion  of  gastric  juice  is  absent  entirely. 
These  states  will  be  considered  under  Achylia  Gastrica  or  In- 
acidity. In  subacidity  HC1  is  still  secreted,  but  in  such  small 
amounts  that  it  enters  into  combination  with  albuminous  foods 
entirely,  and  we  can  detect  it  only  as  combined  HC1.  Cases  in 
which  free  HC1  can  be  detected  by  Congo  paper  after  our  double 
test-meal  do  not  logically  belong  in  this  class  of  subacidity,  because 
the  presence  of  free  HC1  means  that  more  HC1  is  secreted  than  can 
enter  into  combination  with  the  food ; there  is  an  excess  of  acid 
beyond  that  required  for  digestion.  Technically,  we  may,  therefore, 
define  hypochylia  as  a secretory  neurosis  in  which  free  HC1  is 
absent  at  the  test-meal,  but  combined  HC1  and  the  ferments  are 
still  present.  Nervous  hypochylia  is  in  reality  but  a phase  of 
nervous  dyspepsia,  or  neurasthenia  gastrica.  But,  as  it  is  desir- 
able to  represent  all  secretory  neuroses  seriatim,  we  have  here 
abstracted  the  symptoms  of  nervous  depression  of  gastric  secre- 
tion. It  was  formerly  believed  that  subacidity  was  always  con- 
nected with  some  organic  gastric  disease  (carcinoma,  gastritis),  or 
occurred  in  the  train  of  infectious  diseases,  or,  as  a result,  with 
anemia  and  leukemia.  Subacidity,  however,  may  exist  on  a purely 
nervous  substratum,  in  hysteria  and  neurasthenia,  and  in  psychoses. 
It  then  occurs,  independently  of  anatomical  changes  in  the  stomach, 
as  a functional  disturbance  of  the  secretory  nerves,  the  irritability 
of  which  has  been  reduced.  Functional  disturbances  of  this  char- 
acter may  be  limited  to  the  secretory  nerves  and  not  involve  the 
remaining  nervous  apparatus  of  the  stomach.  The  amount  of  HC1 
secreted  is  not  sufficient  to  saturate  the  albumin  present  in  the 
proteid  food  : in  other  words,  an  HC1  deficit  exists.  It  is  probable 


848 


NEUROSES  OF  SECRETION. 


that  the  secretory  nerves  become  exhausted  sooner  than  the  motor 
nerves,  and  that,  therefore,  subacidity  may  be  an  expression  of  ex- 
haustion or  weakness  in  the  secretory  apparatus.  In  this  way  we 
have  repeatedly  observed  prolonged  subacidity  followed  by  pro- 
nounced hyperacidity. 

Etiology. — Nervous  subacidity  or  hypochylia  is  a secondary 
phenomenon  occurring  with  neurasthenia,  hysteria,  tabes,  and  the 
psychoses. 

Symptomatology. — When  the  motor  function  of  the  stomach  is 
good,  symptoms  may  be  absent  entirely,  but  the  slightest  insuffi- 
ciency of  the  motor  power  is  rapidly  followed  by  decomposition  in 
the  gastric  contents,  caused  by  bacteria,  for  the  amount  of  HC1 
secreted  is  not  sufficient  to  inhibit  or  prevent  the  action  of  micro- 
organisms. As  a consequence  of  this  organic  acids  are  formed, 
and  gaseous  formations  create  gastric  discomfort,  and,  at  times, 
intestinal  distention.  There  is  nothing  characteristic  in  the  symp- 
tomatology of  subacidity.  The  result  of  the  depressed  state  of 
the  secretion  and  the  general  symptomatology  are  the  same  as 
those  in  achylia  gastrica,  and  will  be  described  under  that  heading. 
It  is  natural  that  amylolysis  should  proceed  more  rapidly  in  the 
absence  of  free  HC1,  since  nothing  can  disturb  the  activity  of  the 
ptyalin  in  that  case.  On  the  other  hand,  the  digestion  of  meats, 
eggs,  etc.,  is  most  unsatisfactory.  As  HC1  is  one  of  the  principal 
normal  stimulants  to  peristalsis,  the  disease  is  frequently  accom- 
panied by  constipation,  which,  in  turn,  produces  increasing  putre- 
faction of  the  intestinal  contents,  being  in  this  case  more  pro- 
nounced because  the  disinfecting  action  of  the  HC1  is  missing. 

Differential  Diagnosis. — Carcinoma  and  chronic  gastritis  might 
be  confounded  in  the  incipient  stages  with  nervous  subacidity 
(for  the  differential  diagnosis  from  carcinoma  and  gastritis,  we 
refer  to  the  chapters  on  these  diseases) ; but  when  the  enzymes, 
pepsin  and  rennin,  can  be  demonstrated  in  the  gastric  contents,  or 
even  if  only  the  proenzymes,  pepsinogen  and  rennin-zymogen,  can 
be  demonstrated,  one  can  not,  as  a rule,  exclude  chronic  gastritis 
and  carcinoma.  A patient  and  prolonged  study  of  nervous  sub- 
acidity will  not  fail  to  demonstrate  that  great  variations  exist  in  the 
amount  of  hydrochloric  acid  that  is  secreted.  Occasionally  it  may 
be  found  that  a transition  to  a normal  acidity,  or  even  to  hyper- 
chylia,  has  taken  place.  Lactic  acid  is  a very  rare  occurrence  in 
nervous  subacidity;  its  presence  and  the  Oppler-Boas  bacillus 
would  speak  for  carcinoma. 


TREATMENT  AND  DIET  IN  SUBACIDITY.  849 

Treatment. — In  most  cases  it  will  be  sufficient  to  supply  an 
amount  of  dilute  HC1  which  is  commensurate  with  the  deficit.  In 
rare  instances  it  will  be  impossible  to  administer  sufficient  HC1  to 
give  the  reaction  for  free  IIC1,  because  it  is  not  well  tolerated  in 
this  quantity.  In  that  case  we  advise  adding  the  HC1  to  beef- 
juice,  either  Wyeth’s,  Valentine’s,  or  the  Mosquera  beef-jelly. 
This  makes  a sauce  which  can  be  poured  over  the  finely  divided 
meat  foods  that  are  to  be  eaten.  The  meat-dissolving  power  of 
the  acid  is  not  destroyed  by  this  method  of  preparing  it,  although 
the  acid  may  be  partly  in  a combined  state.  Abnormal  fermentations 
and  decompositions  are  rare,  and  therefore  the  stomach-tube  can, 
as  a rule,  be  dispensed  with.  The  bitter  tonics — quassia,  cinchona, 
calumbo,  gentian — and  the  basic  orexin  (in  five-grain  doses  three 
times  a day)  very  often  increase  the  appetite  and  favor  a secretion 
of  HC1.  Strychnin  and  the  intragastric  use  of  the  faradic  current 
we  warmly  recommend  for  this  purpose.  Pilocarpin,  according  to 
Riegel,  increases  the  secretion  of  gastric  juice,  but  in  my  experi- 
ence it  is  too  dangerous  a drug  to  use  with  that  persistence  that 
is  requisite  in  these  cases.  When  the  motility  is  good,  those 
mineral  waters  which  are  rich  in  sodium  chlorid  are  worth  a trial. 
(See  section  on  Mineral  Waters.) 

The  Diet. — It  is  an  interesting  fact  that  patients  with  sub- 
acidity instinctively  avoid  a meat  diet,  and  are  large  carbohydrate 
eaters.  It  is  well,  however,  not  to  let  them  persist  on  the  exclusive 
use  of  carbohydrates,  but  to  train  up  the  digestive  capacity  of  the 
stomach  to  a more  abundant  digestion  of  proteids.  All  meats 
should  be  given  in  a finely  divided  state.  The  extractive  materials 
in  meat  are  useful  stimulants  to  appetite  (Pawlow).  Before  the 
meal,  it  is  well  to  stimulate  the  appetite  and  secretion  by  giving  a 
few  sardels  or  the  roe  of  potted  herring,  or,  what  is  more  palat- 
able and  easier  to  procure,  a sandwich  spread  with  Russian  caviar. 
Surf-baths,  cold  sponge-baths  at  home,  proper  movements  of  the 
bowels,  and  at  least  eight  to  nine  hours  of  sleep,  are  indispensable 
agents  in  the  management  of  this  secretory  defect. 


850 


ACHYLIA  GASTRICA. 


CHAPTER  XIII. 

ACHYLIA  GASTRICA. 

Synonyms. — Absence  of  the  Secretion  of  Gastric  Juice;  Nervous  Inacidity; 
Atrophy  of  the  Stomach;  Anadenia  Ventriculi ; Phthisis  Ventriculi ; Achlor- 
hydria. 

Nature  and  Concept. — The  term  achylia  gastrica  means,  liter- 
ally, without  gastric  chyle,  and  was  first  proposed  by  Einhorn 
(“  New  York  Medical  Record,”  June  11,  1892)  to  designate  a class 
of  diseases  in  which  no  gastric  juice  is  secreted. 

The  affection  is  found  to  exist  in  two  varieties — first,  the  pri- 
mary, idiopathic,  possibly  inherited,  achylia;  secondly, the  acquired 
or  secondary  achylia.  The  primary  idiopathic  or  symptomatic 
achylia  is  characterized  by  the  fact  that  absence  of  secretion  is 
evident  before  any  marked  anatomical  changes  have  occurred  in 
the  mucosa  which  could  explain  the  loss  of  function.  It  is,  there- 
fore, as  a rule,  not  regarded  as  a result  acquired  from  a real 
disease,  but  as  an  individual  peculiarity,  possibly  an  inherited 
functional  debility.  There  are  undoubtedly  persons  in  whom 
gastric  secretion  may  be  absent  for  years,  or  permanently  wanting; 
yet  who,  apparently,  may  enjoy  robust  health.  The  majority  of 
these  individuals,  however,  have  suffered  from  frequent  dyspeptic 
complaints,  which  are  partly  of  a purely  nervous  character.  In 
these  cases  severe  anemic  and  cachectic  conditions  are  usually 
absent,  and  while  the  general  nutrition  may  occasionally  be  found 
disturbed,  it  is  easily  remedied  with  proper  dietetic  treatment. 

The  last-named  type  of  cases  demonstrates  that  the  function  of 
the  stomach  may  be  permanently  lost,  so  far  as  its  digestive  power 
is  concerned,  yet  with  no  apparent  effects  upon  the  general  con- 
stitution. A very  convincing  argument  for  the  compensatory 
digestive  power  of  the  intestine!  Lubarsch  (“  Achylia  Gastrica,” 
etc.,  von  Martius  u.  Lubarsch,  1897,  p.  74)  raises  the  question 
whether  gastric  digestion  may  not  be  entirely  dispensed  with,  or 
whether  it  is  not  superfluous,  which  of  course  implies  that  the 
secretion  of  HC1  may  possibly  be  an  unnecessary  function.  There 
can  be  no  doubt,  however,  that  deficiency  of  gastric  secretion  is  a 
disease.  Individuals  affected  with  symptomatic  achylia  are  very 
much  more  sensitive  in  general,  and  more  susceptible  to  gastric 


NATURE  OF  ACHYLIA. 


85 


diseases,  than  their  fellow-men  equipped  with  normal  stomachs. 
The  idea  that  gastric  digestion  is  superfluous  and  dispensable  im- 
presses us  as  being  a reactive  opinion  induced  by  the  other 
extreme  view  formerly  held,  according  to  which  the  stomach  was 
the  most  important  of  all  digestive  organs.  Gastric  secretion  is 
by  no  means  a useless  function.  Lubarsch  says:  “Those  who 
have  lost  it,  have  one  weapon  less  in  the  struggle  for  existence,” 
and  clinical  experience  teaches  that  persons  who  have  no  secretion 
of  gastric  juice  are  much  more  liable  to  diseases  of  the  stomach. 
When  such  are  attacked  by  intestinal  diseases  and  this  supple- 
mentary digestion  is  interfered  with,  the  prognosis  becomes 
serious. 

Achylia  may  exist  upon  a nervous  basis,  it  may  be  congenital 
or  acquired,  in  consequence  of  some  organic  gastric  disease. 

The  results  of  the  examination  of  the  gastric  contents,  in  simple, 
uncomplicated  achylia,  are  quite  characteristic : The  fasting  stom- 
ach, examined  in  the  morning  before  any  food  has  been  taken,  is 
empty.  I have  never  been  able  to  obtain  more  than  twenty 
to  thirty  cubic  centimeters  of  neutral,  slightly  mucoid  liquid; 
remnants  of  ingesta  of  the  previous  day  are  never  observed.  One 
hour  after  the  Ewald  test-breakfast  the  contents  of  the  stomach 
have  the  same  appearance  as  they  have  in  the  mouth  before  they 
are  swallowed.  This  appearance  is  claimed  by  Einhorn  and  others 
to  be  quite  characteristic.  Contents  drawn  in  this  manner  are 
generally  slightly  acid.  Blue  litmus  paper  is  very  slightly  red- 
dened. The  total  acidity  varied  in  our  cases  from  two  to  eight. 
This  degree  of  acidity  can  be  found  in  the  test-meal  before  it  is 
eaten.  Whenever  the  acidity  of  the  drawn  stomach-contents  does 
not  exceed  that  of  the  meal  before  it  is  swallowed,  it  may  be  safely 
assumed  that  free  and  combined  HC1  is  absent;  in  other  words, 
no  HC1  has  been  secreted.  Whenever  the  total  acidity  is  equal  to 
four  only,  it  is  due  to  acid  that  has  been  introduced  in  the  food; 
with  a total  acidity  no  higher  than  four,  one  hour  after  a test- 
breakfast,  it  is,  therefore,  unnecessary  to  make  further  analyses  for 
the  detection  of  HC1.  The  gastric  contents,  when  filtered  and 
mixed  with  HC1  sufficient  to  produce  the  reaction  with  Congo 
paper,  can  not  digest  discs  of  egg-albumen. 

Milk  taken  by  achylic  patients  may  be  drawn  out  twenty  or  thirty 
minutes  afterward  perfectly  unchanged,  or,  rather,  uncoagulated. 
The  secretion  of  pepsin  and  rennin  is,  therefore,  absent.  By 
proper  tests  it  can  also  be  found  that  pepsinogen  and  rennin- 


852 


ACHYLIA  GASTRICA. 


zymogen  are  also  wanting.  Lubarsch  and  Martius  assert  that  the 
isolated  loss  of  HC1,  without  loss  of  secretion  of  pepsin  and  ren- 
nin,  does  not  exist ; and  for  these  cases  of  loss  of  gastric  secre- 
tion (not  the  HC1  simply,  but  all  the  constituents  of  gastric  juice) 
the  terms  anacidity,  inacidity,  and  achlorhydria  are  not  so  expres- 
sive and  logical  as  the  designation  “ achylia  gastrica.”  We  may 
assert,  however,  on  a very  large  personal  experience,  that  isolated 
loss  of  HC1  secretion  and  preservation  of  formation  of  ferments 
does  occur.  In  the  progressive  destruction  of  the  mucosa  accom- 
panying carcinoma  and  gastritis  there  are  stages  in  which  HClis 
totally  wanting,  and  yet,  by  proper  methods,  secretion  of  enzymes, 
or  of  the  proenzymes,  can  be  detected.  All  other  cases  of  loss  of 
secretion  not  due  to  carcinoma  or  atrophic  gastritis  may  logically 
be  classed  as  achylia.  A further  pronounced  sign  of  achylia  is  the 
abnormally  small  quantity  of  gastric  contents  found  one  hour  after 
the  test-breakfast.  Biedert  (“  Diatetik  u.  Kochbuch,”  etc.,  1895), 
who  suffers  from  this  affection  himself,  found  that  his  stomach  was 
very  rapidly  emptied,  so  that  he  had  to  draw  the  contents  within 
forty-five  minutes  if  he  wished  to  obtain  any  at  all. 

Julius  Miller  (/.  c.,  “Archiv  f.  Verdauungskrankh.,”  Bd.  i,p.  233) 
found  that  strong  solutions  of  sodium  chlorid  are  very  much 
diluted  when  they  are  brought  into  the  human  stomach.  It  is 
further  known  that  strong  solutions  of  common  salt,  when  brought 
into  the  stomach,  arrest  HC1  secretion.  The  tendency  to  dilute 
solutions  that  are  put  into  the  stomach  is  so  persistent  that  it  con- 
tinues even  after  the  concentration  of  these  solutions  has  inhibited 
the  HC1  secretion.  Alcohol,  various  forms  of  sugar,  dextrin,  and 
peptone  are  absorbed,  and  a more  or  less  active  excretion  of  water 
goes  on  hand  in  hand  and  simultaneously  with  such  absorption. 
In  achylia  gastrica,  however,  the  stomach  differs  very  much  in  this 
respect  from  the  normal  organ,  since  it  has  then  lost  its  power 
of  diluting  the  gastric  contents. 

The  fact  that  concentrated  solutions  of  sodium  chlorid  inhibit 
the  secretion  of  HC1  has  been  made  available  in  the  treatment 
of  hyperacidity.  From  this  fact  it  is  very  probable  that,  in 
achylia,  we  are  dealing  not  only  with  loss  of  the  characteristic 
secretion,  the  gastric  juice  with  its  HC1  and  ferments,  but  also  that 
there  seems  to  be  no  secretion  of  any  kind  issuing  from  the 
mucosa.  The  diluting  secretion  of  the  stomach  is,  under  normal 
conditions,  not  exclusively  made  up  of  the  normal  gastric  juice, 
and  we  are  here  confronted  with  a physiological  function  of  a very 


GASTRIC  ATROPHY  WITH  ANEMIA. 


*53 


complicated  character,  concerning  which  very  little  of  a positive 
nature  is  known.  There  is  a general  consensus  of  opinion,  which 
we  can  confirm,  that  in  achylia  there  is  an  exceptionally  great 
vulnerability  of  the  mucosa.  It  is  a frequent  experience  with 
achylic  patients  to  find  that  particles  of  the  mucosa  showing  slight 
hemorrhages  are  unintentionally  scraped  or  torn  off  during  the 
drawing  of  the  test-meals. 

Lubarsch  (/.  c .),  Einhorn  (/.  c.),  Biedert  (/.  c .),  Cohnheim  (“  Archiv 
f.  Verdauungskrankh.,”  Bd.  1,  p.  274),  Jaworski  (“  Munch,  med. 
Wochenschr.,”  1887,  Nr.  7 und  8),  have  observed  this  phenomenon, 
and  the  first-mentioned  author  asserts  that  the  vulnerability  of  the 
mucosa  in  achylia  is  as  great  as  in  carcinoma.  In  achylia  it  is 
almost  impossible  to  avoid  the  scraping  off  of  portions  of  the 
superficial  mucous  membrane,  no  matter  what  shaped  tube  is  used, 
and  if  it  is  desired  to  avoid  scraping  the  mucosa  at  all,  it  is  safer 
to  use  a tube  which  is  entirely  closed  at  its  lower  end  and  has  but 
one  velvet  eye-opening  at  the  side  (Tiemann  & Co.,  New  York). 
Scraping  off  of  minute  particles  is  a harmless  procedure,  but  the 
tearing  of  larger  pieces  by  suction  may  be  followed  by  extensive 
hemorrhages. 

Total  loss  of  gastric  secretion,  even  as  a consequence  of  a 
fully  developed  atrophy  of  the  mucosa  (anadenia),  can  not  cause 
anemia  or  cachexia  per  se.  Those  cases  in  which  anemia  has 
been  observed  in  connection  with  achylia  were  most  probably 
complicated  by  a mechanical  insufficiency  of  the  stomach,  or  by 
other  diseases ; thus,  in  some  cases,  syphilis  or  tuberculosis,  and 
extension  of  the  atrophic  process  to  the  mucosa  of  the  intestine, 
have  complicated  the  gastric  derangement. 

The  credit  of  having  first  pointed  out  the  association  of  gastric 
atrophy  with  anemia  is  usually  attributed  to  S.  Fenwick  (lecture 
on  “Atrophy  of  the  Stomach,”  “The  Lancet,”  July  7,  1877;  also 
“ On  Atrophy  of  the  Stomach  and  Certain  Nervous  Affections 
of  the  Digestive  Organs,”  London,  1880,  J.  and  A.  Churchill). 
Both  Einhorn  (/.  c.,  p.  321)  and  Martius  (/.  c.,  p.  16)  assert  that 
Fenwick’s  report  is  the  pioneer  observation  on  this  subject.  As 
a matter  of  fact,  it  was  our  countryman,  Austin  Flint,  who  first 
called  attention  to  the  relation  between  anemia  and  atrophy  of  the 
gastric  glands  (Austin  Flint,  “ The  American  Medical  Times,”  1 860). 
He  expressed  the  opinion  that  some  cases  of  profound  anemia  are 
dependent  upon  atrophy  of  the  glands  of  the  stomach.  (The  fur- 
ther contributions  of  Flint  to  this  subject  are  to  be  found  in  the 
56 


854 


ACHYLIA  GASTRICA. 


“ New  York  Med.  Jour.”  for  March,  1871,  and  in  his  “ Principles 
and  Practice  of  Medicine,”  p.  477,  Philadelphia,  1881.)  The  pri- 
ority of  Flint’s  publications  have  been  emphasized  by  Professor 
William  H.  Welch  (“  A System  of  Medicine  by  American  Authors,” 
vol.  11,  p.  616  *). 

Although  the  anemia  which  supervenes  in  these  cases  of  achylia 
can  not  be  directly  ascribed  to  the  gastric  atrophy,  and  too  much 
importance  was  attributed  by  Flint  and  others  to  the  state  of 
the  gastric  mucosa,  the  reports  of  this  author  are,  nevertheless, 
very  valuable,  because  the  secondary  states,  which  we  have  men- 
tioned as  really  causing  the  anemia  and  cachexia,  are  most  prob- 
ably brought  about  by,  and  owe  their  origin  to,  the  primary 
degenerative  changes  in  the  gastric  mucosa  which  Flint  and  Osier 
have  described. 

In  the  first  part  of  this  work  I have  reported  examinations 
of  fragments  of  mucosa  derived  from  twelve  cases  of  anacidity 
or  subacidity;  of  these,  ten  were  cases  of  typical  achylia  gas- 
trica.  In  these  twelve  cases  proliferation  of  glands,  with  marked 
round-cell  infiltration,  was  found  once.  The  fragment  was  appar- 
ently normal  in  two  cases,  but  of  the  ten  cases  of  typical  achylia, 
granular  gastritis  and  atrophy  of  the  mucosa  could  be  established 
in  nine.  In  making  the  diagnosis  of  simple  achylia  gastrica  we 
excluded  all  those  cases  of  permanent  loss  of  secretion  evidently 
due  to  carcinoma  or  pronounced  chronic  atrophic  gastritis.  In 
fact,  before  making  these  detailed  examinations,  I supposed  it 
was  possible  that  this  form  of  achylia  existed  simply  as  a neu- 
rosis, because  all  of  the  ten  cases  which  we  described  occurred 
in  neuropathic  patients.  I had  also  inclined  to  Einhorn’s  view, 
that  some  forms  of  achylia  might  be  of  purely  nervous  origin.  We 
have  since  then  examined  a number  of  new  cases  in  addition  to 
those  reported,  making  in  all  fourteen.  In  none  was  the  mucosa 
found  perfectly  normal.  It  seems  improbable  that  a permanent 


* Since  Flint’s  publications,  cases  have  been  reported  by  Quincke,  Brabazon,  Noth- 
nagel,  Rosenheim,  and  G.  Meyer.  The  purely  American  contributions  to  this  subject 
are  very  valuable.  They  have  been  made  by  Henry  and  Osier  (“  Atrophy  of  the  Stom- 
ach, with  Clinical  Features  of  Progressive  Pernicious  Anemia,”  “ Amer.  Jour.  Med. 
Sciences,”  April,  1887) ; F.  P.  Kinnicutt  (“  Atrophy  of  the  Gastric  Tubules  : Its  Rela- 
tion to  Pernicious  Anemia,”  “Amer.  Jour.  Med.  Sciences,”  vol.  xciv,  p.  419,  1887)  ; 
Allen  Jones  (“Gastric  Anacidity,”  “New  York  Med.  Jour.,”  p.  573,  May,  1893); 
D.  D.  Stewart  (“  Amer.  Jour.  Med.  Sciences,”  Nov.,  1895) ; Einhorn  (“  Med.  Record,” 
June  11,  1892) ; also  in  Boas’  “Archives  of  Digestive  Diseases,”  vol.  1,  p.  158. 


ACHYLIA  GASTRICA  AS  A CAUSE  OF  NEURASTHENIA.  855 

cessation  of  a normal  function  could  be  caused  by  a neurasthenic 
condition.  This  explanation  of  achylia  would  be  justifiable  only 
in  case  we  could  demonstrate  that  in  this  affection  the  gastric 
mucosa  was  perfectly  normal.  To  our  knowledge,  there  is  no  case 
of  well-authenticated  achylia  on  record  in  which  a cure  or  an 
improvement  in  the  neurasthenia  was  reported  to  have  cured  or 
improved  the  secretory  defect. 

There  are,  no  doubt,  highly  nervous  patients  who  secrete  HC1 
normally,  but  under  the  influence  of  the  nervous  excitement  and 
apprehension  coincident  with  the  drawing  of  the  test-meal,  the 
gastric  secretion  is  temporarily  inhibited.  I have  seen  three  such 
cases  in  which  I could  not  detect  HC1  at  six  consecutive  analyses, 
but  a normal  secretion  was  found  in  the  vomited  matter  brought 
up  by  the  patient  at  home.  Later,  the  secretion  was  also  found 
normal  in  the  test-meals  drawn  at  my  office.  The  question  has 
also  suggested  itself,  whether  achylia  gastrica  could  not  be  the 
cause  of  the  neurasthenia.  Nor  on  this  point  are  there  any  authen- 
ticated observations.  Experience  has  taught,  however,  that  neuras- 
thenic disturbances  disappear  in  these  cases  with  an  improvement 
of  the  general  condition,  while  the  achylia  continues,  which  would 
not  be  the  case  were  the  latter  the  cause  of  the  neurasthenia.  The 
loss  of  function  in  this  disease  is  not  a relative  or  transient  one,  but 
it  is  absolute  and  permanent.  Biedert  (/.  c.f  p.  173)  gives  it  as  his 
opinion  that  the  persistent  loss  of  HC1  and  ferments  gives  the  im- 
pression of  a lasting  defect,  not  of  a variable  increasing  or  decreas- 
ing inhibition.  The  absence  of  the  gastric  secretion  is  the  same, 
whether  the  patients  are  very  much  run  down  and  emaciated  and 
subject  to  much  suffering  or  whether  they  are  in  a state  of  good 
health.  The  supposition  of  Biedert  that  there  may  be  a great 
many  who  possess  this  defect  and  are  unaware  of  it,  has  been  veri- 
fied by  a number  of  observations  among  the  students  at  my  clinic. 
While  studying  the  question  whether  the  normal  healthy  stomach 
contained  digestive  juice  in  the  fasting  condition,  we  discovered 
an  athletic,  robust  student  who  had  no  HC1  whatever  in  his  stom- 
ach, whether  fasting  or  after  meals.  The  total  acidity,  taken  after 
test-meals  on  six  different  occasions,  varied  between  one  and 
four;  as  these  analyses  were  made  shortly  before  the  examinations 
for  the  degree  of  M.D.,  we  did  not  inform  the  candidate  of  the 
physiological  defect  in  his  stomach,  fearing  that  it  might  cause 
him  some  mental  annoyance,  and  for  all  that  we  know  he  may 
still  be  unaware  of  his  achylia  and  continue  in  vigorous  health. 


856 


ACHYLIA  GASTRICA. 


My  results  concerning  the  condition  of  the  gastric  mucous  mem- 
brane are  in  accordance  with  those  of  Cohnheim  (/.  c.),  Einhorn 
(“  N.  Y.  Med.  Record,”  June  27,  1896),  Hayem  (“  Allgem.  Wiener 
med.  Zeitung,”  1894,  Nr.  2-17),  and  have  recently  been  supported 
by  Martius  and  Lubarsch  (“  Achylia  Gastrica,”  pp.  1 12-170),  and 
H.  Strauss  (“  Virchow’s  Archiv,”  Bd.  cliv).  The  results  of  the 
very  exact  investigations  of  these  last  authors  make  it  probable 
that  a more  or  less  pronounced  granular  gastritis  exists  in  the 
majority  of  cases  of  achylia. 

The  anatomical  changes,  however,  are  not,  in  all  cases,  suffi- 
ciently advanced  to  explain  the  permanent  loss  of  function. 
There  is  no  indication  at  present  for  determining  whether  glandular 
gastritis  is  the  cause  or  result  of  achylia.  It  is  self-evident  that  a 
weak  gastric  parenchyma  should  be  less  resistant  to  exterior  detri- 
mental influences — such  as  bacterial  invasion— than  a robust  gas- 
tric tissue.  The  secretion  of  HC1  being  the  normal  disinfectant, 
though  not  an  absolute  antiseptic,  it  largely  protects  the  mucosa 
from  infection. 

It  is  evident  from  what  has  been  said  in  the  etiology  of  the 
various  diseases  of  the  stomach  that  the  organ  is  exposed  to  many 
external  aggressions  of  a thermic,  chemical,  mechanical,  and  bac- 
terial nature,  and  it  is  a matter  of  astonishment  what  intense  mal- 
treatment a healthy  stomach  will  endure  without  reacting  patho- 
logically. It  is,  therefore,  conceivable  that  the  anatomical  loss  of 
the  glandular  apparatus  will  render  those  individuals  afflicted  with 
primary  simple  achylia  more  susceptible  to  bacterial  invasion. 
Most  observers  agree  that  the  increased  vulnerability  of  the  mucosa 
goes  hand  in  hand  with  the  loss  of  secretion ; this  lessens  the 
power  of  resistance,  and  eventually  induces  a state  of  chronic 
granular  gastritis,  effected  by  causes  which  a healthy  stomach 
would  resist  without  any  change. 

Symptoms. — The  disturbances  of  function  may  long  remain 
latent.  Persons  with  achylia  may  for  many  years  have  no  subjec- 
tive or  objective  disturbances  of  any  kind  ; but  sooner  or  later  dys- 
peptic complaints  arise.  The  subjective  sensations  are  not  charac- 
teristic, but  are  essentially  those  of  nervous  dyspepsia,  accompanied 
by  eructation,  fullness,  and  pressure  after  eating,  gradually  leading 
to  attacks  of  severe  gastralgia.  The  symptomatology,  as  based 
upon  the  complaints  of  the  patient,  is  most  accentuated  in  neuras- 
thenics. In  persons  with  a perfectly  sound  nervous  system  achylia 
may  exist,  and  the  individual  may  be  unaware  of  it ; this  is  proved 


SYMPTOMS  OF  ACHYLIA  GASTRICA. 


857 


by  the  case  of  the  medical  student  reported  in  the  preceding. 
Oppler  (“Deutsche  med.  Wochenschr.,”  1896,  Nr.  32,  S.  5 1 1 ) has 
reported  a number  of  cases  which  make  it  probable  that  loss  of  gas- 
tric secretion  predisposes  to  diarrhea  and  intestinal  catarrhs,  which 
are  not  benefited  until  the  achylia  is  discovered,  when  rational  treat- 
ment effects  improvement.  The  personal  description  which  Pro- 
fessor Biedert  (/.  c.)  gives  of  his  own  case  is  a weighty  argument 
pointing  to  the  fact  that  achylic  patients  are  very  much  predisposed 
to  diarrhea.  Among  the  achylic  patients  which  I have  studied 
(fourteen  in  all),  I observed  attacks  of  diarrhea  in  five.  So  far  as  I 
could  determine,  the  colon  and  the  duodenum  were  in  normal  con- 
dition. I also  studied  the  state  of  the  duodenum  by  my  method  of 
duodenal  intubation,  showing  the  pancreatic  and  hepatic  secretions 
to  be  normal.  This  makes  it  probable  that  these  diarrheas  are  pos- 
sibly not  due  to  an  extension  of  the  anatomical  changes  in  the 
stomach  to  the  intestine,  but  to  fermentative  processes,  developed 
in  the  absence  of  HC1  secretion.  These  diarrheas  confirm  Bunge’s 
view  that  at  least  one  effect  of  the  HC1  secretion  is  that  of  a par- 
tial antiseptic. 

Martius’  conclusions  (/.  c.}  p.  101)  are  the  following:  Achylia 
gastrica  is  due  to  two  conditions  : (1)  a primary  secretory  de- 

bility of  the  stomach,  constituting  simple  achylia  gastrica;  (2) 
atrophy  of  the  gastric  mucosa  (anadenia),  which  is  secondary 
achylia  gastrica.  The  primary  achylia  gastrica  is  either  congenital 
or  developed  on  the  basis  of  a very  early  predisposition.  It  is 
associated  with  inherited  debility  of  the  nervous  system,  and  pre- 
vails among  so-called  neuropathic  patients. 

Primary  secretory  debility  of  the  stomach  is  an  individual 
peculiarity,  which  may  remain  latent  for  years,  and  without  demon- 
strable detriment  to  the  general  organism.  This  is  particularly 
the  case  when  the  motor  function  is  well  preserved,  and  the  motor, 
secretory,  and  resorptive  functions  of  the  intestine  continue 
normal. 

The  mucosa,  which  is  devoid  of  secretion,  exhibits  a diminished 
vital  resistance  to  all  external  detrimental  influences.  This  explains 
the  fact  that  anatomical  alterations  of  varying  intensity  are  rarely 
absent  in  simple  achylia  gastrica.  The  structural  changes  bear  no 
proportionate  relation  to  the  absolute  gravity  of  the  loss  of 
function. 

It  is,  therefore,  probable  that  there  are  forms  of  so-called  atrophy 
of  the  gastric  mucosa  (the  primary  noncarcinomatous  anadenia) 


858 


ACHYLIA  GASTRICA. 


which  develop  preferably  on  the  basis  of  this  congenital  secretory 
weakness  of  the  stomach. 

Accordingly,  there  are  gradual  transitions,  clinically  and  ana- 
tomically, from  congenital  simple  achylia  with  but  immaterial 
alterations  of  the  mucosa,  to  achylia  with  chronic  granular  gas- 
tritis eventuating  in  complete  atrophy  of  the  secretory  mucosa. 

The  grave  results  for  the  total  organism  (progressive  anemia, 
malnutrition,  etc.)  which  have  been  ascribed  to  the  latter  type  do 
not  in  reality  develop  until  the  mucous  membrane  of  the  intestine 
is  extensively  involved  by  the  atrophy. 

Pathological  Histology.— The  investigations  made  by  the 
authors  quoted  in  the  literature  at  the  end  of  this  chapter  show  in 
general  a marked  increase  in  the  interstitial  connective  tissue.  The 
surface  epithelium  contains  many  goblet  cells.  The  vestibules  to 
the  glandular  alveoli  are  very  tortuous,  and  so  dilated  that  they 
resemble  minute  cysts,  filled  with  homogeneous,  slightly  granular 
masses,  that  stain  with  acid  anilin.  The  epithelial  cells  lining  the 
vestibules  present  marked  variations  in  structure  and  staining 
qualities.  Those  most  prominent  are:  (i)  Ordinary,  long,  cylin- 
drical, epithelial  cells.  (2)  Somewhat  shorter,  cylindrical  cells  with 
dark  protoplasm  and  dark-staining  nucleus,  the  upper  end  of  which 
has  disappeared.  (3)  Goblet  cells.  (4)  Cells  as  in  type  2,  but  with 
a very  dark  protoplasm  (Stohr  cells).  (5)  Cells  with  a marked 
fuchsinophilic  granulation.  In  some  vestibules  only  cells  answer- 
ing to  the  description  of  type  2 are  found,  and  in  them  an  abund- 
ance of  mitotic  figures.  In  other  vestibules  we  find  goblet  cells 
in  addition  to  these.  There  are  very  few  vestibules  which  contain 
normal  surface  epithelium. 

Among  the  other  characteristics  that  were  found  in  freshly  hard- 
ened stomachs  of  achylic  patients  are  : (1)  Immigration  and  per- 
meation of  leukocytes.  (2)  The  occurrence  of  mitoses  in  the 
surface  epithelium  and  in  that  lining  the  vestibular  alveoli.  The 
author’s  cases  were  especially  examined  with  regard  to  atypical  or 
pathological  mitoses,  but  the  results  were  negative.  (3)  Occurrence 
of  acidophilic  leukocytes.  (4)  Frequency  of  goblet  cells.  (5) 
Occurrence  of  so-called  Stohr’s  and  Nussbaum’s  cells.  (6)  Occur- 
rence of  hyaline  spheres. 

Referring  to  No.  1 of  the  above  observations,  it  should  be  stated 
that  Sachs  (“  Zur  Kenntniss  d.  Magendriisen  b.  krankhaften 
Zustanden,”  Breslau,  1886)  has  found  an  abundance  of  lymph-cells 
migrating  through  the  surface  epithelium  and  glandular  substance. 


HISTOLOGICAL  CHANGES  IN  ACHYLIA  GASTRICA. 

The  pyloric  region  seems  to  be  more  invaded  than  any  other  part 
of  the  stomach.  Stintzing  considers  the  immigration  ofleukocytes 
in  the  normal  stomach  a very  rare  occurrence.  Permeation  of  the 
gastric  mucosa  with  leukocytes  at  the  height  of  digestion  is  a 
normal  occurrence,  and  has  been  frequently  observed  in  animals. 
The  difference  in  the  achylic  stomach,  with  regard  to  the  permea- 
tion of  leukocytes,  is  simply  one  of  degree.  Lubarsch  found  that 
the  glandular  lumina  were  actually  packed  full  with  acidophilic 
leukocytes;  this  property  has  not  been  found  in  the  leukocytes  of 
the  normal  stomach.  It  is  probable  that  the  invasion  of  the  mucosa 
with  acidophilic  leukocytes  to  such  a degree  as  Lubarsch  describes 
is  pathological. 

Concerning  No.  2,  the  presence  of  mitoses  in  the  epithelia  of  the 
normal  stomach  is  denied  by  Sachs  (/.  c .)  and  Oppel  (“  Lehrbuch 
der  vergleich.  mikroskop.  Anatomie  d.  Wirbelthiere,”  Bd.  i : 
“ Magen”),  and  the  occurrence  of  karyokinetic  figures  in  the  chief 
and  border  cells  is  extremely  rare.  For  a closer  study  of  the  char- 
acter and  significance  of  the  mitotic  processes  I refer  to  my  article 
(Hemmeter,  “ Histological  Studies  Relating  to  the  Early  Diagno- 
sis of  Cancer  of  the  Stomach,”  “ Phila.  Med.  Journ.,”  Feb.,  1900). 
The  hyaline  spheres  which  Lubarsch  describes  are  composed  of  cell 
granules  that  have  become  confluent  and  enlarged,  but  are  still 
contained  within  the  body  of  the  original  cell.  These  hyaline 
spheres  are  considered  pathognomonic  for  atrophic  processes  in 
the  gastric  mucosa. 

The  histological  changes  found  by  various  authors  in  achylia, 
and  which  we  have  been  enabled  to  confirm  in  cases  which  we 
had  opportunity  to  examine  at  autopsies  shortly  after  death,  in- 
dicate the  proliferation  of  the  interstitial  connective  tissue,  the 
occurrence  of  acidophilic  migrating  cells;  and,  in  addition,  the 
disappearance  of  the  specific  glandular  elements  and  cell  prolifera- 
tion, emanating  from  the  vestibules  of  the  glands;  also  trans- 
formation of  the  gastric  mucosa  into  intestinal  mucosa.  The  pro- 
cess eventuates  in  complete  atrophy  of  the  mucosa.  Einhorn 
has  reported  a case  of  achylia  in  which  a bit  of  gastric  mucosa 
was  found  in  the  wash-water,  which  under  the  microscope  appeared 
normal.  We  obtained  normal  mucosa  from  two  cases  of  achylia, 
when  strips  were  cut  from  achylic  stomachs  running  from  the 
esophagus  along  the  greater  curvature  to  the  duodenum ; on 
serial  sections  made  at  intervals  of  one  inch  apart,  small  areas 
of  microscopically  normal  mucosa  were  found,  particularly  near 


86o 


ACHYLIA  GASTRICA. 


the  cardia,  while  most  other  portions  of  the  stomach  showed  distinct 
atrophic  changes,  with  profuse  immigration  of  leukocytes,  and 
proliferation  of  the  interstitial  connective  tissues.  A small  bit  of 
mucosa  accidentally  found  in  the  wash-water  does  not  indicate  the 
state  of  the  entire  stomach.  When  such  normal  fragments  are 
found  in  achylia,  it  is  still  probable  that  other  portions  of  the 
stomach  may  be  diseased,  and  what  may  be  a normal  condition 
in  a fragment  from  the  fundus  *or  pyloric  region,  will  be  pathological 
for  the  intermediate  zone  (Martius  and  Lubarsch,  /.  c.;  also  Hem- 
meter,  /.  c .).  We  do  not,  therefore,  consider  the  evidence  satis- 
factory that  achylia  may  exist  with  a perfectly  normal  gastric 
histology. 

In  the  great  majority  of  cases  of  achylia,  a progressive  atrophic 
gastritis  may  be  found  to  exist.  There  may  be  periods  in  the 
history  of  achylia  when  this  condition  exists  without  any  apparent 
alteration  in  the  gastric  mucous  membrane,  and  the  fact  that  most 
patients  do  not  consult  the  physician  until  the  process  has  devel- 
oped to  a very  advanced  state  may  explain  the  observation  that  the 
occurrence  of  achylia  with  perfectly  normal  stomachs  is  thus  far 
supported  by  very  few  reliable  microscopic  examinations  of  gastric 
tissue  fragments.  All  achylic  patients  give  a history  of  years  of 
gastric  disturbances  when  they  first  present  themselves  for  treat- 
ment, the  anamnesis  thus  making  it  probable  that  the  gastric 
changes  must  have  progressed  very  far.  In  the  case  of  the  healthy 
medical  student  in  whom  we  found  achylia  on  six  different  exami- 
nations, we  did  not  succeed  in  obtaining  a piece  of  the  gastric 
mucosa.  In  these  cases  frequent  examinations  for  fragments  of 
mucosa  are  necessary  to  decide  the  relation  between  the  histological 
alteration  and  the  clinical  history.  These  examinations  should  be 
made  at  frequent  and  regular  intervals,  and  in  case  of  autopsies  on 
achylic  patients  the  stomach  should  be  previously  preserved  by 
pouring  in  alcohol  or  Zenker’s  fluid  within  a half  hour  after  death, 
so  as  to  prevent  autodigestion.  What  relation  exists  between  the 
atrophic  process  of  the  intestines  and  that  of  the  stomach  is  un- 
known. It  may  be  a direct  continuation  of  the  progressive  gastri- 
tis, since  it  is  very  probable  that  the  same  detrimental  agencies 
that  cause  the  disease  of  the  stomach  give  rise  to  the  intestinal 
atrophy.  One  might  assume  also  that  excessive  demands  are  made 
upon  the  digestive  power  of  the  intestines  in  the  absence  of  the 
preparatory  digestive  function  of  the  stomach.  Again,  it  is  probable 
that  bacterial  fermentations  occur  to  a much  greater  degree  when 


ETIOLOGY  OF  ACHYLIA  GASTKICA. 


86 1 

the  disinfecting  power  of  the  HC1  is  lost.  In  two  autopsies  on  sub- 
jects who  had  shown  the  symptoms  of  achylia,  the  author  observed 
that  the  coeliac  axis,  and  all  branches  arising  from  it,  were  of  un- 
usually small  size.  The  gastric  arteries  were  smaller  than  those 
of  normal  stomachs.  The  intestinal  and  mesenteric  arteries  were 
also  smaller  in  diameter  than  normal.  The  dimensions  of  the 
hepatic  and  splenic  arteries  were  smaller.  The  arteries  of  the 
heart,  spleen,  kidney,  and  liver  appeared  normal  in  size.  On  in- 
jecting the  arteries  of  the  stomach  from  the  celiac  axis,  the  diminu- 
tive caliber  of  the  arteries  was  evident  even  without  micrometric 
measurements.  There  was  in  this  case  no  atrophic  gastritis. 

Etiology. — Aside  from  the  probability  that  achylia  may  be 
either  congenital  or  developed  upon  a neuropathic  basis,  not  much 
is  known  of  the  causation  of  the  progressive  atrophic  gastritis. 
It  has  been  supposed  that  bacterial  infection  is  an  etiological 
factor  in  bringing  about  this  state  of  the  mucosa.  We  may  con- 
ceive the  bacterial  invasion  to  have  occurred  in  a similar  manner 
to  that  pictured  under  the  head  of  ulcus  carcinomatosum.  In  one 
of  our  drawings  the  presence  of  bacilli  is  represented  beneath 
the  floor  of  the  ulcer,  some  of  them  located  in  the  muscularis. 
(Plate  VIII  and  Fig.  38,  p.  532.)  It  is  not  known  whether  this  bac- 
terial invasion  is  a cause  or  result  of  these  processes.  Syphilis 
and  tuberculosis  may  be  predisposing  factors. 


Example  of  Clinical  History. — Mr.  L.  W.,  thirty-two  years  old,  reporter  on 
a daily  newspaper.  Up  to  1894  he  was  physically  well  and  in  good  health, 
although  he  admits  to  have  frequently  abused  his  stomach  by  overeating  and 
overdrinking.  His  mother  is  a highly  neurasthenic  woman,  who  imagines  she 
is  afflicted  with  all  sorts  of  ailments;  father,  high-strung  and  arbitrary.  His 
duties  necessitate  that  he  should  be  awake  during  the  night  and  sleep  during 
the  day.  As  a consequence  of  this,  he  is  compelled  to  take  his  meals  at  very 
irregular  hours.  He  frequently  does  not  obtain  sufficient  sleep,  being  awak- 
ened by  noises  in  the  street  (trolley  cars,  etc.)  and  about  the  house  in  which  he 
lives.  He  usually  gets  to  bed  about  five  o’clock  in  the  morning,  and,  if  his 
nerves  are  quiet,  sleeps  until  eleven  or  twelve  ; then,  arising,  he  takes  his  break- 
fast. His  main  meal  is  taken  between  five  and  six  o’clock  in  the  afternoon. 
At  seven  o’clock  he  must  report  for  duty  as  night  clerk  or  reporter  of  the  Asso- 
ciated Press.  The  work  he  has  to  perform  is  frequently  of  an  exciting  and 
enervating  character.  During  the  summer  of  1894,  while  it  was  very  hot,  he  had 
indulged  in  very  cold  beer  during  the  night  while  following  up  some  sporting 
occasion,  and  since  then  has  suffered  from  dyspepsia,  nausea,  eructation,  etc. 
Sometimes,  after  a meal,  he  will  be  attacked  with  palpitation  of  the  heart  and 
a feeling  of  giddiness,  which  has  recently  been  associated  with  sensations  of 
precordial  fear.  His  appetite  in  the  summer  of  1895  was  very  poor  ; the  food 


862 


ACHYLIA  GASTRICA. 


was  described  as  weighing  down  his  stomach  like  a lump  of  lead.  Heart  pal- 
pitation so  strong  that  he  can  not  sleep  because  of  the  noise  his  heart  makes. 
In  one  month  of  the  summer  of  1895  he  lost  eleven  pounds. 

Analysis  of  Test-meal. — The  first  test-meal  had  disappeared  from  the 
stomach  entirely  fifty-five  minutes  after  it  had  been  eaten.  The  second  test- 
meal  was  drawn  fifty  minutes  after  it  had  been  taken  ; the  amount  was  about 
three  ounces,  and  it  consisted  of  chewed  particles  of  wheat  bread  entirely  un- 
changed. Total  acidity  = 5 ; free  HC1  = negative  ; combined  HC1,  negative  ; 
lactic  acid,  trace ; propeptone  and  peptone,  absent.  On  test  by  milk  digestion, 
rennin  and  rennin-zymogen,  absent ; pepsinogen,  absent;  very  slight  quantity 
of  mucus ; very  slight  amount  of  filtrate  gained  by  pressing  the  drawn  ingesta 
through  a sieve.  Test  of  motor  function,  by  the  Hemmeter  method,  shows  a 
rather  increased  peristalsis. 

Absorption  (Penzoldt  and  Faber’s  method)  is  abnormally  delayed.  Exam- 
ination of  a fragment  of  mucosa  shows  irregular  dilations  of  the  peptic  gland- 
ducts  ; there  is  some  increase  of  the  interglandular  connective  tissue,  which 
is  infiltrated  with  tremendous  numbers  of  leukocytes,  which  have  also  per- 
vaded the  epithelial  cells  of  the  vestibules.  Here  and  there  the  entire  lumen 
of  the  gland-duct  is  packed  full,  and  apparently  pushed  apart  with  an  enormous 
invasion  of  lymphoid  cells.  The  characteristic,  spindle-shaped,  connective- 
tissue  cells  are  present,  but  unless  carefully  sought  for,  they  escape  detection, 
on  account  of  a copious  round-cell  infiltration,  and  of  the  invasion  of  leuko- 
cytes, to  which  reference  has  been  made.  Many  eosinophilic  cells  present.  In 
the  epithelia,  cells  with  numerous  chromosomes  and  others  containing  more 
than  one  nucleus.  The  nuclei  in  these  cells  are  in  various  stages  of  indirect 
division,  showing  typical  mitotic  figures. 

Anatomical  diagnosis,  chronic  granular  gastritis.  This  patient  improved 
very  much  after  a vacation  of  six  weeks  in  the  summer,  which  brought  him  the 
necessary  sleep  at  night  and  rest.  Remedies  to  restore  HC1  secretion  have  been 
tried  persistently  for  one  year  and  six  months  without  effect.  He  repeatedly 
suffered  in  the  hot  season  of  the  year  from  attacks  of  diarrhea,  which  were 
easily  controlled  by  administering  HC1  and  subnitrate  of  bismuth,  together 
with  a proper  diet.  The  patient  has  relapses  whenever  he  indulges  in  over- 
work, with  loss  of  sleep.  Since  1895,  twenty-three  test-meal  analyses  have 
been  made,  not  one  showing  a trace  of  HC1  or  ferments. 

Treatment. — At  my  clinic  we  are  in  the  habit  of  prescribing 
dilute  HCl  for  all  these  cases  whenever  the  acid  agrees  well.  As 
considerable  HCl  is  needed  to  effect  any  appreciable  digestive 
action  and  to  exert  a disinfecting  influence,  we  give  twenty  drops  of 
the  official  dilute  HCl  every  half-hour  after  meals  until  sixty  drops 
have  been  taken.  The  acid  must  be  largely  diluted  and  taken  in  a 
double  gelatin  (Aaron)  capsule  or  through  a glass  tube.  Our 
experience,  which  is  based  upon  a large  number  of  cases  of  this 
sort,  has  convinced  us  that  the  acid  is  not  only  well  tolerated, 
but  is  almost  indispensable  to  the  patient.  Although  it  may  be 
argued  that  achylic  patients  sometimes  get  along  without  any 


DIET  IN  ACHYLIA  GASTKICA. 


863 


treatment  whatever,  simply  because  they  exhibit  no  symptoms, 
nevertheless  when  they  do  apply  for  treatment  they  generally 
present  a complexity  of  symptoms,  which  are  much  benefited  by 
carefully  selected  but  nutritious  diet,  sometimes  rest  in  bed,  strych- 
nin, and  HC1.  When  the  appetite  is  absolutely  lost,  it  may  be 
restored  by  washing  out  the  stomach  with  bitter  tonics,  such 
as  gentian  and  quassia.  In  neurasthenic  patients,  strychnin  sul- 
phate improves  not  only  the  local  gastric  symptoms,  but  also 
the  symptoms  of  the  general  neurasthenia.  A number  of  gastric 
patients  of  this  kind  refuse  to  eat,  because  they  fear  that  distress 
will  be  caused  by  the  food.  In  such  cases  it  may  become  neces- 
sary to  place  the  patient  in  a well-managed  institution  for  the 
dietetic  treatment  of  digestive  diseases.  They  must  gradually  be 
convinced  that  food  that  is  ingested  with  appetite  can  do  no  harm. 
When  the  motility  is  interfered  with  and  symptoms  of  dilation  are 
manifest,  gastric  lavage  is  indispensable.  Concerning  the  use  of 
pepsin  and  pancreatin  see  pages  344  and  345. 

Diet. — The  achylic  patient  is  an  individual  who  has  an  internal 
infirmity,  due  either  to  a congenital  defect,  or  to  an  acquired  abnor- 
mality in  the  gastric  structure.  Whatever  may  be  the  condition 
and  the  cause,  we  are  dealing  with  individuals  who  are  essentially 
weak  and  debilitated.  We  have  found  it  expedient  not  to  be  too 
exacting  with  diet  orders.  In  fact,  we  make  it  a rule  never  to  give 
a standing  diet  order  to  an  achylic  patient  without  carefully  inquir- 
ing as  to  the  food  which  he  knows  from  experience  agrees  best 
with  him.  The  stomach  is  a protective  and  selective  organ,  pre- 
paring the  food  for  the  intestines.  By  its  selective  property,  when 
the  motility  is  in  a normal  condition,  it  permits  only  the  semisolid 
and  liquid  masses  to  pass  first,  while  the  more  consistent  masses 
are  retained,  to  be  further  softened  and  disintegrated.  We  have 
shown,  in  the  preceding  pages,  that  the  stomach  of  the  achylic 
patient  has  lost  the  power  to  dilute  its  contents  by  a secretion  from 
its  walls.  This  is  one  of  the  main  reasons  why  we  permit  the  in- 
gestion of  liquids  during  meals,  and  of  largely  diluted  HC1  after 
meals.  For  the  same  reason  all  foods  should  be  well  chewed,  or 
preferably  finely  divided  during  the  process  of  cooking,  for  the 
main  object  of  all  treatment  must  be  to  preserve  the  peristalsis , 
and  to  insure  a healthy  state  of  the  mucosa.  Therefore,  the  food 
should  generally  be  taken  in  the  form  of  gruels,  pastes,  or  in  any 
semisolid,  easily  swallowed  state.  The  meat  should  be  very  soft, 
scraped,  or  run  through  the  meat-grinder.  Fish,  sweetbread, 


864 


NERVOUS  DYSPEPSIA. 


calf’s  brain,  and  soft-boiled  eggs  are,  as  a rule,  of  such  soft  con- 
sistency that  they  need  no  further  preparation.  Our  experience  is 
that  the  more  food  is  ingested  and  well  tolerated,  the  better  for  the 
patient  in  these  cases.  We  will  give  no  outline  here  of  detailed 
diet  list,  but  refer  the  reader  to  the  diet  order  for  anacidity  and 
Penzoldt  graded  diet  order  given  in  the  chapter  on  Dietetics.  In 
many  cases  physical  and  mental  rest,  hygienic  surroundings,  and  a 
nourishing  diet  will  be  all  that  are  needed  for  insuring  comparative 
well-being  of  the  patients.  Where  the  motor  power  becomes  de- 
fective, the  treatment  will  be  that  outlined  in  the  chapter  on  Motor 
Insufficiency. 

A remedy  little  known,  but  a very  valuable  adjuvant  in  treat- 
ment for  lack  of  dietetic  ferment,  is  the  juice  of  fresh  pineapple. 
This  has  decided  proteolytic  power,  and,  besides,  is  a pleasant, 
easily  procured  remedy.  The  ferment  is  only  active  in  the  fresh 
fruit,  and  is  destroyed  in  the  preserved  pineapple.  The  name 
“ Bromelin  ” has  been  given  to  the  ferment  by  Chittenden  (“  Journ. 
Physiol.,”  xv,  1894). 

There  is  no  treatment  that  is  universally  applicable  to  all  cases 
of  achylia.  The  ability  of  the  practitioner  in  discerning  the  special 
indications  for  each  individual  case  is  put  to  the  test  severely  in 
the  therapeutic  management  of  this  disease.  Sometimes  the  treat- 
ment will  be  that  of  chronic  gastritis,  sometimes  that  of  nervous 
dyspepsia.  Excessive  strictness  in  dietetic  regulation  has,  in  the 
author’s  opinion,  occasionally  developed  gastric  “ hypochondriacs.” 
It  is  more  advisable  to  train  up,  or,  as  Broadbent  says,  “ level  up,” 
the  gastric  digestion  to  a higher  plane.  We  make  it  a rule  to  show 
these  gastrophobic  patients  the  contents  of  their  stomach  at  a 
proper  time  after  full  meals,  to  convince  them  that  they  can  digest 
thoroughly,  for,  as  a rule,  every  vestige  of  food  will  have  passed 
out  of  the  organ  within  one  and  one-half  hours. 

The  literature  on  achylia  gastrica  will  be  found  compiled  in  the 
article  by  Martius  and  Lubarsch,  published  by  Franz  Deuticke, 
Leipzig,  1897. 


DEFINITION  OF  NERVOUS  DYSPEPSIA. 


865 


CHAPTER  XIV. 

NERVOUS  DYSPEPSIA  (Leube).— NEURASTHENIA 
GASTRICA  (Ewald). 

The  original  definition  which  Leube  gave  of  this  affection  char- 
acterized it  as  a neurosis  of  sensibility,  without  any  well-defined 
and  constant  objective  disturbances  of  digestion,  but  exhibiting  a 
large  variety  of  subjective  symptoms  connected  with  the  digestive 
act  and  occurring  independently  of  any  demonstrable  changes  in 
the  stomach. 

In  his  first  paper  Leube  (“  Ueber  nervose  Dyspepsie,”  “ Deutsch. 
Arch.  f.  klin.  Med.,”  Bd.  xxm,  1879)  emphasized  that  the  gastric 
digestion  may  be  perfectly  normal  so  far  as  the  chemistry  and 
motility  are  concerned,  and  that  he  has  used  the  term  “ dyspepsia,” 
or  difficult  digestion,  because  this  act  is  accompanied  by  manifold 
complaints  that  are  traceable  to  an  abnormal  excitability  of  the 
sensory  gastric  nerves.  Since  then  Leube  has  expanded  the  con- 
ception of  nervous  dyspepsia  to  the  effect  that  it  includes  anoma- 
lies of  secretion  and  motility. 

R.  Geigel  and  Abend  (pupils  of  Leube)  later  on  demonstrated 
that  the  secretion  of  HC1  may  be  extremely  variable  in  nervous 
dyspepsia,  and  that  we  may  have  a normal  acidity,  or  euchlorhydria, 
subacidity,  anacidity  or  achylia,  or  hyperacidity.  Accordingly,  the 
important  symptoms  of  the  trouble — viz.,  the  annoying  gastric  dis- 
tress— can  not  be  traced  to  fermentations  of  the  gastric  contents 
with  sub-  or  inacidity,  nor  to  the  products  of  this  decomposition, 
nor  to  irritation  of  the  gastric  nerves  in  superacidity.  It  is  natural 
that  the  definitions  and  conceptions  of  various  authors  concerning 
a disease  that  is  so  vague  and  indefinite  in  its  clinical  history  and 
pathology  should  differ  greatly.  Leube  distinguishes  more  re- 
cently between  two  kinds  of  nervous  dyspepsia : ( a ) Nervous 
dyspeptic  symptoms  in  which  the  nervous  channels  are  sympa- 
thetically involved  by  anatomical  changes  in  the  stomach,  and 
altered  chemistry  of  digestion  caused  by  these  changes.  (/?)  Ner- 
vous dyspepsia  with  an  apparently  normal  anatomical  state  of  the 
organ.  Boas  distinguishes  a third  form  of  nervous  dyspepsia, 
which  originates  reflexly  from  other  organs  : for  instance,  the  kid- 
neys, uterus,  ovaries,  male  genito-urinary  apparatus,  and  intestine. 


866 


NERVOUS  DYSPEPSIA. 


Constitutional  diseases,  such  as  tuberculosis,  syphilis,  diabetes 
mellitus,  anemia,  uric  acid  diathesis,  may  form  the  basis  of  this 
complexity  of  symptoms.  The  disease  may  occur  in  an  idiopathic 
form,  independently  of  any  demonstrable  gastric  changes,  or  in  a 
secondary  form  consequent  upon  neurasthenia,  hysteria,  and  the 
other  pathological  states  referred  to.  Whatever  the  underlying 
basis  or  etiology  of  the  disease,  the  ultimate  symptoms  can  be  as- 
scribed  to  a functional  sensory  neurosis  and  overexcitability  of  the 
gastric  nerves,  which  may  become  so  acute  that  they  react  in  a 
pathological  manner  upon  the  influence  of  normal  digestive  stimu- 
lation. 

Pathology. — Jurgens  has  discovered  total  degeneration  of  the 
plexus  of  Meissner  and  Auerbach  in  forty-one  cases  of  nervous 
dyspepsia.  In  one  of  the  cases  in  which  the  sensory  disturbances 
were  predominant,  and  the  intestinal  functions  involved  also,  this 
author  found  a distinct  degeneration  of  the  muscularis  of  the 
stomach  and  intestine.  F urther  exact  pathological  and  histological 
investigation  will  very  probably  restrict  the  number  of  cases  at 
present  classed  under  nervous  dyspepsia.  The  > conceptions  of 
various  authors  concerning  the  nature  of  nervous  dyspepsia  vary 
considerably.  Leube,  as  is  well  known,  states  that  nervous  dys- 
pepsia is  of  central  origin,  while  Stiller  applies  the  name  to  all 
digestive  disturbances  that  are  transmitted  to  the  stomach  through 
the  central  or  the  sympathetic  nervous  system.  Stiller  attributes 
greater  importance  than  Leube  to  disturbances  of  the  secretory 
function,  which  he  could  demonstrate  in  a majority  of  his  cases. 
We  interpret  the  disease  as  a mixed  neurosis,  in  which  the  motor 
secretory  and  sensory  nerve  apparatus  are  affected  contemporane- 
ously or  alternately ; an  anatomical  substratum  is  present  in  one- 
half  of  the  cases,  but  it  is  not  of  a constant  type. 

Etiology. — Neurasthenia  gastrica  has  been  observed  after  intense 
emotional  excitement,  exhaustive  mental  work,  alcoholic  and 
sexual  excesses,  after  abuse  of  tobacco,  and  associated  with  pul- 
monary phthisis,  nephritis,  and  malaria.  The  sensibility  of  the 
normal  gastric  mucosa  is  very  slight,  and  the  digestive  irritation 
causes  no  distinct  sensation  in  the  normal  individual,  but  when  a 
healthy  person  transgresses  the  customary  amount  of  food,  unpleas- 
ant sensations  of  pressure,  distention,  fullness,  eructation,  and 
nausea  will  ensue,  indicating  that  the  organ  has  been  overloaded. 
These  sensations  cease  when  a part  of  the  chyme  has  passed  out 
into  the  intestine. 


SYMPTOMATOLOGY  OF  NEURASTHENIA  GASTKICA.  867 

Narcotic  substances,  such  as  very  strong  coffee,  tea,  or  tobacco, 
may  relieve  or  remove  these  symptoms,  showing  that  they  are  of 
a purely  nervous  character.  If  the  excitability  of  the  sensory 
nerves  is  for  any  reason  increased,  then  the  normal  digestive  irrita- 
tion brings  about  such  gastric  difficulty.  It  is  characteristic  of 
nervous  dyspepsia  that  gastric  distress  is  perceived  only  after  meals, 
and  is  absent  when  the  stomach  is  empty.  With  an  intensely  excit- 
able nervous  apparatus  in  the  stomach,  such  symptoms  as  we  have 
described  may,  in  exceptional  cases,  come  on  even  when  the  organ 
is  empty.  The  nervous  dyspepsia  associated  with  malaria  should 
induce  the  physician  to  examine  the  blood  of  the  patient  for  the 
malarial  parasite.  The  symptoms  in  these  cases  generally  abate 
under  the  influence  of  quinin. 

As  a secondary  neurosis,  neurasthenia  gastrica  is  generally  the 
result  of  general  neurasthenia  or  hysteria.  Grave  anatomical  alter- 
ations of  the  brain  and  spinal  cord,  which  frequently  bring  on  other 
gastric  neuroses,  are,  so  far  as  we  know,  not  reported  to  have  any 
causal  relation  to  nervous  dyspepsia. 

Reflexly,  the  disease  may  result  from  irritation  arising  from  the 
genito-urinary  organs  in  both  sexes,  from  menstrual  and  puerperal 
disturbances.  The  dyspepsia  during  the  puerperal  period  has  been 
attributed  to  traction  or  compression  of  the  sympathetic.  In  a 
portion  of  the  cases  it  is  impossible  to  attribute  any  cause.  It  is  a 
disease  which  prevails  among  the  male  sex. 

Symptomatology. — The  clinical  picture  of  neurasthenia  gas- 
trica is  extremely  variable.  It  is,  therefore,  impossible  to  give  a 
well-defined,  typical  representation  of  the  disease  that  can  be 
applicable  to  the  majority  of  the  cases.  We  will,  therefore,  simply 
designate  the  most  important  and  frequent  symptoms.  It  is  char- 
acteristic of  nervous  dyspepsia  that  the  gastric  distress  is  directly 
dependent  upon  the  ingestion  of  food — that  it  occurs  as  a rule 
only  after  meals,  and  not  on  an  empty  stomach. 

Furthermore,  it  is  characteristic  that  the  quality  and  the  quantity 
of  the  food  and  dietetic  errors  exert  no  influence  upon  dyspepsia. 
At  times  the  most  indigestible  food  causes  no  difficulty  whatever, 
and  at  other  times  the  most  digestible  food  brings  on  distress. 
The  sensations  of  the  patient  are  very  much  under  the  influence 
of  the  emotional  state.  The  dyspeptic  symptoms  are  : Unpleasant 
sensations,  pressure,  fullness,  distention  of  the  stomach,  occurring 
shortly  after  meals.  After  the  patients  have  slept  well,  they  are  in 
a cheerful  state  of  mind  in  the  morning,  but  immediately  after 


868 


NERVOUS  DYSPEPSIA. 


breakfast  they  are  tormented  by  manifold  sensations  in  the  stomach. 
The  suffering  is  most  severe  when  the  neurasthenia  gastrica  is  ac- 
companied by  hyperacidity.  In  this  case  it  increases  during  the 
second  period  of  digestion,  as  the  acidity  becomes  greater.  Such 
types  are  relieved  by  the  administration  of  alkalies,  which,  how- 
ever, are  useless  with  achylia.  The  epigastric  region  is  not  very 
sensitive,  nor  are  there  any  characteristic  pain-points,  so  far  as  we 
could  determine. 

Leven  (“  Estomac  et  Carvau,”  Paris,  1884)  attributes  great  im- 
portance to  the  appearance  of  these  so-called  painful  spots,  which 
are  supposed  to  be  due  to  an  irritation  of  the  solar  plexus.  Burk- 
hart (“Pathol,  der  Neurasthenia  Gastrica,”  Bonn,  1882),  Fleischer, 
Ewald,  Bouveret,  and  Richter  do  not  attribute  much  importance 
to  this  symptom.  In  some  cases  very  peculiar  sensations  are  de- 
scribed by  these  patients.  Some  have  a crawling  feeling  in  the 
stomach,  as  if  some  live  animal  were  moving  about  in  it.  Some 
have  a sensation  of  tickling,  others  describe  it  as  a beating,  burn- 
ing, or  sticking  sensation.  A most  unusual  sensation  is  that  de- 
scribed as  a restless,  wavy,  or  undulating  motion.  Persistent 
eructation  is  a very  frequent  and  annoying  symptom.  The  eruc- 
tations occur  in  an  explosive  manner,  and  without  any  regard  for 
the  surroundings.  If  there  is  hyperacidity,  these  eructations  are 
accompanied  by  severe  pyrosis.  Emesis  is  rare,  but  when  it  does 
occur,  the  character  and  consistency  of  the  vomit  depend  upon 
the  composition  of  the  gastric  juice.  With  normal  acidity  or  hyper- 
acidity it  has  a very  sour  taste  and  is  void  of  proteid  food  when 
the  acid  is  present  in  excess.  With  subacidity  or  inaeidity  it  con- 
tains much  undigested  meat  and  eggs  and  but  little  carbohydrate 
food.  Although  inacidity  may  be  present,  the  gastric  contents  do 
not  decompose,  because  there  is  no  stagnation.  The  appetite  is 
variable.  There  may  be  a normal  appetite,  bulimia,  or  anorexia. 
As  a rule,  thirst  is  increased.  The  behavior  of  the  sensory  gastric 
nerves  is  capricious.  When  the  patient  is  in  a cheerful,  pleasant 
humor,  or  occupied  with  a congenial,  interesting  piece  of  work,  he 
will  digest  articles  of  diet  which  will  cause  very  great  distress 
when  he  is  emotionally  depressed  or  otherwise  indisposed.  Exces- 
sive mental  or  bodily  work,  cares  and  worries  concerning  the 
vocation,  disappointments  in  business  enterprises,  grief,  etc.,  all 
cause  a condition  of  excitability  in  which  digestion  is  much 
impaired. 

Secretory  Function. — In  neurasthenia  gastrica  there  may  be  a 


DIAGNOSIS  OF  NEURASTHENIA  GASTKICA.  869 

normal  secretion,  hyperacidity,  or  inacidity.  When  inacidity  exists, 
the  ferments  can  still  be  demonstrated  in  the  gastric  contents. 
This  important  fact  will  serve  to  distinguish  this  type  of  nervous 
dyspepsia  from  typical  achylia  gastrica. 

Motor  Function. — The  peristalsis  of  the  stomach  is  in  most 
cases  undisturbed  in  neurasthenia  gastrica,  but  there  are  cases  in 
which  temporary  motor  insufficiency  occurs. 

Intestinal  Disturbances. — The  most  constant  symptom  is  obstinate 
constipation.  Very  frequently  there  are  rumbling  noises  in  the 
intestines  and  extensive  flatulence. 

Nervous  Symptoms. — These  consist  of  pain  and  pressure  in  the 
head,  giddiness,  tinnitus  aurium,  flashes  before  the  eyes,  rapid 
pulse,  exhaustion,  cool  extremities,  attacks  of  fainting,  palpitations 
of  the  heart,  dyspnea.  It  is  very  probable  that  all  these  symptoms 
are  connected  with  the  deranged  intestinal  digestion,  and  that  they 
are  due  to  the  absorption  of  toxic  products  formed  during  the 
putrefaction  of  food  in  the  intestines.  C.  A.  Herter  and  E.  E. 
Smith  (“  N.  Y.  Med.  Jour./’  June  22  and  29,  July  6,  13,  and  20, 
1895)  have  published  clinical  histories  and  detailed  analyses  show- 
ing the  relations  of  psychical  disturbances,  melancholia,  etc.,  to  the 
toxicity  of  the  urine.  It  is  conceivable  that  the  production  of 
these  symptoms,  particularly  frontal  headache,  beating  in  the  head, 
congestions,  pulsations  of  the  large  arteries,  globus  hystericus,  mel- 
ancholia, and  insomnia,  is  in  some  way  related  to  excessive  intes- 
tinal putrefaction.  When  the  nervous  dyspepsia  is  comparatively 
recent,  the  symptoms  are  limited  to  the  gastro-intestinal  tract,  but 
when  the  disease  is  of  long  standing,  the  nervous  symptoms  may 
submerge  the  digestive,  and  it  may  be  difficult  to  decide  whether 
the  latter  or  the  former  constitute  the  primary  derangement. 

Diagnosis. — As  a general  rule,  it  will  be  found  that  the  nervous 
dyspepsia  is  connected  with  some  organic  disease  of  one  of  the 
digestive  organs.  We  refer  to  the  various  anomalies  of  position 
of  the  intra-abdominal  organs  that  are  described  in  the  chapter  on 
Gastroptosis  and  Enteroptosis.  Frequently,  dislocated  kidneys, 
small  tumors,  herniae  of  the  median  linea  alba,  morbid  changes  in 
the  male  or  female  sexual  organs,  and  organic  diseases  of  the 
stomach  and  intestines,  will  be  found  to  exist.  There  will  be  no 
connection  between  the  quality  and  quantity  of  the  food  and  the 
digestive  difficulties,  but  sleep,  emotional  state,  and  psychical  con- 
dition will  be  influential  factors.  The  complaints  of  the  patient  are 
frequently  described  in  exaggerated  language.  One  of  our  patients, 
57 


870 


NERVOUS  DYSPEPSIA. 


who  is  the  owner  of  a brickyard,  describes  his  feelings  as  “ similar 
to  the  rolling  of  a ton  of  bricks  in  his  belly”  ; another  compares 
his  sensation  to  being  “ stabbed  with  a red-hot  knife  ” ; still  another 
describes  her  abdomen  as  being  “ distended  to  bursting,  like  a bal- 
loon,” or,  at  other  times,  as  feeling  compressed  as  though  it  were 
in  a vise.  At  other  times  these  same  patients,  without  recognizable 
reason,  will  make  no  complaints  at  all,  will  be  very  happy  and  cheer- 
ful, and  digest  well.  These  variations  in  the  functional  powers  of 
digestion  are  very  characteristic  of  nervous  dyspepsia.  Leube  has 
called  our  attention  to  the  emptiness  of  the  stomach  seven  hours 
after  a rather  heavy  test-meal. 

Prognosis. — Inasmuch  as  the  course  of  the  disease  is  a chronic 
one,  it  may,  in  severe  cases,  by  continued  and  progressive  loss  of 
strength  and  emaciation,  prove  fatal.  In  those  cases  in  which  a 
cure  has  been  effected  relapses  may  occur,  so  that  the  prognosis 
should  be  guarded.  Sometimes,  when  the  fundamental  disease  is 
remediable, — for  instance,  in  genito-urinary  disturbances,  malaria, 
etc., — or  when  the  cause,  such  as  sexual  excesses,  abuse  of  alcohol 
and  tobacco,  bodily  and  mental  overexertion,  can  be  removed,  the 
resulting  nervous  dyspepsia  may  be  permanently  cured. 

Heterochylia  (from  erepos,  meaning  “ other  ” or  “ different,”  and 
yuloq,  meaning  “juice  ” or  “ secretion  ”). — This  term  is  suggested 
by  the  author  to  denote  a rapidly  alternating  state  of  secretion, 
occurring  chiefly  in  nervous  dyspepsia.  In  making  a large  num- 
ber of  analyses  in  these  cases,  Dr.  E.  L.  Whitney  and  the  author 
have  observed  within  one  week  that  euchlorhydria,  hyperchlor- 
hydria,  and  inacidity  will  be  found  after  the  same  test-meals.  In 
the  discussion  of  a paper  read  before  the  American  Medical 
Association,  in  Philadelphia,  June  4,  1897,  a colleague,  Dr.  E.,  of 
Brooklyn,  stated  that  in  his  own  case  he  had  ;observed  hyper- 
acidity and  inacidity  on  the  same  day,  after  he  had  taken  the 
identical  meals  and  drawn  a sample  within  one  hour  after  they 
had  been  ingested.  Dr.  E.,  who  is  an  able  chemist,  made 
quantitative  analyses  of  his  gastric  juice  on  many  occasions, 
and,  so  far  as  he  can  tell,  these  variations  in  the  secretion  are 
independent  of  his  emotional  state.  In  a number  of  the  cases 
examined  by  Dr.  Whitney  and  the  author  they  found  hyperacidity 
with  rapid  digestion  of  proteids,  and  defective  carbohydrate  diges- 
tion, with  symptoms  of  pyrosis  and  eructation  that  were  relieved 
by  alkalies.  Two  days  afterward  the  author  examined  the  same 
cases,  to  find  that  two  of  them  showed  no  reaction  with  Congo 


D I F FER  ENT  I A L D I A G NOS  IS. 


871 


paper,  no  free  nor  combined  HC1,  and  a pronounced  HC1  deficit. 
There  was  no  pyrosis  nor  eructation,  but  the  patients  complained  of 
a sense  of  fullness  and  weight  in  the  stomach,  together  with  anorexia, 
which  symptoms  were  relieved  by  two  doses  of  dilute  HC1  (thirty 
drops  per  dose).  At  the  end  of  the  same  week  we  had  occasion  to 
examine  the  same  cases  again,  and  found  the  acidity  normal.  For 
want  of  a better  expression  we  have  designated  these  rapidly  alter- 
nating states  of  secretion  by  the  name  heterochylia.  When  the  acid 
is  in  excess,  the  proteids  are  absent  from  the  test-meals,  and  rice 
and  bread  almost  undigested.  When  the  acid  is  absent,  one  may 
frequently  find  a defective  proteid  digestion  but  a rapid  carbo- 
hydrate digestion.  We  have  no  explanations  to  offer  for  these 
cases  beyond  those  which  are  purely  hypothetical,  but  it  is  conceiv- 
able that  a closer  histological  study  of  the  finer  ramifications  of  the 
gastric  nerves,  such  as  has  been  carried  out  with  such  admirable 
regard  for  detail  by  Henry  J.  Berkley  in  other  organs  of  the  body, 
may  throw  some  light  upon  this  puzzling  phenomenon.  For 
instance,  we  may  sooner  or  later  be  instructed  that  the  oxyntic  or 
border  cells  receive  a different  nervous  supply  from  the  chief  or 
central  cells,  or  that  both  chief  and  border  cells  are  supplied  by 
nerves  of  widely  differing  character,  one  set  exciting  the  function, 
the  other  inhibiting  it, — i.  e.,  anabolic  and  catabolic  secretory 
fibers, — but  all  this  is  premature  and  problematic.  Dr.  Frank  H. 
Murdoch,  of  Pittsburg,  in  a report  to  the  American  Gastro-entero- 
logical  Association  (Washington,  May,  1898),  gave  a large  number 
of  analyses  on  cases  of  this  type,  showing  a secretion  varying  from 
achylia  to  hyperacidity. 

Differential  Diagnosis. — Nervous  dyspepsia  with  inacidity  may 
be  confounded  with  chronic  gastritis  or  carcinoma,  and  nervous 
dyspepsia  with  hyperacidity  may  be  confounded  with  ulcer,  while 
still  other  forms  may  bear  a striking  resemblance  to  atony  or 
myasthenia.  For  the  separation  of  chronic  gastritis  from  nervous 
dyspepsia,  the  following  facts  are  of  importance : Chronic  gastritis 
is  accompanied  more  frequently  by  vomiting;  the  stomach  con- 
tains large  quantities  of  mucus  and  a few  blood  streaks;  we  may 
have  also  stagnation  of  the  contents.  The  course  of  chronic  gas- 
tritis is  more  uniform  and  typical,  and  the  dyspeptic  symptoms  are 
directly  influenced  by  the  quality  and  quantity  of  the  ingesta.  In 
carcinoma  the  distress  is  present  at  all  times,  even  on  an  empty 
stomach,  vomiting  is  frequent,  and  the  ferments  are  absent  when 
the  HCl  secretion  is  lost.  In  nervous  dyspepsia  the  ferments  are 


Syz 


NERVOUS  DYSPEPSIA. 


still  present,  though  HCl  may  be  absent.  When  symptoms  of 
stenosis  have  occurred,  there  can  be  no  difficulty  about  the  diag- 
nosis. The  differentiation  of  nervous  dyspepsia  from  ulcer  becomes 
difficult  only  in  those  cases  in  which  there  has  been  no  hemat- 
emesis.  The  constant  dependence  of  gastric  pain  upon  the  food, 
the  sharply  circumscribed  pain-points  in  the  epigastric  region  and 
in  the  back,  are  unmistakable  criteria.  We  have  spoken  more 
fully  of  the  differential  diagnosis  in  the  sections  on  the  various 
gastric  diseases  with  which  nervous  dyspepsia  may  be  confounded. 
It  must  not  be  overlooked,  however,  that  nervous  dyspepsia  may 
be  associated  with  some  form  of  organic  gastric  disease. 

Treatment. — The  fundamental  causes  of  disease  should  be 
hunted  up,  and,  if  possible,  removed.  The  prospects  of  doing  this 
are  favorable  if  the  cause  can  be  found  in  the  existence  of  intestinal 
parasites,  floating  kidney,  malaria,  and  certain  remediable  diseases 
of  the  genito-urinary  organs.  In  those  forms  of  nervous  dys- 
pepsia which  depend  upon  an  undue  excitation  of  the  nervous 
system,  due  to  sexual  excesses,  abuse  of  alcohol  and  nicotin,  or 
excessive  mental  and  bodily  exertion,  improvement  can  not  be 
hoped  for  unless  these  states  are  remedied.  Patients  must  be 
impressed  with  the  fact  that  drugs  and  other  treatment  will  not 
improve  them  if  they  persist  in  their  bad  habits.  Particularly 
American  business  men,  who,  with  admirable  energy,  but  with 
little  regard  for  their  own  health,  persist  in  executing  work  which 
is  too  severe  for  their  mental  and  physical  constitution,  must 
be  taught  that  the  prime  factor  in  successful  treatment  is  rest  ! 
This  class  of  cases  will,  in  the  long  run,  prove  to  be  very  grate- 
ful patients  if  this  truth  is  emphasized,  and  false  expectations 
concerning  the  efficacy  of  drugs  and  washing  out  the  stomach, 
etc.,  corrected  at  the  beginning  of  the  treatment.  Better  results 
can  be  obtained  in  all  of  these  cases  by  a change  of  environment, 
with  absolute  psychical  and  physical  quiet,  removal  from  the  cares 
and  worries  of  business  and  household,  than  by  the  most  detailed 
and  complicated  treatment. 

In  connection  with  this  we  must  emphasize  the  value  of  rational 
psychical  treatment  of  nervous  dyspepsia.  The  physician  must,  in 
a dignified  manner,  attempt  to  merit  the  absolute  confidence  of  his 
patient.  For  this  purpose  we  consider  it  important  that  he  should 
show  a warm,  sincere  interest  in  the  suffering  of  his  patients,  even 
if,  after  a repeated  and  thorough  examination,  he  should  become 
convinced  that  the  patient’s  complaints  are  unreal  and  exaggerated. 


TREATMENT  OF  NEURASTHENIA  GASTRICA. 


«73 


It  is  a great  comfort  to  these  neurasthenics  to  listen  patiently  and 
sympathetically  to  their  complaints,  and  not  to  ridicule  or  criticize 
them.  The  sufferings  of  the  patient,  psychically  considered,  are 
equally  intense,  whether  they  be  real  or  imaginative. 

Gymnastics. — The  author  has  frequently  observed  marked  im- 
provement after  a course  of  mild  gymnastic  training  under  an 
experienced  training-master.  The  bicycle,  moderately  used,  is  a 
better  means  of  promoting  appetite  and  regular  evacuations  than 
drugs.  In  a similar  way  horseback  riding,  rowing,  fencing,  etc., 
are  to  be  recommended. 

Climatic  Treatment. — A sojourn  in  the  mountains  or  at  the  sea- 
shore is  a great  help,  inasmuch  as  it  not  only  removes  the  patient 
from  surroundings  which  maintain  his  disease,  but  at  the  same  time 
insures  rest,  quiet,  and,  above  all  things,  invigorating  fresh  air.  In 
seeking  a resort,  fashionable  places  and  those  thronged  with  society 
should  be  avoided.  The  greater  part  of  the  day  should  be  spent 
in  the  open  air — if  possible,  in  taking  extensive  walks.  This  will 
favor  good  sleep  during  the  night.  If  there  is  persistent  hyper- 
acidity with  constipation,  the  patient  will  be  benefited  by  a sojourn 
at  Bedford  Springs,  Pa. 

Massage. — There  is  no  doubt  that  massage  improves  the  nutri- 
tion of  the  muscles  and  nerves,  and  favors  a vigorous  circulation, 
metabolism,  and  regular  evacuation.  Massage  should  not  be  per- 
mitted to  be  executed  by  the  inexperienced.  Nine-tenths  of  the 
persons  claiming  to  be  masseurs  at  the  present  time  are  charlatans. 
To  be  effective,  the  massage  must  be  studied  by  the  physician  who 
has  the  case  in  hand,  and  though  he  may  not  execute  it  himself,  he 
should,  at  least,  supervise  it. 

Hydrotherapy. — Cold  sponge  baths,  taken  in  the  morning  imme- 
diately after  arising,  have  a bracing  effect.  A good  method  is  to 
wrap  the  entire  body  of  the  patient  in  a sheet  dipped  in  cold  water, 
and  while  the  patient  himself  kneads  and  beats  the  parts  of  his 
body  that  are  accessible  to  him  in  front,  another  person  must  per- 
form the  massage  of  his  back;  after  this  the  patient  is  thoroughly 
rubbed  with  a coarse  Turkish  towel.  These  cold  rubs  should  not 
last  longer  than  three  minutes,  after  which  the  patient  must  dress 
and  take  a walk  of  about  one  mile.  The  favorable  effects  of 
hydrotherapeutic  methods  do  not  become  manifest  until  they  have 
been  applied  for  two  or  three  weeks.  They  are  then  followed  by 
improvement  in  the  appetite  and  sleep.  When  the  insomnia  is 
persistent,  we  are  very  fond  of  prescribing  a warm  salt  bath,  at  the 


874 


NERVOUS  DYSPEPSIA. 


temperature  of  the  body,  containing  four  per  cent,  of  sodium 
chlorid  and  two  per  cent,  of  sodium  carbonate.  The  patient  is 
placed  in  this  bath  about  half  an  hour  before  bedtime,  and  remains 
in  it  for  about  twenty  minutes.  In  highly  neuropathic  patients  the 
bath  before  bedtime  has  in  my  experience  aggravated  the  insomnia 
— it  should  then  be  given  about  4 p.  m. 

Irrigations  and  Douches  of  the  Gastric  Mucosa. — These  are  used  to 
reduce  the  hyperesthesia  of  the  gastric  nerves,  and  for  this  purpose 
carbonated  waters  are  preferable  to  still  waters.  The  gastric  tube 
should  be  used  which  contains  numerous  small  lateral  openings 
instead  of  a few  large  terminal  openings.  If  carbonated  water 
can  not  be  conveniently  obtained,  it  can  be  prepared  by  adding 
citric  acid  or  lemon  juice  to  a one  per  cent,  solution  of  sodium  bi- 
carbonate. The  amount  poured  into  the  stomach  should  not  exceed 
twenty  ounces  at  a time. 

Electricity . — Galvanization  of  the  abdomen  and  the  spinal  region 
and  general  faradization  are  applicable  in  these  cases.  The  faradic 
current  should  be  applied  to  every  muscle  in  the  body,  with  large, 
broad,  felt  electrodes.  A good  method  consists  in  placing  the  feet 
of  the  patient  upon  a large  plate  electrode  (cathode),  while  the 
other  pole  is  placed  on  the  various  muscle  groups  of  the  body.  It 
is  well  to  allow  the  large  electrode  to  remain  on  the  epigastric 
region  for  about  five  minutes,  while  the  remaining  one  is  passed  up 
and  down  over  the  spinal  column.  The  intensity  of  the  current 
and  the  duration  and  localization  of  the  treatment  must  be  varied 
according  to  the  individuality  of  the  case.  According  to  Erb, 
Beard,  and  Rockwell,  this  treatment  improves  the  appetite  and 
sleep,  reduces  the  psychical  irritability,  and  creates  a more  favor- 
able disposition  to  bodily  exercise.  Personally,  we  may,  without 
defining  the  exact  benefits  derived  from  electric  treatment,  pro- 
nounce it  to  be  an  indispensable  adjunct  to  the  treatment  of  neuras- 
thenia gastrica.  Perhaps  it  influences  the  nutrition  of  the  nervous 
centers,  or  perhaps  it  is  nothing  but  systematic  massage.  At  all 
events,  it  effects  an  improvement  in  the  sufferings  of  this  class  of 
patients. 

The  Diet. — In  this  disease,  more  than  in  any  other,  the  physician 
must  see  that  the  articles  of  food  possess  considerable  variety  and 
are  well  cooked  and  appetizing.  The  behavior  of  the  digestive 
functions  are  so  grotesque  that  it  is  impossible  and  useless  to 
suggest  stereotyped  diet  lists.  Experience  is  the  best  guide,  and 
the  common  phrase,  “the  proof  of  the  pudding  is  the  eating  of 


MEDICINAL  TREATMENT. 


875 


it,”  is  certainly  applicable  in  these  cases.  It  is  very  beneficial 
to  the  patient  if  he  can  take  and  well  digest  large  quantities  of 
milk;  aside  from  its  high  nutritive  value,  milk  acts  upon  the 
gastric  mucosa  like  a soothing  liquid  ointment,  and  is  a dietetic 
intestinal  antiseptic.  Sometimes  when  the  patient  is  prejudiced 
against  it,  it  is  possible  to  mix  it  with  the  food  surreptitiously, 
and  our  diet  lists  and  “ dietetic  kitchen  ” give  many  formulas  for 
this  purpose.  In  the  selection  of  the  remaining  foods,  the 
taste,  likes,  and  dislikes  of  the  patient  should  be  consulted  so  far 
as  is  consistent  with  rational  dietetics.  Articles  of  luxury,  such  as 
good  fruit — grapes,  pears,  figs,  dates,  and,  if  anacidity  exists,  fresh 
pineapples — should  not  be  forbidden.  If  constipation  is  obstinate, 
the  diet  should  contain  a large  amount  of  these  foods,  and  par- 
ticularly apples.  Concerning  the  use  of  alcoholic  beverages,  no 
definite  rule  can  be  given.  On  the  whole,  we  believe  that  wines 
and  beer  should  be  avoided,  unless  they  are  needed  for  stimulation 
and  to  improve  the  appetite.  Large  colon  enemata  with  pure  olive 
oil(300c.c.  at  a time)  are  sometimes  curative  in  the  nervous  consti- 
pation, particularly  the  membranous  colitis  present  in  these  patients. 
Perhaps  the  most  effective  treatment,  on  the  whole,  is  that  desig- 
nated as  the  Weir  Mitchell  rest-cure,  a combination  of  hydrothera- 
peutic,  electrical,  and  dietetic  treatment,  with  gymnastics,  rest, 
massage,  and  as  much  sleep  as  possible.  When  the  state  of  the 
nutrition  has  been  much  reduced,  the  so-called  “ Mastkur,”  a sys- 
tem of  fattening  by  highly  nutritious  diet  and  passive  exercise,  is, 
in  our  experience,  very  effective  in  bringing  about  a reduction  of 
the  symptoms  and  improvement  in  the  digestive  functions.  This 
“ Mastkur”  is  not  applicable  to  all  classes  of  patients;  those  of  an 
irritable  and  restless  temperament  and  those  who  have  organic 
gastric  diseases  are  not  improved  by  it. 

Drugs. — Those  that  have  been  employed  in  neurasthenia  gastrica 
are  the  tonics,  sedatives,  and  hypnotics.  In  anacidity  the  basic 
orexin,  five  grains  three  times  a day,  has  been  very  much  lauded 
by  Penzoldt.  The  fluid  extract  of  condurango,  one  teaspoonful 
three  times  a day,  and  the  bitter  tonics,  calumbo,  gentian,  quassia, 
in  doses  of  one  dram  three  times  a day,  are  sometimes  of  value, 
though  personally  we  have  seen  no  marked  results  follow  their 
administration.  The  remedy  we  have  most  faith  in  is  the  sulphate 
of  strychnin,  of  a grain  three  times  a day  continued  for  one 
month,  at  least.  When  malaria  is  associated  with  the  nervous 
dyspepsia,  quinin  is  the  remedy  “ par  excellence.”  Boas  and 


876 


NERVOUS  DYSPEPSIA. 


Einhorn  speak  very  favorably  of  the  use  of  bromids ; both  of 
them  employ  mixtures  of  the  ammonium  and  sodium  bromids. 
While  the  remedies  may  have  a temporary  value  and  are  indis- 
pensable for  producing  sleep  and  diminishing  the  excessive  irri- 
tability of  the  nervous  system,  they  must  not  be  used  continu- 
ously. We  have  assured  ourselves,  by  quantitative  analyses  of 
the  toxic  products  of  the  urine,  similar  to  the  studies  of  Herter 
and  Smith  (/.  c.),  that  the  toxicity  of  the  urine  is  increased  in 
nervous  dyspepsia  as  soon  as  the  total  quantity  of  bromids  admin- 
istered exceeds  six  grams  in  twenty-four  hours.  Maximowitsch 
recommends  the  following  in  neurasthenia  gastrica  existing  on  a 
basis  of  anemia : 


R . Ferri  bromati, 

Chitlin  bihydrobromic, aa  4.0  3 j. 

Ext.  et  pulv.  rad.  rhei,  q.  s.  u.  f.  pil.  No.  CXX.  M. 

SlG. — Two  pills  three  times  daily. 


The  use  of  mineral  spring  waters  is  of  doubtful  efficacy.  When 
an  improvement  is  noticed  at  the  mineral  springs,  it  is  probably 
due  to  the  hygienic  surroundings,  the  removal  from  care  and 
worry  and  responsibility,  and  the  discontinuance  of  the  detrimen- 
tal habits  encouraged  at  the  home  of  the  patient.  For  further  con- 
sideration of  the  effect  of  mineral  waters  we  refer  to  the  chapter  on 
this  subject.  If  the  insomnia  is  persistent,  chloral  may  be  unavoid- 
able. It  should,  in  these  cases,  be  given  by  rectal  enema  and  not 
by  the  stomach.  Fifteen  grains  in  two  ounces  of  starch  water  are 
usually  sufficient  to  secure  rest.  An  effective  combination  con- 
sists of  five  grains  of  chloral  hydrate  and  eight  grains  of  sulphonal. 
Opium  and  belladonna  are  best  excluded  from  the  treatment. 
Chloral  even  in  very  small  doses  (three  grains  at  night)  sometimes 
causes  headache  and  lassitude  the  next  day — it  must  then  never  be 
repeated.  In  uric  acid  diathesis  and  marked  rheumatism  the  sali- 
cylate of  soda  (ten  grains,  t.  i.  d.)  often  produces  not  only  relief  of 
any  existing  pain,  but  even  sleep.  Sulphonal  and  trional  are  avail- 
able remedies  for  the  insomnia,  but,  like  the  chloral,  they  have  a 
deleterious  influence  upon  the  stomach,  and  should  be  preferably 
given  per  rectum.  But  the  treatment  producing  the  most  lasting 
results  is  that  which  tones  up  and  invigorates  the  neuromuscular 
apparatus  and  the  nitrogen  elimination  and  increases  the  will  power. 


AUTHOR’S  SYNOPSIS  OF  SCHEME  FOR  EXAMINING 
STOMACH  PATIENTS  AT  THE  UNIVERSITY  OF 
MARYLAND  HOSPITAL. 

Medical  No — Name Address Age...  Color 

Sex Social  Condition Diagnosis Date 

HEREDITARY  FACTS  OF  IMPORTANCE. 

PREVIOUS  HISTORY. — Severe  constitutional  diseases?  First  appearance  of  symptoms,  and 
cause?  Did  they  appear  suddenly  ? Intensely?  Or  gradually  ? Continuous?  Or  remittent? 
What  intervals?  Occupation?  Habits?  Alcoholism?  Tobacco?  Cold?  Change  of  climate? 
Mental  strain  ? Trauma?  Malaria?  Did  it  begin  with  or  without  a chill ? Fever?  Yellow 
fever?  Constipation?  Diarrhea?  Dysentery?  Typhoid  fever?  Abdominal  diseases? 
Menstrual  irregularity?  Pregnancies? 

PRESENT  HISTORY.— Diseases  of  other  organs?  Pressure?  Local  and  subjective  com- 
plaints? Fullness?  Pain?  Distention?  Restlessness?  Sounds  in  the  digestive  tract? 
Bowel  movements?  Nausea?  Eructation?  Vomiting?  Hematemesis?  Appetite?  Taste? 
Thirst  ? 

LOCAL  SUBJECTIVE  SYMPTOMS. — Any  difficulty  or  pain  on  deglutition?  If  so,  its  regu- 
larity? Intensity?  Duration?  Pain  in  stomach?  Effect  of  food  on  pain?  Does  it  occur 
in  every  position  of  body?  Or  only  in  certain  positions?  Time  of  onset  after  meals?  Pain 
at  night?  On  an  empty  stomach?  Improved  by  eating?  Exaggerated  by  eating?  Is  pain 
diffuse?  Or  circumscribed?  Deglutition  sounds ? 

ERUCTATION. — Duration?  Occurring  on  full  or  empty  stomach  ? Is  gas  tasteless?  Odorless? 

Acid?  Decomposed?  After  what  foods  ? Presence  of  pyrosis,  or  heartburn  ? 

NAUSEA  AND  VOMITING. — Occur  on  full  or  empty  stomach  ? Frequency?  Taste  of  vomit? 
Appearance  of  matter  ? Food  particles?  Proteids?  Starches?  Mucus?  Bile?  Pus?  Blood? 
Food  eaten  several  days  before?  Does  emesis  relieve  symptoms? 

APPETITE  AND  THIRST. — Accustomed  diet  (let  the  patient  state  in  detail  what  iseaten  during 
the  entire  day)?  Mode  of  life?  Anorexia?  Bulimia?  Aversion  to  meat  ? Thirst? 
BOWELS. — Constipation?  Diarrhea?  Undigested  particles  of  food ? Mucus?  Pus?  Blood  and 
source  ? 

RESULTS  OF  BLOOD  EXAMINATION. 

GENERAL  NUTRITION. — Emaciation?  Loss  of  weight  in  pounds?  In  what  time? 

PHYSICAL  EXAMINATION. 

Examination  of  Tongue,  Teeth,  and  Mouth. 

INSPECTION. — Change  of  form  of  abdomen?  Tumor?  Gastric  or  intestinal  peristalsis? 
PALPATION. — Time  of  examination?  Temperature?  Outline  of  stomach?  Upper  border? 
Lower  border?  Presence  of  tumor?  Movement  of  tumor?  Was  stomach  full  or  empty? 
Pain  on  pressure?  Diffuse  or  circumscribed ? Succussion  sound ? Liver?  Kidneys? 
PERCUSSION. — Limits  of  the  stomach? 

DISTENTION  WITH  AIR  OR  GAS. — Limits  of  stomach?  Results  with  intragastric  bag? 

Does  tumor  move  with  distention?  Made  more  or  less  distinct? 

ELECTRODIAPHANY. — Limits  of  stomach?  Tumor? 

EXAMINATION  OF  TEST-MEALS. 

Double  test-meal  (see  p.  121) — a full  meal  at  say  9 a.  m. 

Ewald  test-meal  at  say  2 p.  m.  Contents  drawn  at  say  3 P.  M.  Date, 

MACROSCOPICAL  EXAMINATION.— (Quantity  ? Color?  Odor?  Food  particles  ? Froth  or 
gas?  Pus?  Mucus?  Bile?  Blood?  Fragments  of  tissue ? 

MICROSCOPICAL  EXAMINATION.— Bacteria  ? Oppler-Boas  bacilli  ? Sarcinae? 

CHEMICAL  EXAMINATION. — Reaction?  Free  acid?  Free  HC1  ? Lactic  Acid?  Amount 
freeHCl?  Combined  HC1?  Amount  acid  salts  and  organic  acids  ? Total  acidity ? Erythro- 
dextrin  ? Biuret  reaction  ? Deficit  of  HC1  ? 

PEPSIN. 

Albumin  digested  in  pure  filtrate  in. .. .minutes.  Albumin  digested  in  acidified  filtrate  in.... 
minutes.  Albumin  digested  in  HC1  and  pepsin  filtrate  in minutes. 

RENNIN  OR  CHYMOSIN. 

Milk  coagulated  bj’  rennin  in minutes.  Milk  coagulated  by  rennin-zymogen  in minutes. 

Rennin-zymogen  active  in  dilution  1. 

CONTENTS. — After  meal  previous  evening  at  8 p.  M. 

CONTENTS. — After  lavage  previous  evening  at  8 p.  m. 

TIME  OF  SALOL  REACTION,. ..  .minutes. 

TIME  OF  IODID  OF  POTASSIUM  RESORPTION  TEST,. ..  .minutes. 

URINE.— Amount?  Urea?  Uric  Acid?  Reaction?  Indican?  Preformed  sulphates ? Albumin? 
Tube-casts?  Ethereal  sulphates ? Ratio?  Sugar?  Specific  gravity  ? 

TREATMENT. 

Diet?  Medicines?  Electricity?  Massage?  Hydrotherapy?  Lavage?  Mineral  spring  water ? 
Gymnastics?  Results? 


877 


LIST  OF  AUTHORS. 


Compiled  by  the  author'' s pupils , Dr.  Henry  IV.  Nolle  and  Air.  Thomas  II.  Cannon. 


A. 

Abelous,  bacteria  in  the  stomach,  63 
Adler,  diseases  of  the  heart  and  the  stom- 
ach, 389 ; congenital  atresia  of  the 
pylorus,  657  ; diet  in  hyperacidity,  829 
Adler,  Harry,  carcinoma  and  Oppler-Boas 
bacillus,  564;  gastroptosis,  730;  hy- 
pertrophic stenosis,  614 
Albu,  autointoxication,  374,  798  ; coma 
carcinomatosum,  559  ; gastric  tetany, 
379 

Alt,  merycism,  769 
Ames,  phlegmonous  gastritis,  434 
Anderson,  nutritive  enemata,  206;  absti- 
nence cure  for  ulcer,  514 
Arnold,  cancer,  565 
Atkinson,  digestibility  of  foods,  224 
Atwater,  dietaries,  24 ; effects  of  alcohol 
on  metabolism,  289 

B. 

Bachman,  W. , amylaceous  diet  for  hyper- 
acidity, 829 

Bachmeier,  floating  kidney,  728 
Baginsky,  pepsin  and  trypsin  interaction,  66 
Bamberger,  gastromalacia,  488 
Bardenhauer,  median  hernia  and  gastral- 
gia,  800 

Bardet,  electric  therapy,  303 
Barie,  asthma  dyspepticum,  382 
Bartels,  gastric  inflammatory  atrophy,  450 
Barthez,  mtlaena  neonatorum,  686 
Baruch,  Dr.  Simon,  natural  mineral  waters, 
comparative  charts,  313  et  seq. 

Basch,  Seymour,  gastralgia  in  tabic  patients, 

736 

Bauer,  rectal  alimentation,  21 1 
Beard,  electric  therapy,  302 
Beaumont,  peristalsis,  83,  84;  stomach  sur- 
gery, 348 
Beck,  cancer,  542 

Bensley,  histology  and  physiology  of  the 
gastric  glands,  24 
Bernabes,  myoma,  609 
Bernard,  Claude,  pancreatic  juice,  55,  66  ; 

self-digestion  of  the  stomach,  487 
Bertlielot,  steapsin,  57 


Best,  foreign  bodies  in  the  stomach,  61 1 
Bettman,  H.  W. , malformation  of  the  gas- 
tric cavity,  629,  643 
Beynard,  electric  stimulation,  302 
Biedert,  HC1  therapy,  331  ; achylia,  852 
Biernacki,  kidney  diseases  and  the  stom- 
ach, 392 

Bikfalvi,  alcohol  in  digestion,  292 
Billroth,  surgery,  349,  350,  362 
Bircher.  Dr.  Heinrich,  gastrorrhaphy,  650 
Blake,  Dr.  John  D.,  gastralgia  and  adhe- 
sions, 658,  801 
Blank,  digestion  of  fats,  61 
Boas,  peptic  gland  cells,  23  ; ptyalin  diges- 
tion, 45  ; duodenal  chyme,  66  ; test- 
meal,  1 21  ; bile  and  duodenal  secre- 
tion in  stomach  contents,  132;  epithe- 
lial exfoliation,  137,  139;  lactic  acid 
test-meal,  161  ; analysis  for  HC1, 
method,  168;  lactic  acid  estimation, 
169 ; pepsin  and  pepsinogen  tests, 
174;  rennin  and  rennin-zymogen  esti- 
mation, 174;  dietetics,  192,193,259; 
nutritive  enemata,  205  ; diet  lists,  232— 
246;  massage,  309;  alkali  therapy, 
337,  340;  gastric  surgery  and  secre- 
tion, 358  ; asthma  dyspepticum,  382  ; 
infectious  gastritis,  438 ; gastritis 
acida,  458 ; ulcus  carcinomatosum, 
560 ; autointoxication  in  dilatation, 
634  ; rumination  with  subacidity,  769  ; 
gastralgia,  799  ; gastric  crises,  835  ; 
achylia  gastrica,  854 

Bocci,  electricity,  peristalsis  and  secretion, 
302 

Bollinger,  glanders  in  the  stomach,  590 ; 
foreign  bodies,  612 

Booker,  W.  D. , pathological  gastric  mucosa, 
146  ; acute  gastritis,  423 
Borutteau,  secretion  and  peristalsis,  90 
Bottcher,  infectious  gastritis,  440  ; gastric 
ulcer,  490 

Bouchard,  gastric  diseases  and  respiration, 
376 

Bouchert,  papain,  346 
Bouley,  absorption,  91 
Bouveret.  artificial  stomach  distention,  99  ; 
gastric  diseases  and  respiration,  376; 


879 


88o 


LIST  OF  AUTHORS. 


gastric  secretion,  149 ; alcohol  and 
tetany,  192  ; tetany  and  lavage,  299, 
379 ; acute  gastritis,  421  ; gastritis 
atrophicans,  460  ; nervous  eructation, 
755  ; bulimia,  810;  gastric  crises,  835 
Brabazon,  gastric  inflammatory  atrophy, 
450 

Brandi,  gastric  absorption,  93 
Braun,  organic  acids,  analysis,  1 70 
Brenner,  gastro-enterostomy,  350 
Brigham,  gastrectomy,  361 
Brinton,  gastric  glands,  25,  26;  peristalsis, 
85 

Broadbent,  Sir  Wm.  H.,  anorexia,  191  ; 

motor  insufficiency,  842 
Brock,  galvanism  and  gastric  neuroses,  306 
Brooks,  valvulse  conniventes,  33 
Brown-Sequard,  the  stomach  in  nervous 
diseases,  385  ; gastromalacia,  489 
Briicke,  pepsin  determination,  174 
Brunner,  peristalsis  testing,  71 
Bryant,  Joseph  D.,  cancer  statistics,  545 
Bunge,  HC1  an  antiseptic,  63 
Burkhardt,  dietetics,  207,  208,  249 ; neur- 
asthenia gastrica,  868 
Burton,  pancreatic  juice,  56 
Bush,  digestion  in  the  absence  of  the  usual 
ferments,  215 

C. 

Cabot,  Richard  C. , examination  of  gastric 
contents  for  blood,  135 
Cahn,  predigested  food,  209 
Cannon,  peristalsis,  85,  87 
Canstatt,  electric  therapy,  303 
Capelle,  foreign  bodies  in  the  stomach, 
612 

Captain,  gastric  bacteria,  63 

Cartellieri,  eructation,  754 

Charcot,  gastric  crises,  735  ; anorexia, 

. 8l5 

Chiary,  hour-glass  stomach,  645 
Chittenden,  Prof.  R.  H.,  saliva,  1 7 1 ; 
composition  of  beef  products,  199 ; 
alcohol  in  digestion,  290 
Chomel,  diet  in  dilation,  202 
Chomele,  dilation.  637 
Christomanos,  antiperistalsis,  213 
Church,  food  energy,  227 
Chvostek,  purulent  gastritis,  437 
Cohnheim,  Paul,  mucosa  fragments,  82  ; 

• achylia  gastrica,  853 
Cohnheim,  ulcer,  489,  490  ; cancer,  541 
Colin,  absorption,  91 
Connor,  Dr  , gastric  surgery,  348 
Contejean,  peristalsis  and  secretion,  90 
Cornil,  diagnosis  of  cancer,  563 ; lymph- 
adenoma,  590;  polypi,  607 
Courvoisier,  gastro-enterostomy,  349 
Cruveilhier,  polypi,  608 
Cseri,  massage,  309 

Czerny,  resection,  349 ; pyloroplasty  and 
resection,  364 


D. 

Daettwyler,  gastric  ulcer,  491 
Dauber,  antiperistalsis,  213 
Davis,  gastropexy,  365,  730 
Debove,  secretion  of  the  stomach,  149 
Decker,  gastromalacia,  489 
Deininger,  gastric  abscess,  437 
Deiters,  predigested  foods,  209 
Delafield,  acute  gastritis,  423 
Devic*  gastric  fermentation  and  tetany, 
192  ; tetany  from  lavage,  299,  379 
Dobson,  Nelson  C. , ulcer,  515 
Dock,  George,  cancer,  562 
Donders,  dietetics,  185 
Donkins,  H.  B.,  nutritive  enemata,  206; 

abstinence  cure  for  ulcer,  514 
Dreger,  George  R. , electrical  stimulation, 
82 

Dubey,  hypertrophic  sclerosis,  445 
Duchenne,  electrotherapy,  303 
Dujardin-Beaumetz,  carbohydrates  in  hy- 
peracidity, 196;  dietaries,  221 
Duret,  gastropexy,  365,  730 


E. 

Earl,  Dr.  Samuel  F.,  tuberculous  rectal 
fistula,  389 

Eberth,  carcinoma,  563 
Ebstein,  nervous  diseases  and  the  stomach, 
385  ; gastromalacia,  489  ; polypi,  608 
Edinger,  L. , acute  gastritis,  422 
Edkins,  acid  and  formation  of  pepsin,  27  ; 
absorptions,  91 

Edsall,  D.  L.,  gastrosuccorrhea,  845 
Eichhorn,  subcutaneous  feeding,  219 
Eichhorst,  peristalsis  testing,  71  ; spectro- 
scopic examination  for  blood,  135  ; 
rectal  alimentation,  2 II  ; dietetics, 
238  ; acute  gastritis,  .428 
Einhorn,  Dr.  Max,  gastric  motor  function, 
71  ; gastrograph,  74;  mucosa  exfolia- 
tions, 82;  gastrodiaphany,  104;  stom- 
ach bucket,  120  ; erosions  of  the  stom- 
ach, 137,  140;  their  pathological  sig- 
nificance, 141  ; gastric  secretion  in 
the  fasting  state,  149,  150;  intragas- 
tric  spray,  300 ; electrical  stimulation, 
302,  304,  305  ; intragastric  electrode, 
3°3  > gastritis,  415  ; electricity  in 
chronic  gastritis,  472 ; trauma  and 
ulcer,  491  ; hypertrophic  pyloric  ste- 
nosis, 614;  frequency  of  dislocated 
kidney,  721  ; gastrosuccorrhea,  843  ; 
achylia  gastrica,  850,  854,  856 
Eiselberg,  von,  pylorectomy,  360;  phyto- 
bezoar, 613 

Elsasser,  gastromalacia,  488 
Emmerich,  bile  action,  60 
Engel-Reimers,  cysts,  610 
Escherich,  bacteria  in  digestion,  62,  69 


LIST  OF  AUTHORS. 


88  I 


Ewald,  capacity  of  the  stomach,  1 8 ; fer- 
ment action,  46,  66;  peristalsis,  71; 
test-meal,  121,  122  ; mucosa  exfolia- 
tions, 135,  140;  secretions  from  the 
fasting  stomach,  149,  150;  nutritive 
enemata,  211  ; diet  list,  231,  238; 
massage,  309  ; formula  for  anorexia, 
341  ; tetany,  380;  nervous  diseases 
and  the  stomach,  385;  abscess,  437; 
gastromalacia,  489 ; syphilitic  ulcer, 
601  ; foreign  bodies  in  stomach,  61 1 ; 
fatal  gastric  hemorrhage,  688 ; bu- 
limia, 807 

F. 

Faber,  absorption,  92 
Faust,  action  of  pepsin  on  proteids,  176 
Fenwick,  Samuel,  insufficiency  of  secre- 
tion, 330  ; gastric  inflammatory  atro- 
phy and  anemia,  853 
Fenwick,  W.  Soltau,  poisoning  by  lavage, 
299 ; pulmonary  diseases  and  the 
stomach,  387 ; melsena  neonatorum, 
685 

Fermaud,  gastritis  parasitaria,  440 
Finlder,  papain,  346 

Finney,  J.  M.  F.,  exploratory  laparotomy, 
694 

Fischer,  melsena  neonatorum,  686 
Fitz,  R.  H.,  phantom  tumor  and  dilation 
of  the  colon,  725 

Fleiner,  electrodiaphany,  106;  test-meals, 
1 21,  122;  alcohol  and  tetany,  192; 
carbohydrates  in  hyperacidity,  196 ; 
gastritis,  41 5;  sarcomata,  547 
Fleischer,  gastric  motor  function,  71  ; per- 
istalsis, 72  ; gastrodiaphany,  104  ; 
diet-list,  246  ; HC1  combining  power 
of  foods,  247;  gastritis,  415;  men- 
struation and  gastric  disturbances,  736 
Flexner,  Dr.  S.,  tubercular  ulcer,  591 
Fliess,  gastric  neuroses,  207 
Flint,  Austin,  HC1  as  a medicinal  agent, 
33°  5 gastric  inflammatory  atrophy, 
449  ; anemia  and  atrophy,  853 
Foote,  El  M.,  ulcer,  515 
Foster,  gastromalacia,  488 
Fowler,  intravascular  feeding,  218 
P'ox,  Wilson,  ulcer  cure,  512;  hyperacid- 
ity and  peptic  ulcer,  501 
Frankel,  A.,  asthma  dyspepticum,  383  ; 

fatal  gastric  hemorrhage,  688 
Frankel,  C.,  acute  gastritis,  427 
Frerichs,  gastric  glands,  26 
Friedenwald,  Dr.  Julius,  acidities  after 
test  meals,  122  ; toxic  products  in 
gastric  diseases,  374,  634 
Fubini,  electricity,  peristalsis,  302 


G. 

Gafifky,  infectious  gastritis,  458 
Galeotti,  diagnosis  of  cancer,  563 


Gftrtner,  bacillus  of  melena,  686 
Gerhardt,  C.,  eroded  mucosa,  136;  ulcer, 
287  ; gastritis  parasitaria,  440 
Gersung,  dietetics  in  stenosis,  204 
Gessner,  bacteria  as  ferments,  61 
Gillespie,  interaction  among  bacteria,  63  ; 
gastric  motor  function,  71  ; gastric 
douche,  728 ; absorption  from  the 
stomach,  747 

Glaevecke,  absorption  of  iron,  816 
Glax,  purulent  gastritis,  434 
Gluczinski,  test-meal,  121 
Gmelin,  tryptophan,  57  ; bile  test,  132 
Goldschmidt,  electricity,  peristalsis,  and  se- 
cretion, 307 

Golgi,  mucosa  histology,  24 
Gombauldt,  hypertrophic  sclerosis,  444 
Graaf,  Regnier  de,  intestinal  contents,  52 
Gros,  Dr.  A.  P. , rest  of  the  digestive  or- 
gans, 285 

Grutzner,  digestive  action  of  the  succus 
entericus,  68  ; rectal  alimentation,  21 1, 
212 

Grynfelti,  melaena  neonatorum,  686 
Gull,  anorexia,  815 
Gussenbauer,  gastric  surgery,  348 


H. 

Haberkant,  Dr.,  gastric  surgery,  348; 
statistics  on  surgical  operations,  354, 
37°>  373 

Habershon,  statistics  on  gastric  ulcer, 

494 

Hacker,  von,  gastro-enterostomy,  350,  352, 
359,  3^3  > gastro-anastomosis,  365  ; 
surgery  for  ulcer,  515  ; NaCl  infusion 
for  gastric  hemorrhage,  516;  hour- 
glass stomach,  645 
Haeberlin,  cancer  statistics,  545 
Hahn,  gastrolysis,  351  ; surgical  treatment, 
359>  363 

Haig,  Alexander,  rest  of  the  stomach, 
286  ; gout  of  the  intestines,  391 
Halliburton,  W.  G. , pancreatic  juice,  56 
Halliday,  Andrew,  merycism,  768 
Hamilton,  Dr.  Alice,  tuberculous  ulcers, 
593 

Hammarsten,  rennin-zymogen  test,  51  ; 

composition  of  bile,  59  ; bile  action,  65 
Hammersclilag,  test  for  peptonizing  power 
of  gastric  juice,  173 
Hanot,  hypertrophic  sclerosis,  444 
Hanseman,  mitosis  in  diagnosis  of  cancer, 
563  ; tumors,  613 
Hartung,  mucosa  fragments,  136 
Hauser,  cancer,  541 ; ulcus  carcinomato- 
sum,  560 

Hayem,  mucosa  pathology,  140 ; anemia, 
chlorosis,  and  gastric  diseases,  386; 
“ gastrite  hyperpeptique,”  844;  achylia 
gastrica,  856 


882 


LIST  OF  AUTHORS. 


Hehner-Seeman,  organic  acid  estimation, 

. !7°  . 

Heidenhain,  peptic  gland-cells  and  their 
secretions,  22,  23,  24,  48;  function 
of  bile,  60 

Heinecke,  von,  pyloroplasty,  363  ; puru- 
lent gastritis,  437 

Heinsheimer,  metabolism  in  gastro-enter- 
ostomy,  369 

Hemmeter,  Dr.  John  C.,  duodenal  intuba- 
tion, 52;  intestinal  putrefaction,  64; 
gastric  motor  function,  71  ; peristalsis, 
74,  87,  90 ; gastrograph,  intragastric 
stomach-shaped  rubber  bag,  76,  79, 
82,  89;  test  for  absorption,  94-97  ; 
entero-  and  gastro-diaphany,  105, 
108,  1 12;  double-current  stomach- 
tube,  1 16  et  seq.;  acidity  after  test- 
meals,  124;  significance  of  mucosa 
exfoliations,  141-145  ; digestibility  of 
foods,  187 ; digestion  of  enemata, 
213;  dietaries,  232,  236;  alcohol  and 
gastric  motility,  293  ; electric  stimula- 
tion, 304  ; formula  for  anorexia,  340  ; 
gastrectomy,  361  ; gastric  tetany,  381  ; 
kidney  disease  and  the  stomach,  392 ; 
phlegmonous  gastritis,  434;  chronic 
hypertrophic  gastritis,  443  ; electricity 
and  chronic  gastritis,  472 ; gastro- 
malacia,  487  ; gastric  ulcer  treatment, 
512  ; cancer  statistics,  546  ; ulcus  car- 
cinomatosum,  560 ; carcinoma,  early 
diagnosis,  566 ; duodenal  intubation, 
622-642,  670;  Rontgen-ray  photog- 
raphy of  the  stomach,  641  ; deter- 
mination of  length  of  the  esophagus, 
655  ; pathogenesis  of  enteroptosis, 
706 ; histology  of  stomach-glands  in 
hyperacidity,  734  ; absorption  of  iron, 
815  ; proliferation  of  glandular  ele- 
ments in  hyperacidity,  817  ; hyper- 
acidity, 822  ; achylia  gastrica  ; 859  ; 
merycism,  769  ; pyloric  sounding, 
773  ; schema  for  examination  of 
stomach  patients,  877 
Hemmeter,  Mrs.  J.  C.,  dietetics,  281 
Henne,  HC1  therapy,  33 1 
Henoch,  asthma  dyspepticum,  381  ; the 
tongue  in  chronic  gastritis,  455 
Henry,  red  corpuscles  in  carcinoma,  404  ; 

gastric  atrophy  and  anemia,  854 
Hensen,  Hans,  bacterial  invasion  of  the 
digestive  tract,  64 
Herschel,  absorption,  93 
Herter,  nervous  dyspepsia,  869 
Heryng,  transillumination,  105,  106 
Herz,  malaria  and  gastric  hemorrhage, 
685 

Hildebrandt,  gastritis  parasitaria,  440 
Hippocrates,  dietetics,  185 
Hirschler,  carbohydrates  and  putrefaction, 
68 

H odder,  intravascular  feeding,  218 


Hodge,  C.  F. , effect  of  electricity  on  nerve 
elements,  301 

Hoffmann,  secretion  in  the  jejune  stomach, 
148,  150 ; electricity  and  secretion, 
302  ; gastritis,  447 
Hofmeister,  peristalsis,  83 
Honigman,  dietetics,  194;  HC1  therapy, 
330 

Hoppe-Seyler,  gases  in  the  stomach,  405; 
effect  of  exanthematous  diseases  on 
the  gastric  mucosa,  415 
Horner,  gastralgia  and  lipoma,  800 
Howell,  W.  H.,  amylolysis,  46  ; peris- 
talsis, 83 

Huber,  peristalsis  test,  72 ; gastric  secre- 
tion, 149,  150;  rectal  alimentation, 
21 1 ; dietetics,  238 
Hiif  ler,  gastrodiaphany,  104 
Hunter,  autodigestion  of  the  stomach,  487 
Huseman,  infectious  gastritis,  438 
Hutchinson,  pulmonary  diseases  and  the 
stomach,  388 


J- 

Jacobson,  diaphany  106,  107  108 
Jaksch,  von,  rectal  contents,  68  ; detection 
of  blood,  135  ; carbohydrates  and 
hyperacidity,  196;  on  the  diazo  re- 
action, 428 ; coma  carcinomatosum, 
559 

Jaworski,  rennin  test,  51  ; colon  contents, 
67;  test-meal,  121 ; secretion  stimu- 
lation, 150;  secretion  and  peristalsis 
after  gastric  operations,  358  ; catarrhus 
acida,  844  ; achylia  gastrica,  853 
Johnson,  Dr.  R.  W.,  gastric  surgery,  842 
Johnson,  Wyatt,  acute  gastritis,  427 
Jones,  Allen  A.,  gastric  secretion,  150; 
electrotherapy,  306 ; renal  diseases 
and  the  stomach,  393  ; anacidity,  854  ; 
gastralgia,  597 

Jones,  Bence,  urinary  changes  in  stomach- 
diseases,  407 

Jurgens,  nervous  dyspepsia,  866 
Jiirgensen,  Chr.,  amylaceous  diet  in  hyper- 
acidity, 829 

Justesen,  J.,  amylaceous  diet  in  hyper- 
acidity, [829 


K. 

Kaiser,  surgery,  348,  568 
Kansche,  surgical  treatment,  secretion, 
and  peristalsis,  358 
Karst,  subcutaneous  feeding,  219 
Kaufman,  Oppler-Boas  bacillus,  1 30 
Kazzander,  valvulae  conniventes,  33 
Keen,  Prof.  W.  W.,  gastric  surgery,  350, 
675  ; ulcer  statistics,  518  ; gastropexy, 
730 

Kelly,  Dr.  H.  A.,  gastric  surgery,  761 


LIST  OF  AUTHORS.  883 


Key,  Axel,  ulcer,  490 
Kinnicutt,  F.  P. , gastric  atrophy  and 
anemia,  330,  854 

Klebs,  ulcer,  489;  cancer,  542  ; infectious 
granulomata,  593 
Kleinwachter,  acute  gastritis,  429 
Klemperer,  peristalsis,  71,  72;  test-meal, 
121  ; acute  gastritis,  422 
Klikowicz,  alcohol  in  digestion,  292 
Knapp,  uterine  displacements  as  a cause 
of  nephroptosis,  714;  frequency  of 
dislocated  kidney,  721 
Koch,  nervous  diseases  affecting  the 
stomach,  385  ; gastromalacia,  489 
Kolliker,  gastric  glands,  25 
Kooyker,  foreign  bodies  in  the  stomach, 
612 

ICorcynski,  catarrhus  acida,  844 
Kramer,  stomach  operations,  358 
Kraus,  the  mouth  in  gastritis,  456 
Kretschy,  menstruation  and  gastric  dis- 
turbances, 736 

Krompecher,  cancer-diagnosis,  563 
Krueg,  subcutaneous  feeding,  219 
Kuhn,  F.,  absorption,  94;  HC1  action  on 
yeast,  15 1;  predigested  foods,  209; 
gases  in  the  stomach,  405  ; pyloric 
sounding,  642 

Ktihne,  trypsin  and  pepsin  interaction,  66 
Kundrat,  infectious  gastritis,  439  ; sarco- 
mata, 547  et  seq. 

Kupffer,  border  cells  in  fundus,  23 
Kussmaul,  alcohol  and  tetany,  192  ; diet  in 
dilation,  202;  gastric  douche,  299; 
electric  therapy,  303  ; gastric  tetany, 
379  ; stenosis  of  the  duodenum,  660 
Kuttner,  diaphany,  106,  107,  108 ; gastric 
surgery,  350 


L. 

Lambl,  polypi,  608 

Lancaster,  fatal  gastric  hemorrhage,  683 
Landau,  splanchnoptosis,  717 ; mekena 
neonatorum,  685  ; etiology  of  floating 
kidney,  696  ; intestinal  stenosis,  719 
Landenberger,  hypodermic  feeding,  219 
Landois,  dietetics,  220 
Langerhans,  recognition  of  gastroptosis, 
104  ; etiology  of  enteroptosis,  702 
Langermann,  HC1  therapy,  331 
Langley,  ferment  and  acid  cells,  27  ; pepsin 
and  trypsin  interaction,  66 
Larrey,  stomach  surgery,  348 
Lauenstein,  gastro-enterostomy,  349  ; gas- 
trolysis,  351 

Lauterbach,  asthma  dyspepticum,  382 
Lebert,  infectious  gastritis,  438 
Legroux,  transfusion  for  hemorrhage  in 
ulcer,  516 

Lemoine,  alkali  therapeutics,  334 

Leo,  secretions  in  the  fasting  stomach,  149  ; 


estimation  of  IIC1,  167;  estimation 
of  fatty  acids,  1 70;  bulimia,  807 
Leonard,  diagnosis  of  renal  calculus,  804 
I .eroy,  transfusion  in  hemorrhagic  ulcer,  516 
Lctulle,  ulcer,  490 

Leube,  peristalsis,  71  ; test- meal,  121  ; 
gastric  secretion  test,  150;  nutritive 
enema,  21 1 ; subcutaneous  feeding, 
219;  dietaries,  241;  alkali  therapy, 
334  > gastric  and  intestinal  vertigo, 
378  ; acute  gastritis,  428  ; gastric  ab- 
scess, 4}7  ; gastromalacia,  488  ; ulcer 
cure,  512  ; nervous  dyspepsia,  865 
Leven,  nervous  dyspepsia,  868 
Levertin,  absorption,  96 
Lewin,  bacterial  invasion  of  the  walls  of  the 
digestive  tract,  64 

Leyden,  dietetics,  194,  204;  alcohol  and 
metabolism,  289  ; juvenile  vomiting, 
760 

Leydig,  gastric  glands,  25 
Lindner,  gastric  surgery,  350 
Linossier,  therapeutics  of  alkalies,  234 
Litten,  chronic  gastritis,  460;  dislocation 
of  the  kidneys,  710 
Littmann,  papain,  346 
Lobker,  pyloroplasty  and  pylorectomy, 

363 

London,  ulcer,  489 

Loreta,  digital  divulsion  of  pylorus,  364 
Loye,  electrical  stimulation,  302 
Lubarsch,  O. , insufficiency  of  gastric  se- 
cretion, 329  ; achylia  gastrica,  850 
Luclcsdorf,  bacteria  of  mouth  and  intestine, 

63 

Ludwig,  electricity  and 1 the  motor  func- 
tion, 302;  mineral  springs,  313  et 
seq. 

Liittke,  HC1  determination,  166 


M. 

MacDonald,  gastrectomy,  361 
Macfayden,  bacteria  in  economy  of  diges- 
tion, 62;  ileum  contents,  67 
Macleod,  abscess,  436 
Magendie,  vomiting,  756 
Maisoneuve,  surgery,  349 
Malbranc,  gastric  douche,  299 
Mall,  F. , anatomy  of  the  stomach,  17; 
peptic  gland  cells  and  their  secre- 
tion, 23,  25,  27,  90;  antiperistalsis, 
216 

Maly,  HC1  formation,  48 ; bile  and  putre- 
faction, 60 

Mannaberg,  sustenance  of  colon  bacteria, 
70 

Marfan,  stomach  in  pulmonary  diseases, 

387 

Martin,  interaction  of  secretions,  66 ; 
gastric  absorption,  93  ; detection  of 
sarcinse,  129  ; gastritis,  415  ; anthrax 
gastritis,  439  ; ulcerations,  491 


884  LIST  OF  AUTHORS. 


Martius,  secretions  in  the  fasting  stomach, 
148,  149;  HC1  determination,  166; 
insufficiency  of  secretion,  329,  330, 
850 

Mathieu,  total  quantity  of  gastric  contents, 
150;  gastritis,  415  ; acidity  of  the 
urine  and  gastric  contents,  820 
Mayer,  gastric  vertigo,  378 ; autodigestion, 
488 

McCall,  treatment  of  ulcer  by  nutritive 
enemata,  206 

Meckel,  J.  E.,  vertical  position  of  stomach, 
697 

Mehring,  von,  starch  digestion,  46  ; gas- 
tric absorption,  65,  91,  93,  95,  191  ; 
analysis  for  fatty  acids,  172 
Meinert,  acute  gastritis,  429 
Meisenbach,  foreign  bodies  in  stomach, 
613 

Meltzer,  S.  J.,  electrical  stimulation,  79, 
305,  364;  absorption,  91  ; electricity 
in  chronic  gastritis,  472  ; subphrenic 
abscess,  5 11  ; congenital  pyloric  ste- 
nosis, 657,  660 

Meltzing,  gastrodiaphany,  107,  108 
Mendel,  alcohol  and  digestion,  290 
Mensche,  bitter  tonic  treatment,  340 
Menzel,  hypodermic  feeding,  219 
Merrem,  stomach  surgery,  348 
Meschede,  gastritis  parasitaria,  440 
Mesnil,  du,  alkali  therapy,  334 
Metschnikoff,  interaction  among  bacteria, 
62 

Meyer,  G , HC1  in  gastric  therapy,  330 
Michaelis,  gastric  hemorrhage,  516 
Michel,  gastric  hemorrhage,  5 15 
Mikulicz,  gastroscopy,  178;  statistics  in 
gastrectomy  and  gastrotomy,  353 ; 
pyloroplasty,  363 

Miller,  mouth  microbes,  63 ; absorption, 

95 

Milliot,  transillumination,  104 
Minassian,  H.  A.,  merycism,  768 
Minkowski,  bacteria  in  the  stomach,  130 
dietetics,  202 

Mintz,  HC1  as  a remedial  agent,  331 ; 
pylorectomy,  359 

Mitchell,  Weir,  fattening  rest  cure,  207 
Miura,  alcohol  as  a food,  288,  289 
Morau,  HC1  in  gastric  antisepsis,  63 
Moritz,  stomach  support,  19  ; intragastric 
apparatus,  76,  82  ; circulation  of  gas- 
tric ingesta,  89  ; dietetics,  194 
Morris,  Henry,  gastrotomy,  352 
Moss,  analysis  of  a man,  220 ; percentage 
nutrition  of  foods,  224 
Muller,  peptone  test,  177  ; intestinal  auto- 
intoxication, 375 

Munk,  J.,  bile  and  absorption,  60  ; prepar- 
ation of  food,  193 
Murphy,  surgery,  368 
Murray,  lipoma,  608 


N. 

Naunyn,  abnormal  retention  of  ingesta,  201 
Nencki,  bile,  agency  of,  in  pancreatic  diges- 
tion, 60;  fat  decomposition,  61  ; bac- 
teria in  digestion,  62  ; ileum  contents, 
67 

Neubauer,  absorption,  97 
Neumeister,  schemata  of  digestion  : amylol- 
ytic,  46 ; proteolytic,  49,  58 ; biliary 
diastatic  ferment,  59 

Noorden,  von,  deficiency  of  gastric  juice 
and  health,  329  ; HC1  therapy,  330 ; 
malnutrition,  374  ; gastric  crises,  757, 

835 

Nothnagel,  antiperistalsis,  212,  213;  in- 
sufficient secretion,  330 ; gastric  in- 
flammatory atrophy,  450 
Novarro,  gastro-enterostomy,  367 
Nuttal,  bacteria,  not  essential  to  digestion, 
62 

O. 

Obalinski,  secretory  and  motor  functions 
as  affected  by  surgical  operations,  358 
Ogata,  albumin  as  food,  209 
Oppel,  anatomy  of  the  stomach,  17;  gas- 
tric glands,  25  ; achylia  gastrica,  859 
Oppler,  gastrodiaphany,  109 ; sarcinae, 
129  ; asthma  dyspepticum,  382  ; achy- 
lia gastrica,  857 
Oppolzer,  gastromalacia,  487 
Orth,  acute  gastritis,  422;  infectious  gas- 
tritis, 439  ; gastritis  polyposa,  445  ; 
carcinoma,  527  et  seq.  ; infectious 
granulomata,  590 

Oser,  infectious  gastritis,  438  ; faradic  cur- 
rent in  gastralgia,  805 
Osier,  gastric  atrophy  and  pernicious 
anemia,  330,  854;  carcinoma,  368; 
acute  gastritis,  416,  428  ; chronic  gas- 
tritis, 450;  abdominal  tumors,  554, 
555 > 558  ; tubercular  ulcer,  592  ; dila- 
tion, 637;  splanchnoptosis,  720 
Ott,  infusion  treatment  for  ulcer,  516  t 


P. 

Pancanowski,  location  of  the  stomach,  779 
Panecki,  gastralgia  and  the  uterus,  800 
Panum,  gastromalacia,  489 
Park,  Roswell,  cancer,  543 
Pasteur,  bacteria  in  digestion,  6 1 
Pavy,  self-digestion,  488 
Pawlow,  innervation  of  gastric  glands,  48  ; 
738  ; secretory  nerve  of  pancreas,  48  ; 
gastric  secretion,  197 
Pean,  resection,  349 

Pedioux,  cutaneous  diseases  and  the  stom- 
ach, 396 

Penzoldt,  absorption,  92  ; stomach- tube, 
1 17;  dietetics,  194,  203;  dietaries, 
228-231,  235,  241  ; bitter  tonics,  339  ; 


LIST  OF  AUTHORS. 


885 


gastritis,  415  ; dilation,  631  ; hunger, 
814 

Pepper,  effect  of  electricity  on  peristalsis, 
302 ; dilation,  637 
Perco,  hypodermic  feeding,  219 
Perry,  E.  C\,  intestinal  stenosis,  719 
Petruscky,  tuberculous  ulcer,  515,  594 
Pettenkofer,  bile-acid  demonstration,  133 
Peyer,  bulimia,  809  ; gastralgia  and  genito- 
urinary diseases,  800 
Pliaff,  bile,  59 

Pick,  secretion  in  the  empty  stomach,  148; 
gastritis,  416  ; autointoxication  in  di- 
lation, 634 

Pitt,  lymphadenoma,  609 
Playfair,  fattening  rest  cure,  207 
Podwyssozki,  pepsin  production,  27 
Posner,  bacterial  invasion  of  bowel  wall, 
64 

Potain,  asthma  dyspepticum,  383 
Preuschen,  von,  melaena  neonatorum,  686 
Pribam,  gastric  vertigo,  378 
Prudden,  acute  gastritis,  423 

Q. 

Quincke,  insufficient  secretion,  330 ; 
chronic  gastritis,  450  ; ulcer,  491 

R. 

Rachford,  digestion  in  the  duodenum,  330 
Ranke,  bile,  59 
Ranvier,  lymphadenoma,  590 
Rauber,  villi,  34 
Reaumur,  stomach  contents,  52 
Reiche,  hour-glass  stomach  and  ulcer,  510 
Reichert,  alcohol  as  a food.  288 
Reichmann, transillumination,  106;  gastric 
secretion,  149 ; HC1  as  a medicinal 
agent,  331  ; alkali  therapy,  336  ; bitter 
tonics,  339 ; gastrosuccorrhea,  334, 
836,  858 

Remond,  stomach  secretion,  149,  150 ; 

hour-glass  stomach,  643 
Remsen,  Ira,  mineral  spring  water,  470 
Richards,  Mrs.  E.  H.,  rations,  225 
Richardson,  gastrectomy,  361 
Richet,  acid  and  pepsin,  28 
Rieder,  cancer,  562 

Riegel,  peristalsis  test,  71  ; determination 
of  location,  Size,  and  capacity  of  the 
stomach,  methods,  9,  102,  106; 

test-meal,  121  ; sarcinse,  1 29 ; Oppler- 
Boas  bacillus,  130;  secretion  in  the 
■ fasting  stomach,  149 ; nutritive  ene- 
mata,  206,  212;  predigested  foods, 
209 ; gastric  douche,  3C0 ; massage, 
309  ; hyperacidity  and  ulcer,  501  ; 
HC1  in  therapeutics,  330;  bitter 
tonics,  340 ; asthma  dyspepticum, 
381  ; hypersecretion,  832,  840 
58 


Rillet,  melama  neonatorum,  685 
Rindfleisch,  ulcer,  490 
Ritter,  gastromalacia,  489 
Roberts,  Sir  William,  effects  of  cooking 
on  food,  250;  “indications  of  the 
palate,”  251  ; alcohol  in  digestion, 
292,  296,  297  ; hyperacidity,  818 
Rockwell,  electrotherapy,  302 
Rohmann,  bile  and  intestinal  peristalsis, 
60 

Rokitansky,  gastromalacia,  488 
Rollet,  gastric  gland  cells,  22,  26 
Romeyn,  alcohol  and  metabolism,  289 
Rondeau,  myoma,  609 
Roseman,  alcohol  and  metabolism,  289 
Rosenbach,  asthma  dyspepticum,  381 
Rosengarth,  Jos.,  pathogenesis  of  entero- 
ptosis,  702 

Rosenheim,  gastric  cells,  22 ; stomach- 
tube,  1 1 7 ; gastroscopy,  178,  181, 

184;  pancreatic  ferment,  215  ; gastric 
douche,  299;  massage,  309;  secre- 
tion and  the  motor  function  following 
surgical  operations, 358  ; gastritis,  4 1 5 ; 
chronic  gastritis,  450  ; carcinomatous 
ulcer,  510,  560  ; carcinoma  diet,  575  ; 
gastralgia  and  median  hernia,  800 
Rosenstein,  stomach  in  diabetes  mellitus, 
391 

Rosenthal,  hydrotherapy,  308;  anorexia, 
815  ; gastroxynsis,  834 
Rosin,  secretion  in  the  jejune  stomach, 
148 

Rossbach,  gastroxynsis,  834 
Rossi,  electric  stimulation  to  secretion,  302 
Rotch,  acute  gastritis,  421 
Roth,  gastralgia  and  median  hernia,  801 
Roux,  W.,  proteids  and  carbohydrates  in 
hyperchlorhydria,  196 
Rummo,  carbohydrates  vs.  proteids  in  the 
treatment  of  hyperacidity,  196 
Runeberg,  artificial  stomach  distention,  99 
Rupp,  resection,  361 
Ruysch,  cysts,  610 
Rydygier,  resection,  349 


S. 

Sachs,  achylia  gastrica,  858 
Salkowsky,  absorption  test,  97 
Salzer,  Henry,  test-meal,  121,  124 
Scammell,  relative  value  of  foods,  223 
Schafer,  absorption  of  fats,  56 
Schech,  the  mouth  in  gastritis,  456 
Scheperlen,  chronic  gastritis,  450 
Schetty,  acute  gastritis,  422 
Schiff,  pepsin  and  acid,  27  ; gastric  ulcer, 
488 ; stomach  in  nervous  diseases, 
385 

Schillbach,  electricity  and  peristalsis,  302 
Schlatter,  gastrectomy,  361 
Schlesinger,  Oppler-Boas  bacillus,  130; 
sarcoma,  546 


886 


LIST  OF  AUTHORS. 


Schmidt,  Adolph,  digestibility  of  mucus, 
1 31  ; mucosa  in  gastric  diseases,  146 ; 
alcohol  and  metabolism,  289 
Schmidt,  F.,  gastric  fever,  427 
Schmidt,  H.,  nephroptosis,  714 
Schmidt,  John,  frequency  of  dislocated 
kidney,  721 

Schonborn,  foreign  bodies  in  the  stomach, 
611 

Schreiber,  secretions  in  the  fasting  stom- 
ach, 148,  149,  836,  840;  dilation, 
457  5 gastrosuccorrhea,  838 
Schreiner,  Dr.  E.  R.,  diet-list,  192 
Schuchardt,  pylorectomy,  360 
Schiitz,  peristalsis,  83 
Schwartz,  infusion  of  salt  solution  in  hem- 
orrhage from  ulcer,  516 
See,  Germain,  test-meal,  121 ; alkali  treat- 
ment, 338 

Sehrwald,  physiology  of  cells,  23 
Seifert,  the  mouth  in  gastritis,  456 
Senator,  asthma  dyspepticum,  384  ; gas- 
tritis parasitaria,  440 

Senn,  N.,  gastric  distention  with  hydro- 
gen, 367  ; bone  plates,  368 
Shaw,  L.  E.,  intestinal  stenosis,  719 
Sieber,  bacteria  in  the  digestive  economy, 
62,  69  ; contents  of  ileum,  67 
Sievers,  gastric  motor  function,  71 
Silbermann,  asthma  dyspepticum,  381  ; 

ulcer,  489  ; melsena  neonatorum,  686 
Simon,  Chas.  E.,  indican  in  gastric  dis- 
eases, 197  ; HC1  therapy,  332  ; urine 
in  stomach-diseases,  410 
Smith,  E.  E.,  neurasthenia  gastrica,  869 
Sohlern,  von,  carbohydrates  vs.  proteids  in 
hyperacidity,  196 

Sohnan,  gastric  functions  affected  by  surgi- 
cal operations,  358 
Spalteholz,  gastric  anatomy,  17 
Stammreich,  alcohol  and  metabolism,  289 
Stansfield,  gastro-enterostomy,  368 
Stein,  absorption  from  the  stomach,  747 
Stern,  stomach  in  heart-disease,  389 
Stewart,  D.  D.,  neuroses,  effect  of  elec- 
tricity on,  306 ; ulcus  carcinomatosum, 
560;  relation  of  anemia  to  gastric 
atrophy,  854 

Stiller,  enteroptosis,  702 ; pylorospasm, 
746;  nervous  vomiting,  759  ; hunger, 
806  ; nervous  dyspepsia,  866 
Stintzing,  dietetics,  203 
Stockton,  Chas.  G. , neuroses — electricity, 
3°3>  3°6 

Stokes,  chronic  hypertrophic  gastritis,  445 
Strauss,  Herman,  lavage,  120  ; total  acid- 
ity, 123;  gastric  secretion,  150;  lac- 
tic acid  test,  168;  diet  in  hyperacid- 
ity, 829  ; achylia  gastrica,  850 
Streit,  gastric  operations,  358 
Strieker,  ulcer,  487 

Strobe,  mitoses  in  gastric  carcinoma,  563 
Strumpell,  asthma  dyspepticum,  381 


Swieten,  von,  dilation,  202 
Swiezicki,  von,  cell  physiology,  23 
Swiezynski,  antiperistalsis,  213 


T. 

Talma,  hyperesthesia  toward  HC1,  333 ; 

gastric  ulcer,  489 
Tanchon,  cancer  statistics,  544 
Tappeiner,  gastric  absorption,  91,  93 
Thierfelder,  bacterial  relation  to  digestion, 
62 

Thomas,  T.  G.,  intravascular  feeding,  218 
Thompson,  Gilman,  food  classes,  43  ; die- 
tetics, 193 ; intravascular  feeding, 
281;  dietetics  of  alcohol,  288;  min- 
eral springs,  313  et  seq. 

Tinker,  ulcer  statistics,  515 
Topfer,  free  H Cl  estimation,  163 
Treheux,  acidity  of  the  urine  and  gastric 
contents,  820 

Trousseau,  gastric  vertigo,  377 
Turck,  F.  B.,  bacteria,  128;  pyloric  intu- 
bation, 642 


U. 

Uffelmann,  lactic  acid  test,  161  j;  dietetics, 
193 

V. 

Velden,  von  der,  secretion,  gastric,  in  neo- 
plasms, 550 

Virchow,  erosions  of  mucosa,  136;  ulcer, 
488,  489 ; splanchnoptosis,  707  ; en- 
teroptosis, 708 

Vogel,  absorption  test,  97 

Voit,  bile,  59,  60 ; rectal  alimentation, 

311 

Vulpius,  gastralgia  and  median  hernia, 
800 


W. 

Waldeyer,  cancer,  540 
Wassmann,  gastric  glands,  25 
Weber,  guaiacum  test,  134 ; electricity  as 
a stimulus  to  peristalsis,  302 
Wegele,  dietetics,  194  et  seq.;  electric 
therapy,  303 

Weir,  Robert  F. , ulcer,  515 
Welch,  William  H.,  chronic  gastritis,  450  ; 
ulcer,  494,  495 ; carcinoma,  537  > 
vicarious  hemorrhage  from  stomach, 
683  ; nephritis  and  fatal  gastric  hem- 
orrhage, 685  ; idiopathic  gastric  hem- 
orrhage, 687  ; achylia  gastrica,  854 
Welti,  ulcer,  489 

Westphalen,  gastro-enterostomy,  479 
Whitney,  Edward  L. , gastric  absorption, 


LIST  OF  AUTHORS. 


887 


97 ; chemistry  of  gastric  digestion, 
148  et  see].;  the  blood  and  urine  in 
stomach-diseases,  400-413;  gases  of 
the  stomach,  404  ; heterochylia,  870 
Whittaker,  subcutaneous  feeding,  219 
Widal,  acute  gastritis,  427 
Wiel,  dietetics,  193 
Williams,  pancreatic  juice,  66 
Winniwarter,  von,  surgical  treatment,  348 
Winslow,  Professor  Randolph,  gastroplica- 
tion,  365 

Wisting,  von,  bile  function,  60 

Wittich,  bile,  59 

Witzel,  gastrotomy,  352 

Wolf,  L.,  bitter  tonics  and  secretion,  339 

Wolfler,  surgery,  349,  362,  365 

Woltering,  dietetics,  194 

Woodruff,  C.  E.,  food  rations,  227 

Wurtz,  papain,  346 


Y. 

Yeo,  dietetics,  194  ; food  energy,  226 
Yeo,  Burney,  gout  and  dyspepsia,  391 


Z. 

Zabludowsky,  massage,  309,  3 1 1 
Zawadski,  secretion  and  peristalsis  in  sur- 
gery, 358 

Zawardsky,  pancreatic  secretion,  56 
Zesas,  gastrostomy,  353,  368 
Ziegler,  acute  gastritis,  423,  434 
Ziemssen,  von,  gastric  secretion,  180  ; elec- 
tricity and  secretion,  302 ; hydro- 
therapy, 308  ; massage,  309 ; gas- 
tritis, 472 ; ulcer,  512 
Zweifel,  pancreas  diastase,  56 ; gastric 
absorption,  93,  94 


LIST  OF  SUBJECTS. 


Compiled  by  Dr.  Henry  IV.  Nolle  and  Mr.  Thomas  II.  Cannon . 


A. 

Abdominal  regulatory  center,  378 
Abscess,  gastric  (see  Gastritis,  Phleg- 
monous); subphrenic,  510 
Absorption  : of  various  substances,  65  ^de- 
pendence on  the  motor  func- 
tion, 70,  90;  variations  in, 
90  ; testing  methods,  92  ; a 
conditioning  factor  in  diet, 
189, 191 ; influence  of  alcohol, 
2 94 

Acetic  acid  : intestinal  fermentation,  61  ; 
analysis,  163 

Acetone,  412 

Achlorhydria,  850 

Achroodextrin,  45,  46 

Achylia  gastrica  : nature  and  concept,  850  ; 

symptoms,  856;  patho- 
logical histology,  858 ; 
etiology,  861  ; treatment, 
862 

Acidity:  as  affected  by  test-meals,  and 
climatic,  barometric,  and  geo- 
graphic factors,  122,  123,  124; 
of  the  urine  and  gastric  contents, 
820 

Acids:  acetic,  61,  163;  action  of  succus 
entericus,  61  ; amido-,  42,  61  ; 
asparaginic,  57  ; aspartic,  58;  bile, 
65  (detection  in  stomach  contents), 
132  ; butyric,  57,  61,  162  ; caproic, 
61  ; carbonic,  61  ; diacetic,  412; 
fatty,  57,  61,  170;  fatty,  quantita- 
tive estimation  of,  170;  free  (tests), 
156 ; hydrochloric  (see  Hydro- 
chloric Acid) ; lactic,  61,  130,  160, 
168,  169,  564,  565  ; nitrogen-free 
vegetable,  42  ; organic  free,  48 ; 
organic  total  (estimation),  170; 
oxyacids,  6 1 ; phenylacetic,  61  ; 
phenyl  propionic,  61  ; skatol  car- 
bonic, 61  ; stomach  acids  (analysis), 
163  ; valerianic,  61 
Acoria,  81 1 
Adenocarcinoma,  527 
Adenoma,  pedunculated,  610 
Albumin,  acid  (see  Syntonin) 


Albuminoid  decomposition,  67 
Albuminous  substances  (see  Proteids  and 
Albumins) 

Albumins:  digestion — peptic, 48, 49 ; tryp- 
tic, 57,  58 

influence  on  biliary  secretion, 
59;  bile  action  on,  60 ; re- 
lation to  succus  entericus, 
60 ; in  treatment  of  hyperse- 
cretion and  hyperacidity,  194- 
198,  246,  247,  248;  in  urine 
the  result  of  gastric  disorders, 
412 

Albumoses,  62 

Alcohol : in  food  substances,  42  ; an  intes- 
tinal fermentation  product,  6 1 ; 
gastric  absorbability  of,  65  ; diet- 
etics, 287 ; effects  of,  on  meta- 
bolism, 289  ; action  of,  on  peptic 
digestion,  290  ; action  of,  on  pan- 
creatic digestion,  292;  action  of, 
on  salivary  digestion  and  on  the 
motility,  293 ; absorption  affected, 
294 ; summary  of  action,  294, 
295 ; in  certain  pathological 
states,  295  ; Sir  Win.  Roberts’ 
theory  in  respect  to  alcoholic  re- 
tardation of  digestion,  296 
Alimentation,  rectal  (see  Enemata,  Nutri- 
tive) 

Alkalies,  medicinal  agents,  334 
Alkalinity  of  the  blood,  403 
Alkaloids,  42 
Alveoli,  21 
Amidulin,  45,  46 
Ammonia,  61 
Amphopeptone,  49,  58 
Amylaceous  foods  in  hyperacidity,  194- 
198,  248,  828;  in  hy- 
persecretion, 248,  828 
Amylodextrin,  45,  46 
Amyloid  degeneration  of  the  stomach,  464 
Amylolysis : bile  in,  66 ; hyperchylia,  its 
influence  on,  718  ; pancreatic, 
56  ; ptyalic,  44-47,  60 
Amylopsin,  56,  66 

Anacidity  : dietetics,  198  ; indol  formation 
and  putrefaction,  332 


890 


LIST  OF  SUBJECTS. 


Anadenia  ventriculi,  850 
Analysis  : stomach  contents,  technic,  114, 
1 16;  methods, 
127; 

quantitative  chemical,  15 1 ; of 
gastric  juice,  156;  of  stomach 
acids,  163,  17 1 

Anemia  and  gastric  affections,  386,  512, 
853  . 

Anorexia,  nervous:  dietetics,  190;  the 

clinic  of,  814 

Antipeptone,  58 
Antiperistalsis,  211-213 
Antisepsis  of  the  digestive  tract,  47,  64, 
249 

Antizymotics  (see  agents  under  Anti- 
sepsis) 

Antrum  pylori,  18,  83 
Appetite,  anomalies  of  the  sensation  of, 
806 

Asthma  dyspepticum,  381 
Atony  : 

gastric,  myasthenic  : terminology, 
etiology,  etc.,  624, 
625,  629  ; differential 
diagnosis,  639  ; prog- 
nosis, 642 ; treatment, 
dietetic,  201,  207, 
235?.  237,  645-652; 
medicinal,  etc.,  645- 
647 

gastric,  neurotic : definition  and 
etiology,  774-776; 
symptomatology,  776— 
781  ; prognosis  and 
diagnosis,  781  ; treat- 
ment, 781-786  (see 
Dietetic  under  Myas- 
thenic Type) 

Atresia,  643 

Atrophy  of  the  stomach,  850 
Auerbach,  plexus  of,  38 
Autochthonous  vegetation,  63 
Autodigestion,  gastric,  487 
Autointoxication,  intestinal,  65 


B. 

Bacteria : fermentation  and  putrefaction, 
56,61,66,  68,  130;  economic 
and  pathogenic  significance,  62, 
64,  128-130;  species,  61,  62- 
69,  120,  439  ; source  of  food  for 
the  colon  flora,  69  ; analysis  of 
stomach  contents  for,  128,  129  ; 
in  the  walls  of  the  stomach, 
128  ; HC1  and  peristalsis  as  re- 
lated to  propagation  of,  128; 
products  giving  rise  to  patholog- 
ical conditions,  130 

Bag,  intragastric, stomach-shaped,  of  Hem- 
meter,  76,  79-82,  89 

Basement  membrane,  34,  35 


Bile  : composition,  59  ; uses  and  functions, 
59,  60,  65,  66;  detection,  132 
Blood:  supply  to  the  stomach,  28-31; 

supply  to  the  intestines,  32,  34, 
37  ; in  stomach  contents,  tests  for, 
1 33,  134;  in  gastric  diseases,  400- 
404 

Boas’  method,  analysis  of  stomach  acids, 
168 

Braun’s  method,  1 70 

Bulb  for  aspirating  test-meals,  117 

Bulimia : dietetics,  189 ; nature,  806 ; 

causation,  808 ; symptomatol- 
ogy, 809  ; diagnosis,  810  ; treat- 
ment, 813 

Butyric  acid  : steapsin  digestion,  57  ; in 
putrefaction^  61  ; analysis, 
162 


C. 

Calcium,  42 

Cancer  (see  Carcinoma) 

Carbohydrates : economic  function,  42 ; 

effect  on  bile  efflux,  59  ; 
absorption  of,  in  presence 
of  bile,  60;  fermentation, 
61,  62,  67  ; action  of  the 
succus  entericus,  69 ; in 
hyperacidity  and  hyper- 
secretion, 194-198,  247, 
248,  829 

Carbolic  acid,  61 
Carbon,  41 

Carcinoma  : germ  growth  in  walls  of  stom- 
ach in,  128;  blood  changes, 
404;  pathology,  527;  eti- 
ology, 540 ; symptomatology, 
547-561 ; diagnosis,  561-575  ; 
treatment,  203,  240,  568,  570, 
572,  576;  indications  for 

operation,  356 ; prognosis, 
577  ; differential  diagnosis  (see 
Table),  587  ; adeno-,  527 ; col- 
loid, 535;  duodenal,  558; 
medullary,  530;  pancreas, 
557  ; scirrhous,  533,  534 
Cardia  : anatomy  of  the,  18 ; carcinoma  of 
the,  566;  obstruction  of,  652  ; ob- 
struction of,  forms  of,  653  ; symp- 
tomatology, 654;  diagnosis,  654; 
prognosis,  655;  treatment,  655; 
cramp  of  the,  739  ; incontinence 
of  the,  764 
Cardiospasm,  739 
Caroid,  346 

Casein,  51,  57  ; peptones,  57 
Catarrh,  gastric,  234,  235,  443 
Cecum,  40 

Celiac  axis,  28  ; plexus,  38 
Cells : acid,  24 ; adelomorphous,  22 ; 

anilin-staining,  24 ; border,  22,  23, 
24,  27,  28  ; central,  22-24,  27>  2$  ; 


LIST  OF  SUBJECTS. 


89I 


chief,  22-24,  25,  26;  columnar 
epithelial,  21,  32,  35  ; cuboidal 
epithelial,  21  ; cylindrical  epi- 
thelial, 22;  delomorphous,  23; 
eosinophilic,  35  ; epithelial  of  villi, 
35,61;  ferment,  24;  goblet,  36; 
mucous  or  mucin,  21,  22,  26; 
neoplasm,  562  ; Nussbaum’s,  23  ; 
oxyntic,  22,  23;  parietal,  22,  23; 
pyloric  gland,  25 
Cerebral  vomiting,  756 
Chlorids:  in  gastric  HC1  production,  49 ; 

in  urinary  changes,  408 
Chlorin,  42 

Chlorosis  and  gastric  diseases,  386 
Cholelithiasis,  509 
Chyme,  55,  59,  65,  66 
Chymosin  (see  Rennin) 

Cirrhosis:  gastric,  614;  ventriculi,  445, 
553 

Clinic,  the  gastric,  414 
Clysters  (see  Enemata) 

Colon,  40;  diaphany,  105;  observations 
on  dislocation  of,  698 
Coloptosis,  724 
Coma  carcinomatosum,  559 
Constipation,  chronic,  dietetics  in,  245 
Convulsions  of  the  pylorus,  746  ; of  the 
stomach,  748 
Cooking,  dietetical,  253 
Coprostasis,  709 
Coronaria  ventriculi  artery,  30 
Cramp  of  the  cardia,  739  ; of  the  pylorus, 
746 

Creatin,  42 
Crises,  gastric,  757 
Cysts,  gastric,  610 


D. 

Deutero-albumoses,  58 
Deuteroproteoses,  49 

Dextrin  : digestion  product,  ptyalic,  45,  46, 
47 ; amylolytic,  56  ; absorption  of, 

65 

Dextrose,  45-47 

Diabetes  mellitus  and  state  of  the  stomach, 
391 

Diagnosis,  differential,  of  cancer,  ulcer, 
gastralgia,  hyperchlorhydria,  and  gas- 
tritis (see  Table),  587 
Diaphany  of  stomach,  104;  colon,  105; 

duodenum,  105  ; ileum,  106 
Diarrhea,  chronic,  diet,  243-245 
Diastase : of  saliva,  44,  45  ; in  bile,  59  ; 

of  pancreas,  56,  66  ; as  a medic- 
inal agent,  343 

Diazo  reaction,  Ehrlich’s,  413 
Dietetic  exercise,  283 
Dietetics  : historical  retrospect,  185  ; diges- 
tibility, 186;  gastric  functions 
conditioning  diet,  sensation, 
189  ; absorption,  19 1 ; secre- 


tion, 194;  motility,  201 ; hyper- 
secretion and  hyperacidity,  194- 
198 ; anacidity  or  subacidity, 
198;  ulcer,  195,205;  gastritis 
acida,  195  ; ulcus  carcinomato- 
sum, 195,  203;  atony  and  dila- 
tion, 201  ; carcinoma,  203 ; 
neuroses,  207  ; fattening  cures, 
207;  predigested  foods,  208; 
rectal  alimentation,  210 ; intra- 
vascular and  hypodermic  feed- 
ing, 218;  tables  of  dietaries, 
220;  diet  lists,  228;  cooking  of 
food  and  the  palate,  250-254 ; 
rectal  enemata,  varieties  of, 
280  ; alcohol  and  alcoholic  bev- 
erages, 287 ; drinks  and  liquid 
foods,  254 

Diet  lists : Penzoldt’s,  for  the  gradual 
training  of  the  digestive  ca- 
pacity, 228 ; Ewald’s  and 
Boas’,  231  ; Hemmeter’s, 
chronic  gastritis,  etc.,  232 ; 
Wegele’s,  chronic  catarrh, 
234 ; Wegele’s  gastric  atony, 
235,  237 ; Hemmeter’s,  for 
anacid  dilation,  236 ; carci- 
noma, 240  ; ulcer,  241  ; 
chronic  diarrhea,  243  ; hyper- 
acidity, 246 ; hypersecretion, 
247  ; intestinal  antisepsis,  neu- 
rasthenia, and  neuroses,  249  ; 
and  dyspepsia  on  hysterical 
basis,  249 

Digestion  : alcohol  retardation  of,  theory 
of  Sir  William  Roberts,  296  ; 
amylolytic,  44,  47,  56,  59,  66  ; 
fat,  57>  59  5 intestinal,  52,  70, 
826;  pancreatic,  55,  58,  292; 
peptic,  47-52,  290,  295,  296  ; 
proteolytic,  47-52,  58 ; pty- 
alin,  44,  45,  60,  171,  293  ; ren- 
nin, 51,  174,  175  ; salivary, 
44,  45,  171,  293;  starch,  45, 
46,  47,  56,  60;  steapsin,  57; 
tryptic,  57,  58 

Digestive  disturbances  in  connection  with 
renal  diseases,  394 

Dilation,  gastric : classification  and  nomen- 
clature, 624;  obstructed 
form,  625  ; differential 
diagnosis,  639 ; progno- 
sis, 642;  treatment,  201, 
235-238,  647,  652; 

atonic  form,  629  ; differ- 
ential diagnosis,  640; 
treatment,  201,  236,  237, 
645,  652  ; diagnosis  by 
gastrodiaphany,  106-108 

Dilator  pylori,  20 

Dimethyl-amido-azo-benzol  test,  157 

Disinfection  of  digestive  tract,  47,  64,  249 

Divulsion,  digital,  of  the  pylorus,  364 

Douche,  the  gastric,  299 


892 


LIST  OF  SUBJECTS. 


Drinks  and  liquid  foods,  254 
Duodenal  intubation,  52-55  ; secretion, 
interaction,  65,  66  ; secretion, 
detection,  133 
Duodenodiaphany,  106 
Duodenum,  31,  32,  38 
Dyspepsia,  nervous  : nature  and  concept, 
865  ; pathology  and 
etiology,  866  : symp- 
tomatology,  867; 
prognosis,  870 ; diag- 
nosis, 869  ; hetero- 
chylia,  870 ; differ- 
ential diagnosis,  871 ; 
treatment,  249,  872 


E. 

Elastin,  47,  57  ; peptones,  47,  57 
Elastoses,  57 

Electric  stimulation  of  peristalsis,  79-82 
Electricity  in  gastric  therapy,  301  et  seq. 
Electrodiaphane,  105 

Electrodiaphany,  104-112;  criticism  and 
limitations  of  the  method, 
108-1 1 1 

Electrode,  intragastric,  Einhorn’s,  303 
Enemata  : dilation,  202  ; evolution  of,  210; 

ulcer,  205  ; antiperistalsis,  2 1 2, 
21 3 ; digestion  of,  214 ; prepara- 
tion and  administration,  216, 
217;  indications  for  nutritive 
kind,  217;  kinds  of  nutritive, 
280 

Enterodiaphany,  105 

Enteroptosis : etiology  and  symptomat- 

ology, 695-7 1 1 ; historical 
view  of,  700 : treatment, 
726 

Enzymes  (see  Ferments) 

Epileptiform  convulsions,  379 
Erosions,  gastric,  dietetic  treatment,  205 
Eructation,  nervous,  754 
Erythrodextrin,  45,  46 
Esophageal  applicator,  183  ; forceps,  183  ; 

tubal  probe,  1 21 
Esophagoscope,  183 
Ethereal  oils,  42 
Ewald  tube,  124 

Examination  of  stomach  patients,  schema, 

877 


F. 

Faradization,  304,  306 
Fasciae  teniae,  40 

Fats  : economic  import,  43  ; in  pancreatic 
digestion,  57;  effect  on  flow  of  bile, 
59;  bile  action,  60 ; action  on  suc- 
cus  entericus,  60 ; bacterial  action, 

61 


Fatty  acids:  pancreatic  digestion,  57; 

bacterial  product,  61  ; 
analysis,  1 70 

Feeding,  rectal  (see  Enemata,  Nutritive) 
Fermentation : relation  to  the  economy, 
62;  products,  61,  67;  in- 
hibiting agents,  128;  in 
gastrectasia,  15 1 

Ferments:  amylolytic,  44,  45,  56,  60,  66, 
17 1,  342;  amylopsin,  56,  66; 
artificial,  342 ; bacteria  (see 
Bacteria);  diastatic,  44,  45, 

56,  59,  66,  343;  inverting  (of 
succus  entericus),  60 ; milk- 
precipitating  (pancreatic),  56; 
pancreatic  diastase,  56  ; pan- 
creatin  (medicinal  agent),  344  ; 
pepsin  (see  Pepsin) ; pepsin- 
ogen (see  Proenzymes) ; pine- 
apple, 347 ; proteolytic,  49, 

57,  213;  prozymogen,  25,  26; 
ptyalin,  44,  45,  60,  171,  342; 
rennin  (see  Rennin)  ; rennin- 
zymogen  (see  Proenzymes)  ; 
steapsin,  57,  60 ; trypsin,  58, 
66,  67,  68,  69,  70;  interaction, 
65,  70;  tests,  171  ; in  urine, 
413 

Fibromata,  606 

Food  substance : constituents,  and  their 
relation  to  the  economy, 
41,  42;  food  groups  of 
Gilman  Thompson,  43  ; 
kinds  of  food  values,  43 ; 
combining  power  with 
HC1,  248;  drinks  and 
liquid  foods,  254 
Foreign  bodies  in  the  stomach,  610 
Fundus  of  stomach,  18 
Fungi  (see  Bacteria) 


G. 

Galvanization,  306 

Gases:  acetylene,  405;  carbonic  acid,  61, 
404,  405  ; hydrogen,  41,  61,  405  ; 
hydrogen  sulphid,  61,  405  ; marsh,' 
405  ; methyl  mercaptan,  6 1 ; ni- 
trogen, 405,  41 1 ; oxygen,  405; 
“ stomach,”  151,  404 
Gastralgia:  description,  798;  causation, 
799  > types,  801,  802;  symp- 
tomatology, 802 ; diagnosis, 
803  ; differential  diagnosis, 
587  ; treatment,  805  ; idio- 
pathic, 801  ; secondary,  802 
Gastralgokenosis,  806 
Gastrectasia  (see  Dilation,  Gastric) 
Gastrectomy,  361 

Gastric  crises,  757  ; diseases,  influence 
upon  other  organs  and  metabolism, 
374 ; douche,  299  ; idiosyncrasies, 


LIST  OF  SUBJECTS. 


893 


797 ; juice,  physiology,  22,  47, 
52;  stimulation,  148;  chemical 
examination,  156;  periodic  atypi- 
cal flow  of,  834  ; chronic  continu- 
ous flow,  857  ; absence  of  secre- 
tion, 850 

Gastritis : definition  and  classification  of, 
414;  acida,  458;  dietetics,  194; 
anacida,  458  ; atrophicans,  459  ; 
state  of  blood,  403  ; diet,  232  ; 
mucosa  or  mucipara,  459  ; poly- 
posa,  445 ; syphilitic,  597  ; 
sclerosing,  613  ; stenosing,  614 
acute,  simple : nature  and  con- 
cept, 416;  etiol- 
ogy, 419;  path- 
ological histol 
ogy,  422  ; symp- 
tomatology and 
course,  425  ; di- 
agnosis, 427  ; 
prognosis  and 
treatment,  428, 
429  ; condition 
of  the  blood,  403 
infectious  : gastritis  infectiosa, 
438  ; diphtheritica, 
438  ; mycotica,  439  ; 
parasitaria,  439 
venenata,  441 

phlegmonous  or  purulent,  434 
chronic : concept  and  types, 
443  ; etiology,  445  ; 
pathological  anatomy, 
447  ; symptomatology, 
453 ; complications, 
461  ; atypical  forms, 
462 ; diagnosis,  462  ; 
prognosis,  464 ; differ- 
ential diagnosis,  587  ; 
treatment,  231,  232, 
465  ; blood  changes  in, 
403 

Gastro-anastomosis,  365 
Gastrocolic  ligament,  41 
Gastrodiaphany  of  Einhorn,  104 ; as  an 
aid  to  diagnosis,  III 
Gastrodynia  (see  Gastralgia) 
Gastro-enterostomy,  361,  362 
Gastro-epiploic  arteries,  30 
Gastro-gastrostomy,  365 
Gastrograph  of  Einhcrn,  77;  of  Hemme- 
ter,  77,  79-81,  89 
Gastroliths,  61 1 
Gastrolysis,  351 
Gastromalacia,  487 
Gastropexy,  365 
Gastroplasty,  365 

Gastroptosis : observation  on,  697;  symp- 
tomatology, 723;  diagnosis, 
107,  108,  640,  641,  725  ; 
treatment,  726 

Gastrorrhagia  (see  Hemorrhage  from  the 
Stomach) 


Gastrorrhaphy,  353 
Gastrorrhexis,  635 
Gastroscope,  179 
Gastroscopy,  178 
Gastrospasm,  748 
Gastrostomy,  352 

Gastrosuccorrhea  periodica,  834  ; chronica, 

837 

Gastroiomy,  352 
Gastroxie,  834 
Gastroxynsis,  834 

Gelatin,  47,  57,  60;  peptones,  47,  57 
Gelatoses,  57 

Glands:  agrtiinate,  36,  38  ; Brunner’s,  36; 

crypts  of  Lieberkiihn,  36;  gastric 
follicles,  21,  22  ; lymph-follicles, 
36,  37;  mucous,  21  ; peptic,  22, 
23,  27;  Peyer’s  patches,  36,  38; 
pyloric,  27,  37 ; salivary,  45  ; 
solitary,  36,  38 
Glenard’s  disease,  613 
Globulin,  57 
Glucosids,  42 
Glycerin,  56,  61 
Gmelin’s  test,  132 
Gout  and  gastric  disease,  391 
Granulomatous  infections,  590 
Guaiacum  test,  133 
Gymnastics,  abdominal,  726 


H. 

Heart : disturbances  induced  by  gastric 
diseases,  375 ; cardiac  diseases 
affecting  the  stomach,  389 
Hehner-Seeman  method  of  analysis,  170 
Hemialbumoses  (see  Propeptone) 
Hemipeptone,  58 
Hemoglobin,  402 

Hemorrhage  from  the  stomach,  682  ; eti- 
ology, 682-688  ; pathology, 
688 ; symptomatology,  688  ; 
diagnosis,  691  ; prognosis, 
694 ; treatment,  694 
Hepatocolic  ligament,  40 
Hepatoptosis,  724 
Heterochylia,  870 
Heteroproteose,  49 
Hour-glass  stomach,  510,  643 
Hunger,  anomalies  of  the  sensation  of, 
806 

Hydrochloric  acid:  source,  22-24,  27,  28, 

47,  48;  derivation, 
28,  48  ; action,  28,  47, 

48,  49,  332  ; demon- 
stration, 50 ; in  gastric 
antisepsis,  63,  128; 
interaction  among  se- 
cretions in  the  intes- 
tines, 65,  66  ; tests  for 
HC1,  free,  157;  tests 
for  combined,  159  ; 
combining  capacity  of 


894 


LIST  OF  SUBJECTS. 


foods  with  , 248 ; 
effect  of  alcohol  on 
pepsin-  hydrochloric 
acid  digestion,  290 ; 
as  medicinal  agent, 
328 ; in  neoplasms, 
550;  in  hypersecre- 
tion, 840 

Hydrogen,  41,  61 
Hydronephrosis,  720 
Hydrotherapy,  307 

Hyperacidity:  true  index  of,  124;  defini- 
tion and  types,  196-198  ; 
factor  in  bulimia,  190 ; 
dietetics,  195-198,  246, 

248 ; combining  power  of 
various  foods  with  HC1, 
248 ; relation  to  indican- 
uria,  333  ; factor  in  ulcer, 
491  ; the  clinic  of,  charac- 
teristics, 817  ; etiology, 
822 ; nature  and  concept, 
820  ; symptomatology,  823  ; 
prognosis,  826  ; diagnosis, 
827 ; differential  diagnosis, 
587  ; therapeutics,  828 
Hyperchlorhydria  (see  Hyperacidity) 
Hyperchylia  (see  Hyperacidity) 
Hyperesthesia,  794 ; dietetics,  207 
Hypermotility  as  factor  in  bulimia,  190; 

the  clinic  of,  748 
Hyperorexia  (see  Bulimia) 
Hyperperistalsis,  748 
Hyperplasia,  inflammatory,  447 
Hypersecretion,  chronic,  837 ; dietetics, 
194,  247,  248 
Hypochlorhydria,  847 
Hypochylia,  847 


I. 

Icterus,  catarrhal,  analysis  of  stomach  con- 
tents in,  390 

Idiopathic  gastralgia,  801 
Idiosyncrasies,  gastric,  797 
Ileodiaphany,  105 
Ileum,  40 

Inacidity,  nervous,  850 
Incontinence  of  the  cardia,  764  ; pylorus, 
771 

Indican,  62,  197,  332 
Indicanuria,  332 
Indicators,  152,  154 
Indol,  57,  61,  333 

Inflammation  of  the  stomach,  suppurative 
(see  Gastritis,  Phlegmonous) 

Innutritious  materials  in  food  substances, 
41,  42 

Insufficiency  of  the  cardia,  764  ; of  the  py- 
lorus, 771  ; of  the  stomach, 
mechanical,  774  ; motor,  624 
Intestinal  digestion,  52-70,  128,  826  ; fer- 


mentation, 61.  62,  66,  67,  128; 
putrefaction,  60,  62,  67,  128 
Intestine  : anatomy  of  small,  31-41  ; of 
large,  40 ; duodenal  intubation 
of  Hemmeter,  52-55  ; entero- 
diaphany,  105 ; autointoxica- 
tion and  disinfection,  64 
Intragastric  stomach-shaped  bag  of  Hem- 
meter,  52-55 
Inulin,  56 
Iron,  42,  134 
Ischochymia,  651 

J- 

Jejunum,  31,  40 

K. 

Karyokinesis  in  neoplasms,  527 
Kerkring,  valves  of,  33 
Kidneys : diseases  of,  and  the  state  of  the 
stomach,  392 ; dislocation,  in 
gastroptosis  and  enteroptosis, 
710  ; floating  and  movable,  71 2 ; 
etiology  of,  696  ; palpation,  bi- 
manual, 714;  diagnosis  of  pal- 
pable, movable,  and  dislocated 
kidney,  720  ; treatment,  727 


L. 

Lacteals,  32,  34 

Lactic  acid:  intestinal  fermentation,  61  ; 

bacterial  gastric  product, 
130 ; origin,  significance, 
and  detection,  160;  quanti- 
tative estimation,  168,  169  ; 
diagnostic  value  in  cancer, 
564 ; conditions  necessary 
ior  excessive  formation  of, 

695 

Laparotomy,  exploratory,  357 
Lavage:  double-cut  rent  stomach-tube,  114- 
1 1 7 ; contraindications,  118, 
1 19;  in  dilation,  202,203;  in‘ 
dications  for,  etc.,  297 
Leo’s  method  of  analysis  of  stomach  acids, 
167 

Leucin,  58,  61 
Leukocytosis,  401 
Levulose,  48 
Ligamenta  coli,  41 
Lipoma,  608 

Literature:  on  gastrodiaphany,  112;  on 
the  history  and  technics  of  the 
stomach-tube,  125 ; exfolia- 
tions and  erosions  of  gastric 
mucosa,  138  ; correlation  of  dis- 
eases of  the  stomach  to  those 
of  other  organs,  399 ; acute 
and  chronic  gastritis,  478 ; 


LIST  OF  SUBJECTS. 


phlegmonous  gastritis,  482  ; 
ulcer,  517;  carcinoma,  577; 
gastric  tuberculosis,  595  ; gas- 
tric syphilis,  605  ; hypertrophic 
stenosis  of  the  pylorus,  623 ; 
congenital  hypertrophic  ste- 
nosis of  the  pylorus  in  infants, 
663 ; dilation,  675  ; gastro- 
ptosis  and  enteroptosis,  730 ; 
neuroses,  786 ; chronic  gas- 
trosuccorrhea,  845 

Liver,  observations  on  dislocation  of,  699 
Liver-diseases  and  the  stomach,  390 
Lumbago,  724 
Lymphadenoma,  609 
Lymphangioma,  610 

Lymphatics  of  stomach,  29,  30;  of  intes- 
tines, 32,  34,  38 
Lymph-corpuscles,  ameboid,  36 
Lymphoid  tissue,  34,  36 


M. 

Macrocytes,  5 1 1 
Magnesium,  42 
Malaria,  385 

Malformation  of  the  gastric  cavity,  591 
Maltose,  44-47,  56,  65 
Martius  and  Liittke’s  method  of  analysis  of 
stomach  acids,  166 

Massage,  309-3 11  ; and  medicated  irriga- 
tion, technic  of,  312 
Materia  medica,  185  et  seq.,  328 
Medicinal  agents,  important:  HC1,  328; 

alkalies,  334 ; bitter 
tonics,  338 ; digestive 
ferments,  342 
Megalogastria,  624,  641 
Meissner,  plexus  of,  34,  38 
Melena  in  carcinoma,  560,  566 
Merycism,  767 
Mesenteric  plexus,  38 
Metabolism,  35,  374 
Microcytes,  511 
Miliary  tuberculosis,  591 
Mineral  springs,  313;  substances  of  food, 
42 

Mitosis  in  gastric  tumors,  562 
Monobutyrin,  57 
Morgagni,  columns  of,  41 
Mosquera  beef  meal,  199-201 
Motor  function  (see  Peristalsis);  insuffi- 
ciency, 624 

Mouth,  nose,  pharynx,  and  larynx,  effects 
of  diseases  of,  on  the  stomach,  387 
Mucigen,  35 
Mucin,  60 

Mucosa  : structure  of  gastric,  21-31 ; intes- 
tinal, 32-38,  40  ; fragments  of, 
in  wash-water  and  vomit,  135- 
138;  diagnostic  significance  of 
exfoliations  and  erosions,  139 ; 


895 

conductivity  with  reference  to 
electricity,  79-82,  304,  305 
Mucous  membrane  (see  Mucosa) 

Mucus,  21,  23,  25,  131 
Muscular  coat  of  stomach,  20,  28 ; of  in- 
testine, 32 

Muscularis  mucosa:,  22,  32,  35 
Myasthenia,  gastric  (see  Atony,  Gastric) 
Myoma,  609 
Myxoma,  613 

N. 

Neoplasms:  benign  tumors,  606;  granu- 
lomatous infections,  590; 
malignant  tumors,  527 
Nephritis  (see  Kidney,  Diseases) 
Nephroptosis  (see  Kidneys,  Dislocation  of 
the) 

Nerves  of  the  stomach,  31  ; intestine,  32, 
34,  38 

Nervous  diseases  and  the  stomach,  385  ; 

eructation,  754  ; system  and  dis- 
eases of  the  stomach,  376  ; vom- 
iting, 756 

Nessler’s  reagent,  162 
Neurasthenia  gastrica  (see  Dyspepsia, 
Nervous) 

Neuroses  : gastric,  classification  of,  733 ; 

dietetics  of,  207,  249  ; general 
consideration  of,  734  et  seq.  ; 
motor,  739;  secretory,  817; 
sensory,  794 
Nitrogen,  41,  41 1 
Nutrition  in  gastric  diseases,  374 


O. 

Obturator,  183 
Oligocythemia,  400 
Oliguria,  723 

Oppler-Boas  bacillus,  129,  130,  564 
Organic  acids,  free,  48  ; total,  analysis  of, 
170 

Orthopedic  treatment,  307 


P. 

Palpation,  98 
Pancreas,  55 

Pancreatic  digestion,  55-57,  292  ; secre- 
tion, physiological  stimulants 
of,  58 

Pancreatin,  344 
Papain,  346 
Papayotin,  346 
Papillomata,  606 
Papoid,  346 

Parasites,  animal,  and  gastritis,  440 
Pepsin:  source  and  origin,  22,  24,  27,  28, 
172;  action,  47,  49,  172,  175; 
tests,  50,  172,  175  ; nature,  175  ; 
in  the  duodenum,  65  ; ultimate 


896 


LIST  OF  SUBJECTS. 


fate  of,  68;  bile  action  on,  60; 
action  of  alcohol  on  pepsin-hy- 
drochloric acid,  290;  as  a me- 
dicinal agent,  344 
Pepsinogen  (see  Proenzymes) 

Peptone : peptic  product,  49 ; test,  50 ; 

tryptic  product,  58 ; bacterial 
product,  61  ; absorption  of,  65  ; 
in  the  stools,  69  ; diet,  199 
Peptones:  casein,  57;  elastin,  47,  57; 

gelatin,  47,  57 
Peptonuria,  412 
Percussion,  98 

Peristalsis  : influence  of  HC1,  47,  7^  ; bile 
influence,  60 ; comparative  im- 
portance, 70,  90;  tests,  71-90; 
function  of,  74  ; phases,  76,  83, 
84 ; passive  movements,  78 ; 
theories  relating  to  the  move- 
ments of  the  gastric  ingesta, 
84-89  ; study  of,  by  X-rays,  87; 
conclusions  concerning  physi- 
ology of,  89  ; electrical  stimula- 
tion, 79-82  ; intragastric  pres- 
sure, 89  ; factor  in  the  patho- 
logical propagation  of  micro- 
organisms, 128;  relation  to 
digestibility  of  food  substances, 
186,  189  ; antiperistalsis,  2 1 2, 
213  ; influence  of  alcohol,  293  ; 
neuroses  of,  739 ; intestinal 
peristalsis,  32 
Peristaltic  unrest,  748 
Peritonitis,  perforation,  510 
Pexine  (see  Rennin) 

Phenol,  61 

Phloroglucin,  vanillin  test,  158 
Phosphates,  48,  409 
Phosphorus,  41,  42 
Phthisis  ventriculi,  850 
Phytobezoar,  613 
Pineapple  ferments,  347 
Pneumatosis,  755 
Pneumogastric  nerves,  31 
Poikilocytosis,  402,  511 
Polypi,  606 

Proenzymes,  pepsinogen  : source,  23,  24, 
27,  173;  con- 
version into  pep- 
sin, 27,  47,  49, 
172  ; test,  173 

rennin-zymogen  : source,  23, 
24 ; corrver- 
sion  into 
rennin,  47, 
174;  tests, 
5L  175 

Prolapsus  of  the  stomach  (see  Gastropto- 
sis)  ; colon  (see  Coloptosis) ; 
spleen  (see  Splenoptosis)  ; 
liver  (see  Hepatoptosis) 
Propepsin  (see  Pepsinogen  under  Pro- 
enzymes) 


Propeptone',  49,  50 

Proteids  : their  office  in  the  economy,  42  ; 

digestion,  peptic,  47,  49,  175  ; 
tryptic,  57,  58;  proteid  and  bile 
interaction,  60  ; intestinal  putre- 
faction, 61  ; in  hyperacidity, 
194-198,  249,  824 

Proteolysis:  peptic,  47-51,  175;  tryptic, 
57,  58;  in  hyperacidity,  194- 
199,  248,  824 

Proteoses,  49 
Protoproteose,  49 
Prozymogen,  25,  26 

Ptyalin  : salivary  digestion,  44,  45,  1 7 1 ; 

of  the  succus  entericus,  60 ; in- 
fluence of  alcohol  on,  293  ; an 
artificial  ferment,  342 
Pulmonary  diseases  and  the  stomach,  387 
Pus  in  gastric  contents,  1 33 
Putrefaction:  bile  action,  60;  products, 
etc.,  61,  66,  67;  economic 
relation,  62  ; promoting  and 
inhibitory  agencies,  60,  67, 
68,  128;  conjugate  sulphates 
and  indol,  indices  of,  332 
Pylorectomy,  354  et  seq.  ; atypical,  360; 
partial,  360 

Pyloric  ligaments,  18,  20;  spasm,  746; 

valve,  18,  20 
Pyloroplasty,  363,  373 
Pylorospasm,  746 

Pylorus:  hypertrophic  stenosis  of,  613; 

symptomatology, 
618  ; diagnosis, 

620  ; prognosis, 

621  ; treatment, 

622 

insufficiency  of,  771  ; obstruction 
of,  657 ; symptomat- 
ology, 658 

resection  of  the,  354;  spasm  of 
the,  746 

Pyopneumothorax  subphrenicus,  510 


R. 

Rectum,  41 

Reflex  vomiting,  756,  760 
Regurgitation,  765 

Renal  diseases  (see  Kidney,  Diseases) 
Rennin:  source  and  derivation*  22,  24, 
174;  action,  51,  1 74;  action 
destroyed,  66;  test,  56,  174; 
zymogen  (see  Proenzymes) 
Resection  of  the  pylorus,  354;  statistics, 
370-373 

Resorcin  test,  159 
Resorption  (see  Absorption) 

Respiration  in  stomach  diseases,  376 
Rest  and  exercise,  therapy  of,  282-287  : 
cure,  Weir  Mitchell’s,  816 
Rheumatism  and  gastric  disease,  391 


LIST  OF  SUBJECTS. 


897 


Rontgen-ray  photography  of  stomach,  641  ; 

in  studying  peristalsis,  87 

Rugae,  21 
Rumination,  767 

S. 

Saliva:  detection  in  gastric  contents,  1 3 1 ; 

nature  and  action,  44,  45,  1 7 1 ; 
influence  of  alcohol,  293 
Sarcinae,  129,  439 

Sarcomata,  546  ; classification  and  etiology, 
546,  547 ; symptomatology, 

547;  diagnosis,  552;  prog- 
nosis, 577 
Scirrhus,  gastric,  533 

Secretion  or  secretions  : physiological  ex- 
citants of  gastric 
and  pancreatic, 
58  ; contempora- 
neous action  of, 
65  ; admixtures 
of,  65  ; of  water 
by  the  stomach, 
65 ; duodenal, 
66,  132;  in  the 
fasting  stomach, 
148 ; depend- 
ence on  peristal- 
sis, 70,  90  ; con- 
ditioning bacte- 
rial propagation, 
128;  factor  in 
digestibility  of 
foods,  186,  194; 
in  neoplasms, 
550 ; neuroses 
of,  817 

Self-digestion  of  the  stomach,  487 
Semilunar  ganglion,  38 
Sensation,  neuroses  of,  794 
Sensations  of  hunger  and  of  appetite, 
anomalies  of,  800 
Serous  coat  of  intestines,  31 
Sigmoid  flexure,  40 
Skatol,  61 

Skin-diseases  and  digestive  troubles,  396 
Sodium,  42 
Solar  plexus,  31 

Solutions,  standard  and  normal,  152 
Spasm,  pyloric,  746 
Spectroscopic  examination,  135 
Sphincter:  anal,  42  ; pyloric,  20 
Splanchnoptosis,  707 
Splenoptosis,  724 
Spray,  intragastric,  300 
Starches,  44-47,  58 
Steapsin,  56,  60 

Stenosis  : cardiac,  652  ; etiology,  653  ; 

symptomatology,  654 ; 
diagnosis,  654;  progno- 
sis, 655 ; treatment,  655 
hyperplastic  pyloric,  444 
cicatricial  pyloric,  510 


hypertrophic  pyloric,  613  ; 

symptomatology,  618  ; 
diagnosis,  620 ; prog- 
nosis, 621  ; treatment, 
622 

congenital  pyloric,  660;  diagno- 
sis, 662;  prognosis, 
663  ; treatment,  663 
effects  of  various  forms  of,  664- 
675 ; relative  value  of 
diagnostic  factors,  660- 
670 ; continued  superse- 
cretion in,  671 

degree  of  obstruction,  673  ; 
prognosis,  673  ; treatment,  673- 
675  ; diet  in,  651 

Stomach:  macroscopic  anatomy,  17-21  ; 

histology,  20-31 ; location, 
size,  and  capacity — methods 
for  determining  these,  98-112; 
contents,  examination,  114- 
138, 141  ; acidity  in  the  healthy 
and  dyspeptic,  713 ; influence 
of  its  diseases  upon  other  or- 
gans and  metabolism,  374;  in- 
fluence of  other  affections  on 
the,  385  ; the  blood  and  urine 
in  gastric  diseases,  400 ; gases, 
15 1 , 404;  the  clinic,  414  et 
seq.  ; hour-glass,  481,  591  ; 
hemorrhage  from,  682 
Stomachic  remedies,  338 
Stomach-pump,  123 

Stomach-tube  and  technics  of  its  introduc- 
tion, 1 14-125 

Subacidity — dietetics,  189  ; clinical,  847 
Submucosa  of  stomach,  21  ; of  intestine, 
32 

Succus  entericus,  60,  66,  69 
Sugar,  44,  45,  59 

Sugars  : cane,  48,  56,  65  ; grape,  56,  65  ; 

invert,  48,  56  ; milk-,  65 
Sulphates,  63,  332 
Sulphur,  41,  42 

Superacidity  (see  Hyperacidity) 
Supersecretion  (see  Hypersecretion) 
Surgery,  gastric  : historical  review,  348  ; 

forms  of  operations,  351  ; 
fundamental  factors  in 
mortality,  resulting,  366 

Syntonin,  49,  65 
Syphilis  of  the  stomach,  596 


T. 

Telangiectatic  carcinoma,  527 
Test-meals,  121-125 
Tetanus,  379 
Tetany,  379 

Therapy  of  stomach  diseases : dietetics, 
185 ; lavage  and 
the  gastric  douche, 


LIST  OF  SUBJECTS. 


297  ; electricity,  301  ; 
hydrotherapeutic  and 
orthopedic  methods, 
307 ; massage,  309 ; 
mineral  springs,  313  ; 
important  medicinal 
agents,  328 

Titration,  152 
Tonics,  bitter,  338 

Topfer’s  method  in  analysis,  163,  164 
Tormina  ventriculi  nervosa,  748 
Transillumination  (see  Diaphany) 

Trypsin,  57,  58,  66,  68,  69,  70 
Tryptones,  58 
Tryptophan,  58 

Tuberculosis  of  the  stomach,  590;  diagno- 
sis, 594 

Tube,  stomach-,  and  technics  of  its  intro- 
duction, 114-126 

Tumors:  benign,  606;  malignant,  527 ; 

of  colon,  557;  of  gall-bladder, 
557;  of  liver,  556  ; of  omen- 
tum, 557  ; of  peritoneum,  557  ; 
splenic,  556 
Tyrosin,  58,  61 

U. 

Ulcer  of  the  stomach : condition  of  the 
blood  in,  403 ; 
nature  of,  486 ; 
self-digestion  of 
stomach,  487  ; 
etiology,  489  - 
49 1;  symptoma- 
tology, 497,  547  ; 
diagnosis,  507- 
511  ; differential 
diagnosis,  587  ; 
587;  treatment, 
195,  205,  241- 
243,  5 1 1 ; car- 
cinomatous, 108, 
195*  5o6,  559, 
570;  syphilitic, 
600 ; tubercular, 
592 


Ulcus  ventriculi,  pepticum,  rotundum,  per- 
forans,  rodens,  corrosivum  e diges- 
tione,  486 ; carcinomatosum  (see 
Ulcer,  Carcinomatous) 

Urea,  394,  41 1 

Urine : in  gastric  diseases,  406  ; acidity 
in  the  healthy  and  dyspeptic,  820 


V. 

Vagus  nerve,  58 

Valvulae  conniventes,  33 

Vasa  brevia,  30 

Vermiform  appendix,  40 

Vertigo,  gastric,  377  ; intestinal,  378 

Vigoral,  200 

Villi,  33,  34 

Viscera,  reversal  of  their  location,  723 
Vomiting  : cerebral,  central,  spinal,  757  ; 

in  pregnancy,  737 ; juvenile, 
656;  nervous  habitual,  756; 
neurasthenic,  hysteric,  759 ; 
periodical,  758 ; reflex,  756, 
760 

W. 

Water : in  the  animal  economy,  42  ; secre- 
tion and  absorption  in  the  stomach, 

65 

Waters:  natural  mineral,  virtues  of,  313; 

alkaline,  317,  319;  alkaline  sul- 
phur, 318  ; chalybeate,  325,  326  ; 
acidulous,  327,  328  ; saline,  319, 
321  ; sodium  chlorid,  319  ; bitter 
or  purgative,  321,  322  ; sulphur- 
etted, 323,  325 


Y. 

Yeast  fungus,  129,  439 


Z. 

Zymogen  granules,  26 
Zymogens  (see  Proenzymes) 


Catalogue  of  the  Medical,  Dental,  Phar- 
maceutical, Chemical,  and  Scientific  Books 
Published  by  P.  Blakiston’s  Son  & Co., 
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ANATOMY. 

Ballou.  V eterinary  Anat.  $0.80 
Broomell.  Anatomy  and 
Histol.  of  Mouth  and  Teeth.  4.50 
Gordinier.  Anatomy  of  Nerv- 


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Wilson’s  Anatomy,  nth  Ed.  5.00 
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Conn.  Agricultural  Bacteri- 
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Hewlett.  Manual  of  lllus.  3.00 
Williams.  Student’s  Manual 
of.  2d  Edition.  90  lllus.  1.50 

BRAIN  AND  INSANITY. 
Blackburn.  Autopsies.  - 1.25 

Horsley.  Brain  and  Sp.  Cord.  2.50 
Ireland.  Mental  Affections 
of  Children.  ...  4.00 

Lewis.  Mental  Diseases.  7 00 
Mann’s  Psychological  Med,  3.00 
Regis.  Mental  Medicine.  - 2.00 
Shuttleworth.  Mentally  De- 
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Stearns.  Mental  Dis  lllus.  2.75 
Tuke.  Dictionary  of  Psycho- 
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Technol'  g’  l Books . Water , Milk, etc. 
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Vol.  II.  Part  III. 

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Vol.  IV.  - - - 4.50 

Bartley.  Medical  and  Phar- 
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Clinical  Chemistry.  1.00 

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Clowes  and  Coleman.  Quan- 
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Vol.  III.  Gas  Lighting.  3.50 

Vol.  IV.  Elec.  Lighting. 

Holland.  Urine,  Gastric  Con- 
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Food  Analysis.  - - 

Milk  Analysis.  - - 1.25 

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Structural  Formulae.  - 1.00 


Muter.  Pract.  and  Anal.  $1.25 
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Electro-Chem.  Exper.  .75 

Richter’s  Inorganic.  5th  Ed.  1.75 

Organic,  jd  Ed.  2 Vols. 

Vol.  I.  Aliphatic  Series.  3.00 
Vol.lI.Carbocyclic  “ 3.00 

Smith.  Electro-Chem.  Anal.  1.25 
Smith  and  Keller.  Experi- 
ments. 4th  Ed.  lllus.  .60 

Sutton.  Volumetric  Anal.  5.00 
Symonds.  Manual  of.  2.00 

Traube.  Physico-Chem.Meth.  1.50 
Thresh.  Water  Supplies.  - 2.00 
Ulzer  and  Fraenkel.  Tech- 
nical Chemical  Analysis.  1.25 
Woody.  Essentials  of.  4th  Ed.  1.50 

CHILDREN. 

Hale.  Care  of.  - .50 

Hatfield.  Compend  of.  .80 

Meigs.  Milk  Analysis.  - .50 

Power.  Surgical  Diseases  of.  2.50 
Smith.  Wasting  Diseases  of.  2.00 

Starr.  Digestive  Organs  of.  

Hygiene  of  the  Nursery.1.00 

Taylor  and  Wells.  Manual.  4.50 

CLINICAL  CHARTS. 
Griffith’s  Temp’ t’ re  Charts. 

Pads  of  50  - . - .50 

Keen.  Outline  Drawings  of 
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Schreiner.  Diet  Lists.  Pads,  .75 

COMPENDS 
And  The  Quiz- Comp  ends. 
Ballou.  Veterinary  Anat.  .80 
Brubaker’s  Physiol.  10th  Ed.  .80 
Cushing.  Histology  - - .80 

Gould  and  Pyle.  The  Eye.  .80 
Hatfield.  Children.  - .80 

Horwitz.  Surgery.  5th  Ed.  .80 
Hughes.  Practice.  2 Pts.  Ea.  .80 
Landis.  Obstetrics.  6th  Ed.  .80 
Leffmann’s  Chemistry.  4th  Ed.  .80 
Mason.  Electricity.  - .75 

Potter’s  Anatomy,  6th  Ed.  .80 

Materia  Medica.  6th  Ed.  .80 

Schamberg.  Skin  Diseases.  .80 
Stewart,  Pharmacy.  5th  Ed.  .80 
Thayer.  Pathology.  - - .80 

Warren.  Dentistry.  3d  Ed  .80 
Wells.  Gynecology.  2d  Ed.  .80 
Self-Examination.  3500 
Questions  on  Medical  Sub- 
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Harris  and  Beale.  Pulmo- 
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Knopf.  Pulmon. Tuberculosis.  3.00 
Steel.  Physical  Signs  of  .Pul- 
monary Disease.  •-  - - 1.25 

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Barrett.  Dental  Surg.  - 1.00 

Broomell.  Anat.  and  Hist,  of 
Mouth  and  Teeth.  - - 4.50 

Fillebrown.  Op.  Dent.  lllus.  2.25 
Gorgas.  Dental  Medicine.  4.00 
Harris.  Principles  and  Prac.  6.00 
Dictionary  of.  6th  Ed.  5.00 


Heath.  Dis.  of  J aws.  - 4.50 

Richardson.  Mech.  Dent.  5.00 
Smith.  Dental  Metallurgy.  1.75 
Taft.  Index  of  Dental  Lit.  2.00 
Tomes.  Dental  Surgery.  4.00 

Dental  Anatomy.  4.00 

Warren’s  Compend  of.  - .80 

Dental  Prosthesis  and 

Metallurgy.  lllus.  - 1.23 

White.  Mouth  and  Teeth.  .40 


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Tyson’s  Manual.  3d  Ed.  lllus.  1.50 

DICTIONARIES. 
Gould’s  Illustrated  Dictionary 
of  Medicine,  Biology,  and  Al- 
lied Sciences,  etc.  5th  Edi- 
tion. Leather,  $10.00;  Half 
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Gould’sStudent’s  Medical  Die-  | 
tionary.  nth  Ed.,  lllus., 

Mor.,  $2.50;  Thumb  Ind.,  3.00 
Gould’s  Pocket  Dictionary — 
30,000  medical  words.  4th 
Edition.  Enlarged.  Leather,  1.00 
Gould  and  Pyle.  Cyclopedia 
of  Med.  and  Surg.  One  Vol. 
lllus.  Leather,  10.00 

Harris’  Dental.  Clo.  5.00;  Shp.  6.co 
Longley’s  Pronouncing.  .75 

Maxwell.  Terminologia  Med- 
ica Polyglotta.  - - 3.00 

Treves.  German-English.  3.25 


EAR. 

Burnett.  Hearing,  etc.  .40 

Dalby.  Diseases  of.  4th  Ed.  2.50 
Hovell.  Treatise  on.  - 5.50 

Pritchard.  Diseasesof.  3d  Ed.  1.50 


ELECTRICITY. 
Bigelow.  Plain  Talks  on  Medi- 
cal Electricity.  43  lllus.  1.00 
Hedley.  Therapeutic  Elec.  2.50 

Jacobi.  Electrotherapy  - 

Jones.  Medical  Electricity. 

3d  Ed.  lllus.  - 3.00 


EYE. 

Donders.  Refraction. 

Fick.  Diseases  of  the  Eye. 
Gould  and  Pyle.  Compend. 
Gower’s  Ophthalmoscopy. 
Harlan.  Eyesight. 
Hartridge.  Refraction.  10th  Ed. 

Ophthalmoscope.  3d  Ed. 

Hansell  and  Reber.  Mus- 
cular Anamolies  of  the  Eye. 
Hansell  and  Bell.  Clinical 
Ophthalmology.  120  lllus. 
Jessop’s  Manual  of  Diseases 
of  Eye.  - 

Morton.  Refraction.  6th  Ed. 
Ohlemann.  Ocular  Therap. 
Phillips.  Spectacles  and  Eye- 
glasses. 49  lllus.  2d  Ed. 
Swanzy’s  Handbook.  7th  Ed. 
Thorington.  Retinoscopy. 

Refraction.  200  lllus. 

Walker.  Student's  Aid. 
Wright.  Ophthalmology. 


3.00 

1. 00 
i-75 

1. 00 

2.50 
1. 00 

1.50 


GYNECOLOGY. 

Bishop.  Uterine  Fibromyo- 
mata.  Illustrated.  - - 3.50 

Byford  (H.  T.).  Manual.  2d 

Edition.  341  Illustrations.  3.00  • 
Diihrssen.  Gynecological 

Practice.  105  Illustrations.  1.50 
Montgomery.  Text -book 


of.  527  lllus.  - - - 5.00 

Lewers.  Dis.  of  Women.  2.50 

Wells.  Compend.  lllus.  .80 

HEALTH  AND  DOMESTIC 
MEDICINE. 

Bulkley.  The  Skin.  - .40 

Burnett.  Hearing.  - .40 

Cohen.  Throat  and  Voice.  .40 

Dulles.  Emergencies.  5th  Ed.  1.0a 

Harlan.  Eyesight.  - .40 

Hartshorne.  Our  Homes.  .40 


CLASSIFIED  LIST  OF  P.  BLAKISTON'S  SON  &+  CO.'S  PUBLICATIONS 


Osgood.  Dangers  of  Winter.  Jo. 40 
Packard.  Sea  Air,  etc.  .40 

Richardson’s  Long  Life.  .40 

White.  Mouth  and  Teeth.  .40 

Wilson.  Summer  and  its  Dis.  .40 
Wood.  Brain  and  Overwork.  .40 
HISTOLOGY. 

Cushing.  Compend.  - - .80 

Stirling.  Histology.  2d  Ed.  2.00 
Stohr’s  Histology.  Illus.  - 3.00 
HYGIENE. 

Canfield.  Hygiene  of  the  Sick- 
Room.  - - - 1.25 

Coplin.  Practical  Hygiene.  

Ernst.  Prophylaxis.  - - 

Kenwood.  Public  Health 
Laboratory  Guide.  - 2.00 

Lincoln.  School  Hygiene.  .40 
McNeill.  Epidemics  and  Iso- 
lation Hospitals.  - - 3.50 

Notter.  Practical  Hygiene.  7.00 
Parkes’ (L.  C.),  Manual.  3 00 

Elements  of  Health.  1.25 

Starr.  H ygiene  of  the  Nursery.  1.00 
Stevenson  and  Murphy.  A 
Treatise  on  Hygiene.  In  3 


Vols.  Circular  Vol.  I,  6.00 
upon  application.  Vol.  II,  6.00 
Vol.  Ill,  5.00 
Thresh.  Water  Supplies.  2.00 
Wilson’s  Handbook.  8th  Ed.  3.00 
Weyl.  Coal-Tar  Colors,  1.25 
MASSAGE,  Etc. 

Kleen  and  Hartwell.  - 2.25 


Mitchell  and  Gulick.  Me- 
chanotherapy. - - - 

Ostrom.  Massage.  105  Illus.  1.00 
Ward.  Noteson.  Paper Cov.  1. 00 
MATERIA  MEDICA. 


Biddle.  13th  Ed.  Cloth,  4.00 

Bracken.  Materia  Med.  2.75 

Coblentz.  Newer  Remedies.  1.00 
Davis.  Essentials  of.  - 1.50 
Gorgas.  Dental.  5th  Ed.  4.00 

Groff.  Mat.  Med  for  Nurses.  1.25 
Heller.  Essentials  of.  - 1.50 
Potter’s  Compend  of.  6th  Ed.  .80 
Potter’s  Handbook  of.  8th 
Ed.  Cloth,  $5.00  ; Sheep,  6.00 

Sayre.  Organic  Materia  Med. 

and  Pharmacognosy.  - 4.50 

White  and  Wilcox.  Mat. 
Med.,  Pharmacy,  Pharmacol- 
ogy, and  Therapeutics.  4th 
Ed.  Enlarged.  Cl., $3.00;  Sh.  3.50 


MEDICAL  JURISPRUDENCE. 
Mann.  Forensic  Med.  - 6.50 

Reese.  Med.  Jurisprudence  and 
Toxicology,5th  Ed.  $3.00;  Sh.  3.50 
MICROSCOPE. 
Carpenter.  The  Microscope. 

8th  Ed.  800  Illus.  - 

Lee.  Vade  Mecum  of.  5th  Ed.  4.00 
Reeves.  Med.  Microscopy.  2.50 
Wethered.  Medical  Micros- 
copy. Illus.  - 2.00 

MISCELLANEOUS. 

Black.  Micro-organisms.  .75 
Burnet.  Food  and  Dietaries.  1.50 

Cohen.  Organotherapy.  

Da  Costa.  Clinical  Pathology 

of  the  Blood.  ...  

Davis.  Alimentotherapy.  

Duckworth.  On  Gout.  - 6.00 
Fenwick.  Ulcer  ot  Stomach.  3.50 
Goodall  and  Washbourn. 

Infectious  Diseases.  Illus.  3.00 
Gould.  Borderland  Studies.  2.00 
Greene.  Medical  Examination 
in  Life  Insurance.  Lius.  - 4.00 
Haig.  Uric  Acid.  5th  Ed.  3.00 

Diet  and  Food.  3d.  Ed.  1.00 

Hare.  Mediastinal  Disease.  2.00 
Hemmeter.  Diseases  of  Stom- 
ach. 2d  Edition.  Illus.  - 6.00 

Diseases  of  Intestines. 

Henry.  Anaemia.  - - .50 

Leffmann.  Coal  Tar  Products.  1.25 
McCook.  Amer.  Spiders.  50.00 
New  Sydenham  Society's 
Publications,  each  year.  - 8.00 
Osier  and  McCrae.  Cancer 
of  the  Stomach  - - - 2.00 


St.  Clair.  Medical  Latin.  J1.00 
Thorne.  Schott  Methods  in 
Heart  Disease.  - - 1.75 

Tissier.  Pneumatotherapy.  

Treves.  Physical  Education.  .75 
Weber  and  Hinsdale.  Cli- 
mate.   

Winternitz.  Hydrotherapy. 

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Tyson’s  Practice  of  Medicine 

A TEXT-BOOK  FOR  PRACTITIONERS  AND  STUDENTS 

WITH  SPECIAL  REFERENCE  TO  DIAGNOSIS  AND  TREATMENT 

% 

By  JAMES  TYSON,  M.D. 

Professor  of  Medicine  in  the  University  of  Pennsylvania ; Physician  to  the  University  and 
Philadelphia  Hospitals , etc. 


COLORED  PLATES  AND  125  OTHER  ILLUSTRATIONS 
Octavo*  1222  Pages*  Cloth,  $5*50 ; Leather,  $6*50 ; Half  Russia,  $7*50 


The  object  of  this  book  is — first,  to  aid  the  student  and  physician  to  recognize 
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Diagnosis  and  Treatment  receive  special  attention,  while  pathology  and 
morbid  anatomy  have  such  consideration  as  is  demanded  by  their  importance  as  funda- 
mental conditions  of  a thorough  understanding  of  disease.  Dr.  Tyson’s  qualifications 
for  writing,  such  a work  are  unequaled.  It  is  really  the  outcome  of  over  thirty 
years'  experience  in  teaching  and  in  private  and  hospital  practice*  As  a 
teacher  he  has,  while  devoting  himself  chiefly  to  clinical  medicine,  occupied  several 
important  chairs,  notably  those  of  General  Pathology  and  Morbid  Anatomy,  and 
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material  and  illustrations  have  been  added,  and  in  many  respects  it  may  be  considered 
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“ It  is  in  the  writing  and  preparation  of  a work  of  this  character  that  Dr.  Tyson  stands  pre- 
eminent. Those  of  the  profession — and  there  are  many  at  this  time— who  have  been  fortunate  to 
have  been  his  pupils  during  their  medical  student  days,  will  remember  that  he  brought  to  his 
lectures  and  to  his  writings  an  amount  of  industry  and  care  which  many  other  teachers  failed  to 
bring ; and  those  who  know  him  best  as  an  author  and  teacher  have  expected  that  his  book  on  the 
Practice  of  Medicine,  when  it  appeared,  would  be  a credit  to  himself,  and  would  increase  his 
reputation  as  a medical  author.  This  belief  has  proved  correct.  ’ ’ — Therapeutic  Gazette , Detroit , Mich. 

“ After  a third  of  a century  spent  in  the  assiduous  study,  practice,  and  teaching  of  medicine, 
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Professor  Tyson  best  shows  his  modesty  by  making  no  apology  for  the  present  work.” — American 
Journal  of  Medical  Sciences , Philadelphia. 


4 


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Burnett.  Hearing  and  How  to  Keep  It. 

By  Chas.  H.  Burnett,  m.d.,  Professor  of  Diseases  of  the  Ear  at  the  Philadelphia 
Polyclinic.  Illustrated.  Cloth,  .40 

Buxton.  On  Anesthetics. 

A Manual.  By  Dudley  Wilmot  Buxton,  m.r.c.s.,  m.r.c.p.,  Assistant  to  Professor 
of  Medicine  and  Administrator  of  Anesthetics,  University  College  Hospital,  London. 
Third  Edition,  Illustrated.  i2mo.  Cloth,  $1.50 

Butlin.  The  Operative  Surgery  of  Malignant  Disease. 

By  Henry  T.  Butlin,  f.r.c.s.,  Assistant  Surgeon  to,  and  Demonstrator  of  Surgery 
at,  St.  Bartholomew’s  Hospital,  London,  etc.,  assisted  by  James  Berry,  f.r.c.s., 
Wm.  Bruce-Clarke,  m.b.,  f.r.c.s.,  A.  H.  G.  Doran,  f.r.c.s.,  Percy  Furnivall, 
f.r.c.s.,  W.  H.  H.  Jessop,  m.b.,  f.r.c.s.,  and  H.  J.  Waring,  b.sc.,  f.r.c.s. 
Second  Ed.,  Revised  and  Rewritten.  Illus.  Just  Ready.  Octavo.  Cloth,  $4.50 

Byford.  Manual  of  Gynecology.  341  Illustrations. 

A Practical  Student’s  Book.  By  Henry  T.  Byford,  m.d.,  Professor  of  Gynecology 
and  Clinical  Gynecology  in  the  College  of  Physicians  and  Surgeons  of  Chicago  ; 
Professor  of  Clinical  Gynecology,  Women’s  Medical  School  of  Northwestern  Uni- 
versity, and  in  Post-Graduate  Medical  School  of  Chicago,  etc.  Second  Edition, 
Enlarged.  With  341  Illustrations,  many  of  which  are  from  original  drawings  and 
several  of  which  are  Colored.  i2mo.  596  pages.  Cloth,  $3.00 

Caldwell.  Chemical  Analysis. 

Elements  of  Qualitative  and  Quantitative  Chemical  Analysis.  By  G.  C.  Caldwell, 
b.s.,  Ph.  d.  , Professor  of  Agricultural  and  Analytical  Chemistry  in  Cornell  Univer- 
sity, Ithaca,  New  York,  etc.  Third  Edition,  Revised  and  Enlarged.  Octavo. 

Cloth,  $i.oo 

Cameron.  Oils  and  Varnishes. 

A Practical  Handbook.  By  James  Cameron,  f.i.c.  With  Illustrations,  Formulae, 
Tables,  etc.  i2mo.  Cloth,  $2.25 

Soap  and  Candles. 

A Handbook  for  Manufacturers,  Chemists,  Analysts,  etc.  54  Illustrations.  i2mo. 

Cloth,  $2.00 

Canfield.  Hygiene  of  the  Sick-Room. 

A book  for  Nurses  and  others.  Being  a Brief  Consideration  of  Asepsis,  Antisepsis, 
Disinfection,  Bacteriology,  Immunity,  Heating  and  Ventilation,  and  kindred  subjects, 
for  the  Use  of  Nurses  and  other  Intelligent  Women.  By  William  Buckingham 
Canfield,  a.m.,  m.d.,  late  Lecturer  on  Clinical  Medicine,  University  of  Maryland  ; 
Physician  to  Bay  View  Hospital,  Baltimore.  i2mo.  Cloth,  $1.25 


MEDICAL  AND  SCIENTIFIC  PUBLICATIONS. 


9 


Carpenter.  The  Microscope  and  Its  Revelations. 

By  W.  B.  Carpenter,  m.d.,  f.r.s.  Eighth  Edition,  by  Rev.  Dr.  Dallinger, 
f.r.s.  Revised  and  Enlarged,  with  800  Illustrations  and  many  Lithographs. 
Octavo.  Nearly  Ready. 

Cazeaux  and  Tarnier’s  Midwifery.  With  Appendix,  by  Munde. 

The  Theory  and  Practice  of  Obstetrics,  including  the  Diseases  of  Pregnancy  and 
Parturition,  Obstetrical  Operations,  etc.  By  P.  Cazeaux.  Remodeled,  rearranged, 
and  revised  by  S.  Tarnier,  m.d.  Eighth  American  from  the  Eighth  French  and 
First  Italian  Edition.  Edited  by  Robert  J.  Hess,  m.d.,  Physician  to  the  Northern 
Dispensary,  Philadelphia,  etc.  With  an  Appendix  by  Paul  F.  Mund6,  m.d.,  Pro- 
fessor of  Gynecology  at  the  New  York  Polyclinic.  Illustrated  by  Lithographs,  Full- 
page  Plates,  and  numerous  Engravings.  8vo.  Cloth,  $4-5°;  Full  Leather,  $5.50 

Clowes  and  Coleman.  Quantitative  Analysis. 

Adapted  for  the  Use  of  the  Laboratories  of  Schools  and  Colleges.  By  Frank  Clowes, 
Sc. d. , Emeritus  Professor  of  Chemistry,  University  College,  Nottingham,  and  I. 
Bernard  Coleman,  Assoc.  R.  C.  Sci.,  Dublin,  Professor  of  Chemistry,  Southwest 
London  Polytechnic.  Fifth  Edition.  122  Illustrations.  Just  Ready.  Cloth,  $3.50 

Coblentz.  Manual  of  Pharmacy. 

A Text-Book  for  Students.  By  Virgil  Coblentz,  a.m.,  ph.d.,  f.c.s.,  Professor  of 
Chemistry  and  Physics  ; Director  of  Pharmaceutical  Laboratory,  College  of  Phar- 
macy of  the  City  of  New  York.  Second  Edition,  Revised  and  Enlarged.  437  Illus- 
trations. Octavo.  572  pages.  Cloth,  $3.50;  Sheep,  $4-5°;  Half  Russia,  $5.50 

The  Newer  Remedies. 

Including  their  Synonyms,  Sources,  Methods  of  Preparation,  Tests,  Solubilities, 
and  Doses  as  far  as  known.  Together  with  Sections  on  Organo-Therapeutic 
Agents  and  Indifferent  Compounds  of  Iron.  Third  Edition,  very  much  enlarged. 
Octavo.  Cloth,  $1.00 

Volumetric  Analysis. 

A Practical  Handbook  for  Students  of  Chemistry.  Illustrated.  8vo.  In  Press. 

Cohen.  System  of  Physiologic  Therapeutics.  Illustrated. 

A Practical  Exposition  of  the  Methods  Other  than  Drug-giving,  Useful  in  the  Treat- 
ment of  the  Sick.  Edited  by  Solomon  Solis  Cohen,  a.m.,  m.d.,  Professor  of 
Medicine  and  Therapeutics  in  the  Philadelphia  Polyclinic  ; Lecturer  on  Clinical 
Medicine  at  Jefferson  Medical  College  ; Physician  to  the  Philadelphia  and  Rush  Hos- 
pitals ; formerly  Lecturer  on  Therapeutics,  Dartmouth  Medical  College.  To  be 
issued  in  Eleven  Compact  Octavo  Volumes.  Price  for  Set  Complete,  Cloth,  $22.00 

Electrotherapy.  Illustrated.  Two  Volumes. 

By  George  W.  Jacoby,  m.d.,  New  York,  Consulting  Neurologist  to  the  German 
Hospital,  to  the  Infirmary  for  Women  and  Children,  to  the  Craig  Colony  for 
Epileptics,  etc.  Special  articles  by  Edward  Jackson,  a.m.,  m.d.,  Denver, 
Col. ; Emeritus  Professor  of  Diseases  of  the  Eye  in  the  Philadelphia  Polyclinic  ; 
Member  American  Ophthalmological  Society  ; Fellow  and  ex-President  American 
Academy  of  Medicine,  etc. — By  William  Scheppegrell,  m.d.,  New  Orleans, 
Member  American  Laryngological,  Rhinological,  and  Otological  Society. — 
By  J.  Chalmers  Da  Costa,  m.d.,  Clinical  Professor  of  Surgery  in  Jefferson 
Medical  College  ; Surgeon  to  the  Philadelphia  and  to  St.  Joseph’s  Hospitals, 
etc. — By  Franklin  H.  Martin,  m.d.,  Professor  of  Gynecology,  Post-Graduate 
Medical  School  of  Chicago  ; Gynecologist  Chicago  Charity  Hospital ; Chairman 
Section  of  Obstetrics  and  Diseases  of  Women  of  the  American  Medical  Asso- 
ciation (1895),  etc.  By  A.  H.  Ohmann-Dumesnil,  m.d.,  Editor  St.  Louis 
Medical  and  Surgical  Journal ; Member  International  Dermatological  Congress  ; 
formerly  Professor  of  Dermatology,  St.  Louis  Medical  College,  etc. 


10 


P.  BLAKISTON'S  SON  CO.'S 


Cohen.  Physiologic  Therapeutics. — Continued. 

Climatology  and  Health  Resorts,  Including  Mineral  Springs. 
Two  Volumes,  with  Maps. 

By  F.  Parkes  Weber,  m.a.,  m.d.,  f.r.c.p.  (Lond.),  Physician  to  the  German 
Hospital,  Dalston  ; Assistant  Physician  North  London  Hospital  for  Consump- 
tion ; Author  of  “The  Mineral  Waters  and  Health  Resorts  of  Europe  and 
Guy  Hinsdale,  a.m.,  m.d.,  Secretary  of  the  American  Climatological  Associa- 
tion ; President  of  the  Pennsylvania  Society  for  the  Prevention  of  Tuberculosis  ; 
formerly  Lecturer  on  Medical  Climatology  in  the  University  of  Pennsylvania,  etc. 

Prophylaxis — Personal  Hygiene — Care  of  the  Sick.  Illustrated. 
By  Harold  C.  Ernst,  m.d.,  Professor  of  Bacteriology  in  the  Medical  School  of 
Harvard  University,  Boston  ; and  Albert  Abrams,  m.d.  (University  of  Heidel- 
berg), formerly  Professor  of  Pathology,  Cooper  Medical  College,  San  Francisco. 

Dietotherapy.  Food  in  Health  and  Disease. 

By  Nathan  S.  Davis,  Jr.,  a.m.,  m.d.,  Professor  of  Principles  and  Practice  of 
Medicine  in  Northwestern  University  Medical  School ; Physician  to  Mercy  Hos- 
pital, Chicago  ; Member  American  Academy  of  Medicine,  American  Climato- 
logical Society,  etc. 

Mechanotherapy.  Illustrated. 

By  John  Kearsley  Mitchell,  m.d.,  Assistant  Physician  to  the  Orthopedic 
Hospital  and  Infirmary  for  Nervous  Diseases  ; Assistant  Neurologist  Presbyterian 
Hospital,  Philadelphia  ; Attending  Physician  to  the  Pennsylvania  School  for 
Feeble-minded  Children;  Fellow  College  of  Physicians  of  Philadelphia,  etc., 
formerly  Lecturer  on  Symptomology  at  the  University  of  Pennsylvania  ; and 
Luther  Gulick,  m.d.,  of  Brooklyn,  N.  Y.,  formerly  of  Springfield,  Mass.,  Mem. 
American  Association  for  Advancement  of  Physical  Education,  Amer.  Medical 
Association,  etc. 

Rest — Mental  Therapeutics — Suggestion. 

By  Francis  X.  Dercum,  m.d.,  Clinical  Professor  of  Nervous  Diseases  in  Jeffer- 
son Medical  College  ; Neurologist  to  the  Philadelphia  Hospital ; Consulting 
Physician  to  the  State  Asylum  for  the  Chronic  Insane  at  Wernersville,  Penna. ; 
Consulting  Neurologist  to  St.  Agnes’  Hospital ; Neurologist  to  the  Jewish  Hos- 
pital of  Philadelphia. 

Hydrotherapy — Thermotherapy — Balneology— Phototherapy. 

By  Dr.  Wilhelm  Winternitz,  Professor  of  Clinical  Medicine  in  the  University 
of  Vienna  ; Director  of  the  General  Polyclinic  in  Vienna,  etc. ; and  Dr.  E. 
Heinrich  Kisch,  Professor  in  the  University  of  Prague  ; Physician  at  Marien- 
bad  Spa. 

Pneumatotherapy  and  Inhalation  Methods.  Illustrated. 

By  Dr.  Paul  Tissier,  Chief  of  Clinic  of  the  Faculty  of  Medicine  of  Paris. 
Serotherapy — Organotherapy — Blood-Letting,  etc. — Principles  of 
T herapeutics — Digest — I ndex. 

By  Joseph  McFarland,  m.d.,  Professor  of  Pathology  in  the  Medico-Chirurgical 
College,  Philadelphia  ; Pathologist  to  the  Medico-Chirurgical  Hospital  and  to  the 
Rush  Hospital  for  Consumptives  and  Allied  Diseases,  etc. — O.  T.  Osborne, 
m.d.,  Professor  of  Materia  Medica  and  Therapeutics,  Medical  Department,  Yale 
University,  New  Haven. — Frederick  A.  Packard,  m.d.,  Visiting  Physician  to 
the  Pennsylvania  and  to  the  Children’s  Hospitals. — The  Editor,  and  Augustus 
A.  Eshner,  m.d.,  Professor  of  Clinical  Medicine  in  the  Philadelphia  Polyclinic  ; 
Physician  to  the  Philadelphia  Hospital,  etc. 

***  Complete  descriptive  circular  upon  application. 


MEDICAL  AND  SCIENTIFIC  PUBLICATIONS. 


11 


Cohen.  The  Throat  and  Voice. 

By  J.  Solis  Cohen,  m.d.  Illustrated.  i2mo.  Cloth,  .40 

Congdon.  Laboratory  Instructions  in  General  Chemistry. 

By  Ernest  A.  Congdon,  Professor  of  Chemistry  in  the  Drexel  Institute,  Philadelphia  ; 
Member  American  Chemical  Society  ; Fellow  of  the  London  Chemical  Society,  etc. 
With  an  Appendix,  useful  Tables,  and  56  Illustrations.  Interleaved,  Cloth,  $1.00 

Conn.  Agricultural  Bacteriology. 

Including  a Study  of  Bacteria  as  Relating  to  Agriculture,  with  Special  Reference  to 
the  Bacteria  in  Soil,  in  the  Dairy,  in  Food  Products,  in  Domestic  Animals,  and  in 
Sewage.  By  H.  W.  Conn,  Ph.d.,  Professor  of  Biology,  Wesleyan  University, 
Middletown,  Conn.;  Author  of  “Evolution  of  To-day,”  “ The  Story  of  Germ  Life,” 
etc.  With  Illustrations.  In  Press. 

Cooper.  Syphilis.  Colored  Plate. 

By  Alfred  Cooper,  f.r.c.s.,  Senior  Surgeon  to  St.  Mark’s  Hospital ; late  Surgeon 
to  the  London  Lock  Hospital,  etc.  Second  Edition,  Edited  by  Edward  Cot- 
terell,  f.r.c.s.,  Surgeon  London  Lock  Hospital,  etc.  20  Full-page  Plates  contain- 
ing many  Colored  Figures.  Octavo.  Cloth,  $5.00 

Coplin.  Manual  of  Pathology.  Third  Edition.  330  Illustrations. 

Including  Bacteriology,  the  Technic  of  Post-mortems,  and  Methods  of  Pathologic 
Research.  By  W.  M.  Late  Coplin,  m.d.,  Professor  of  Pathology  and  Bacteriology, 
Jefferson  Medical  College  ; Pathologist  to  Jefferson  Medical  College  Hospital  and  to 
the  Philadelphia  Hospital ; Bacteriologist  to  the  Pennsylvania  State  Board  of  Health. 
Third  Edition,  Rewritten  and  Enlarged.  330  Illustrations,  many  of  which  are  origi- 
nal, and  7 Colored  Plates.  8vo.  Just  Ready.  Cloth,  $3.50 

Practical  Hygiene. 

With  Special  Articles  on  Plumbing,  Ventilation,  etc.  138  Illustrations.  8vo. 
Second  Edition.  In  Preparation. 

Crippsl  Ovariotomy  and  Abdominal  Surgery. 

By  Harrison  Cripps,  f.r.c.s.,  Surgical  Staff,  St.  Bartholomew’s  Hospital,  London. 
With  17  Plates  and  1 1 5 other  Illustrations.  Large  Octavo.  Cloth,  $8.00 

Crocker.  Diseases  of  the  Skin. 

Their  Description,  Pathology,  Diagnosis,  and  Treatment,  with  Special  Reference  to 
the  Skin  Eruptions  of  Children.  By  H.  Radcliffe  Crocker,  m.d.,  Physician  to 
the  Department  of  Skin  Diseases,  University  College  Hospital,  London.  92  Illustra- 
tions. Third  Edition.  Preparing. 

Cuff.  Lectures  on  Medicine  to  Nurses. 

By  Herbert  Edmund  Cuff,  m.d.,  late  Assistant  Medical  Officer,  Stockwell  Fever 
Hospital,  England.  Second  Edition,  Revised.  With  25  Illustrations.  Cloth,  #1.25 

Cushing.  Compend  of  Histology. 

Specially  adapted  for  the  use  of  Medical  Students  and  Physicians.  By  H.  H.  Cushing, 
m.d.,  Director  of  Histological  and  Embryological  Laboratories,  Woman’s  Medical 
College  of  Pennsylvania  ; Demonstrator  of  Histology  and  Embryology,  Jefferson 
Medical  College,  Philadelphia.  Illustrated.  No.  17  f Quiz-  Compend  ? Series. 
i2mo.  Cloth,  .80;  Interleaved  for  Notes,  $1.00 

Dalby.  Diseases  and  Injuries  of  the  Ear. 

By  Sir  William  B.  Dalby,  m.d.,  Aural  Surgeon  to  St.  George’s  Hospital,  London. 
Fourth  Edition.  With  38  Wood  Engravings  and  8 Colored  Plates.  Cloth,  $2.50 


12 


P.  BLAKISTON  'S  SON  &*  CO.'S 


Davis.  Dietotherapy.  Food  in  Health  and  Disease. 

See  Cohen,  Physiologic  Therapeutics,  page  io. 

Davis.  Essentials  of  Materia  Medica  and  Prescription  Writing. 

By  J.  Aubrey  Davis,  m.d.,  late  Assistant  Demonstrator  of  Obstetrics  and  Quiz- 
Master  in  Materia  Medica,  University  of  Pennsylvania.  i2mo.  Cloth,  $1.50 

Domville.  Manual  for  Nurses 

and  Others  Engaged  in  Attending  to  the  Sick.  By  Ed.  J.  Domville,  m.d.  Eighth 
Edition,  Revised.  With  Recipes  for  Sick-room  Cookery,  etc.  i2mo.  Cloth,  .75 

Donders.  Refraction.  Portrait  of  Author. 

An  Essay  on  the  Nature  and  the  Consequences  of  Anomalies  of  Refraction.  By  F. 
C.  Donders,  m.d.,  late  Professor  of  Physiology  and  Ophthalmology  in  the  Univer- 
sity of  Utrecht.  Authorized  Translation.  Revised  and  Edited  by  Charles  A. 
Oliver,  a.m.,  m.d.  (Univ.  Pa.),  one  of  the  Attending  Surgeons  to  the  Wills  Eye 
Hospital ; one  of  the  Ophthalmic  Surgeons  to  the  Philadelphia  Hospital,  etc.  With 
a Portrait  of  the  Author  and  a Series  of  Explanatory  Diagrams.  Octavo. 

Half  Morocco,  Gilt,  $1.25 

Da  Costa.  Clinical  Pathology  of  the  Blood.  Colored  Plates. 

A Practical  Guide  to  the  Examination  of  the  Blood  by  Clinical  Methods,  with  Refer- 
ence to  the  Diagnosis  of  Disease.  By  John  C.  Da  Costa,  Jr.,  m.d.,  Assistant 
Demonstrator  of  Clinical  Medicine  in  the  Jefferson  Medical  College,  Philadelphia  ; 
Assistant  in  the  Medical  Clinic,  Jefferson  Medical  College  Hospital ; Haematologist 
to  the  German  Hospital.  With  six  Colored  Plates  and  other  Illustrations.  Octavo. 

In  Press. 

Deaver.  Surgical  Anatomy.  400  Full-page  Plates. 

A Treatise  on  Human  Anatomy  in  its  Application  to  the  Practice  of  Medicine  and 
Surgery.  By  John  B.  Deaver,  m.d.,  Surgeon-in-Chief  to  the  German  Hospital ; 
Surgeon  to  the  Children’s  Hospital  and  to  the  Philadelphia  Hospital;  Consulting 
Surgeon  to  St.  Agnes’,  St.  Timothy’s,  and  Germantown  Hospitals  ; formerly  Assistant 
Professor  of  Applied  Anatomy,  University  of  Pennsylvania,  etc.  With  over  400 
very  handsome  Full-page  Illustrations  engraved  from  original  drawings  made  by 
special  artists  from  dissections  prepared  for  the  purpose  in  the  dissecting-rooms  of  the 
University  of  Pennsylvania.  Three  large  volumes.  Royal  square  octavo.  Sold  by 
Subscription.  Orders  taken  for  complete  sets  only.  Description  upon  Application. 

Cloth,  $21.00  ; Half  Morocco  or  Sheep,  $24.00;  Half  Russia,  $27.00 

Synopsis  of  Contents. 

Volume  I. — Upper  Extremity — Back  of  Neck,  Shoulder,  and  Trunk — Cranium 
— Scalp — Face. 

Volume  II. — Neck — Mouth,  Pharynx,  Larynx,  Nose — Orbit — Eyeball — Organ 
of  Hearing — Brain — Female  Perineum — Male  Perineum. 

Volume  III. — Abdominal  Wall — Abdominal  Cavity — Pelvic  Cavity — Chest — 
Lower  Extremity. 

‘ ‘ In  summing  up  the  general  excellences  of  this  remarkable  work,  we  can  accord  our  unqual- 
ifiedfpraise  for  the  accurate,  exhaustive,  and  systematic  manner  in  which  the  author  has  carried  out 
his  plan,  and  we  can  commend  it  as  a model  of  its  kind,  which  must  be  possessed  to  be  appre- 
ciated.”— The  Medical  Record , New  York. 

Appendicitis.  Second  Edition. 

Its  History,  Anatomy,  Etiology,  Pathology,  Symptoms,  Diagnosis,  Prognosis, 
Treatment,  Complications,  and  Sequelae.  A Systematic  Treatise,  with  22  Plates, 
10  of  which  are  Colored,  drawn  specially  for  this  work.  Second  Edition,  Re- 
vised and  Rewritten.  8vo.  Just  Ready.  Cloth,  $3.50 


MEDICAL  AND  SCIENTIFIC  PUBLICATIONS. 


13 


Dercum.  Rest — Mental  Therapeutics — Suggestion. 

See  Cohen,  Physiologic  Therapeutics,  page  io. 

Duckworth.  On  Gout.  Illustrated. 

A Treatise  on  Gout.  By  Sir  Dyce  Duckworth,  m.d.  (Edin.),  f.r.c.p.,  Physician  to, 
and  Lecturer  on  Clinical  Medicine  at,  St.  Bartholomew’s  Hospital,  London.  With 
Chromo-lithographs  and  Engravings.  Octavo.  Cloth,  $6.00 

Diihrssen.  A Manual  of  Gynecological  Practice. 

By  Dr.  A.  Duhrssen,  Privat-Docent  in  Midwifery  and  Gynecology  in  the  University 
of  Berlin.  Translated  from  the  Fourth  German  Edition  and  Edited  by  John  W. 
Taylor,  f.r.c.s.,  Surgeon  to  the  Birmingham  and  Midlands  Hospital  for  Women  ; 
Vice-President  of  the  British  Gynecological  Society;  and  Frederick  Edge,  m.d., 
m.r.c.p.,  f.r.c.s.,  Surgeon  to  the  Wolverhampton  and  District  Hospital  for  Women. 
With  105  Illustrations.  i2mo.  Cloth,  $1.50 

Dulles.  What  to  Do  First  In  Accidents  and  Poisoning. 

By  C.  W.  Dulles,  m.d.,  Surgeon  to  the  Rush  Hospital ; formerly  Assistant  Surgeon 
2d  Regiment  N.  G.  Pa.,  etc.  Fifth  Edition,  Enlarged.  With  new  Illustrations. 
i2mo.  Cloth,  $1.00 

Edgar.  Text-Book  of  Obstetrics. 

By  J.  Clifton  Edgar,  m.d.,  Professor  of  Obstetrics  Medical  Department  of  Cornell 
University,  New  York  City  ; Physician  to  Mothers’  and  Babies’  Hospital,  and  to  the 
Emergency  Hospital,  etc.  With  many  Illustrations,  a large  number  of  which  are 
Original.  Octavo.  In  Preparation. 

Ernst.  Prophylaxis — Personal  Hygiene — Nursing  and  Care  of  the 

Sick. 

See  Cohen,  Physiologic  Therapeutics,  page  10. 

Fenwick.  Guide  to  Medical  Diagnosis. 

By  Samuel  Fenwick,  m.d.,  f.r.c.p.,  Consulting  Physician  to  the  London  Hospital ; 
and  W.  S.  Fenwick,  m.d.,  m.r.c.p.,  Physician  to  the  Out-Patients,  Evelina  Hospital 
for  Children.  Eighth  Edition,  in  great  part  Rewritten,  with  several  New  Chapters. 
135  Illustrations.  Cloth,  $2.50 

Ulcer  of  the  Stomach  and  Duodenum. 

42  Illustrations.  Royal  octavo.  Just  Ready.  Cloth,  $3.50 

Fick.  Diseases  of  the  Eye  and  Ophthalmoscopy. 

A Handbook  for  Physicians  and  Students.  By  Dr.  Eugen  Fick,  University  of 
Zurich.  Authorized  Translation  by  A.  B.  Hale,  m.d.,  Ophthalmic  Surgeon  United 
Hebrew  Charities  ; Consulting  Ophthalmic  Surgeon  Charity  Hospital,  Chicago  ; late 
Vol.  Assistant  Imperial  Eye  Clinic,  University  of  Kiel.  With  a Glossary  and  158 
Illustrations,  many  of  which  are  in  Colors.  8vo. 

Cloth,  $4.50;  Sheep,  $5.50;  Half  Russia,  $6.50 

Fillebrown.  A Text-Book  of  Operative  Dentistry. 

Written  by  invitation  of  the  National  Association  of  Dental  Faculties.  By  Thomas 
Fillebrown,  m.d.,  d.m.d.,  Professor  of  Operative  Dentistry  in  the  Dental  School  of 
Harvard  University  ; Member  of  the  American  Dental  Association,  etc.  Illustrated. 
8vo.  Cloth,  $2.25 


14 


P.  BLAKISTON' S SON  6-  CO.'S 


Fowler’s  Dictionary  of  Practical  Medicine. 

By  Various  Writers.  An  Encyclopedia  of  Medicine.  Edited  by  James  Kingston 
Fowler,  m.a.,  m.d.,  f.r.c.p.,  Senior  Assistant  Physician  to,  and  Lecturer  on  Patho- 
logical Anatomy  at,  the  Middlesex  Hospital,  London.  8vo. 

Cloth,  $3.00  ; Half  Morocco,  $4.00 

Fullerton.  Obstetric  Nursing. 

By  Anna  M.  Fullerton,  m.d.,  Demonstrator  of  Obstetrics  in  the  Woman’s  Medical 
College  ; Obstetrician  and  Gynecologist  to  the  Woman’s  Hospital,  Philadelphia,  etc. 
41  Illustrations.  Fifth  Edition,  Revised  and  Enlarged.  i2mo.  Cloth,  $1. 00 

Surgical  Nursing. 

Comprising  the  Regular  Course  of  Lectures  upon  Abdominal  Surgery,  Gyne- 
, cology,  and  General  Surgical  Conditions  delivered  at  the  Training  School  of 
the  Woman’s  Hospital,  Philadelphia.  Third  Edition,  Revised.  69  Illustrations. 
i2mo.  Cloth,  $1.00 

Gardner.  The  Brewer,  Distiller,  and  Wine  Manufacturer. 

A Handbook  for  all  interested  in  the  Manufacture  and  Trade  of  Alcohol  and  its 
Compounds.  Edited  by  John  Gardner,  f.c.s.  Illustrated.  Cloth,  $1.50 

Goodall  and  Washbourn.  A Manual  of  Infectious  Diseases. 

By  Edward  W.  Goodall,  m.d.  (London),  Medical  Superintendent  Eastern  (Fever) 
Hospital,  Homerton,  London,  etc.  ; and  J.  W.  Washbourn,  f.r.c.p.,  Assistant 
Physician  to  Guy’s  Hospital  and  Physician  to  the  London  Fever  Hospital.  Illustra- 
ted with  Charts,  Diagrams,  and  Full-page  Plates.  Cloth,  $3.00 

Gould.  The  Illustrated  Dictionary  of  Medicine,  Biology,  and 
Allied  Sciences.  Fifth  Edition." 

Being  an  Exhaustive  Lexicon  of  Medicine  and  those  Sciences  Collateral  to  it : 
Biology  (Zoology  and  Botany),  Chemistry,  Dentistry,  Pharmacology,  Microscopy, 
etc.  By  George  M.  Gould,  a.m.,  m.d.,  Editor  of  American  Medicine ; President, 

1 893-94,  American  Academy  of  Medicine,  etc.  With  many  Useful  Tables  and  numer-' 
ous  Fine  Illustrations.  Large  Square  Octavo.  1633  pages.  Fifth  Edition.  Just 
Ready.  Full  Sheep  or  Half  Dark-Green  Leather,  $10.00 

With  Thumb  Index,  $11.00  ; Half  Russia,  Thumb  Index,  $12.00 

“Few  persons  read  dictionaries  as  Theophile  Gautier  did — for  pleasure;  if,  however,  all 
dictionaries  were  as  readable  as  the  one  under  consideration,  his  taste  for  this  kind  of  literature 
would  be  less  singular.  . . . The  book  is  excellently  printed,  and  the  illustrations  are  admir- 

ably executed.  The  binding  is  substantial  and  even  handsome,  but  the  business-like  ‘ get-up  ’ of 
the  book  makes  it  well  fitted  for  use  as  well  as  for  the  adornment  of  a book-shelf.’ ’ — The  British 
Medical  Journal , London. 

The  Student’s  Medical  Dictionary.  Eleventh  Ed.  Illustrated. 

Enlarged.  Including  all  the  Words  and  Phrases  generally  used  in  Medicine, 
with  their  proper  Pronunciations  and  Definitions,  based  on  Recent  Medical 
Literature.  With  Tables  of  the  Bacilli,  Micrococci,  Leukomains,  Ptomains, 
etc.,  of  the  Arteries,  Muscles,  Nerves,  Ganglia,  and  Plexuses;  Mineral  Springs 
of  the  U.  S.,  etc.,  and  a new  Table  of  Eponymic  Terms  and  Tests.  Rewritten, 
Enlarged,  and  Improved.  With  many  Illustrations.  Small  octavo.  840  pages. 

Half  Morocco,  $2.50;  Thumb  Index,  $3.00 

“ One  pleasing  feature  of  the  book  is  that  the  reader  can  almost  invariably  find  the  definition 
under  the  word  he  looks  for,  without  being  referred  from  one  place  to  another,  as  is  too  commonly 
the  case  in  medical  dictionaries.  The  tables  of  the  bacilli,  micrococci,  leukomains,  and  ptomains 
are  excellent,  and  contain  a large  amount  of  information  in  a limited  space.  The  anatomical  tables 
are  also  concise  and  clear.  . . .We  should  unhesitatingly  recommend  this  dictionary  to  our 

readers,  feeling  sure  that  it  will  prove  of  much  value  to  them.” — The  American  Journal  of 
Medical  Science. 


MEDICAL  AND  SCIENTIFIC  PUBLICATIONS. 


15 


Gould.  The  Pocket  Pronouncing  Medical  Lexicon.  Fourth  Edition. 
(30,000  Medical  Words  Pronounced  and  Defined.) 

A Student’s  Pronouncing  Medical  Lexicon.  Containing  all  the  Words,  their  Defini- 
tions and  Pronunciations,  that  the  Student  generally  comes  in  contact  with  ; also 
elaborate  Tables  of  the  Arteries,  Muscles,  Nerves,  Bacilli,  etc.,  etc.;  a Dose  List  in 
both  English  and  Metric  Systems,  a new  table  of  Clinical  Eponymic  Terms,  etc., 
arranged  in  a most  convenient  form  for  reference  and  memorizing.  Thin  64010. 
(6  x 3^  inches.)  838  pages.  The  System  of  Pronunciation  used  in  this  book  is  very 
simple.  A New  Edition. 

Full  Limp  Leather,  Gilt  Edges,  $1.00  ; Thumb  Index,  $1.25 

“ This  ‘ Dictionary  ’ is  admirably  suited  to  the  uses  of  the  lecture-room,  or  for  the  purposes  of 
a medical  defining  vocabulary — many  of  the  words  not  yet  being  found  in  any  other  dictionary, 
large  or  small,  while  all  of  the  words  are  those  of  the  living  medical  literature  of  the  day.” — The 
Virginia  Medical  Monthly. 

***  120,000  copies  of  Gould’s  Dictionaries  have  been  sold. 

Sample  pages  and  descriptive  circulars  of  Gould' s Dictionaries  free  upon  application. 

Borderland  Studies. 

Miscellaneous  Addresses  and  Essays  Pertaining  to  Medicine  and  the  Medical 
Profession,  and  their  Relations  to  General  Science.  350  pages.  i2mo.  Cloth,  $2.00 

Gould  and  Pyle.  Cyclopedia  of  Practical  Medicine  and  Surgery. 
72  Special  Contributors.  Illustrated.  One  Volume. 

A Concise  Reference  Handbook,  Alphabetically  Arranged,  of  Medicine,  Surgery, 
Obstetrics,  Materia  Medica,  Therapeutics,  and  the  various  specialties,  with  Particular 
Reference  to  Diagnosis  and  Treatment.  Compiled  under  the  Editorial  Supervision 
of  Drs.  George  M.  Gould  and  W.  L.  Pyle.  With  many  Illustrations. 

Large  Square  8vo.  To  correspond  with  Gould’s  “Illustrated  Dictionary.” 

Full  Sheep  or  Half  Dark-Green  Leather,  $10.00  ; With  Thumb  Index,  $11.00 

Half  Russia,  Thumb  Index,  $12.00 

***  The  great  success  of  Dr.  Gould’s  “Illustrated  Dictionary  of  Medicine”  sug- 
gested the  preparation  of  this  companion  volume,  which  should  be  to  the  physician  the 
same  trustworthy  handbook  in  the  broad  field  of  general  information  that  the  Dictionary 
is  in  the  more  special  one  of  the  explanation  of  words  and  the  statement  of  facts.  The 
aim  has  been  to  provide  in  a one-volume  book  all  the  material  usually  contained  in  the 
large  systems  and  much  which  they  do  not  contain.  Instead  of  long,  discursive  papers 
on  special  subjects  there  are  short,  concise,  pithy  articles  alphabetically  arranged,  giv- 
ing the  latest  methods  of  diagnosis,  treatment,  and  operating — a working  book  in  which 
the  editors  and  their  collaborators  have  condensed  all  that  is  essential  from  a vast 
amount  of  literature  and  personal  experience. 

The  seventy-two  special  contributors  have  been  selected  from  all  parts  of  the 
country  in  accordance  with  their  fitness  for  treating  special  subjects  about  which  they 
may  be  considered  expert  authorities.  They  are  all  men  of  prominence,  teachers, 
investigators,  and  writers  of  experience,  who  give  to  the  book  a character  unequaled  by 
any  other  work  of  the  kind. 

At  each  reprinting  this  Cyclopedia  is  carefully  revised  and  augmented  so  as  to  in- 
clude important  innovations  and  in  order  to  keep  it  up-to-date. 

“ The  book  is  a companion  volume  to  Gould’s  ‘Illustrated  Dictionary  of  Medicine,’  which 
every  physician  should  possess.  With  these  two  books  in  his  library,  every  busy  physician  will  save 
a vast  amount  of  time  in  having  at  hand  an  instant  reference  cyclopedia  covering  every  subject  in 
surgery  and  medicine.” — Chicago  Medical  Recorder. 

Compend  of  Diseases  of  the  Eye  and  Refraction. 

Including  Treatment  and  Operations,  with  a Section  on  Local  Therapeutics. 
With  Formulae,  Glossary,  and  several  Tables.  Second  Edition.  109  Illustra- 
tions, several  of  which  are  Colored.  No.  8 ? Quiz-  Compend  ? Series. 

Cloth,  .80  ; Interleaved  for  Notes,  $1.00 


16 


P.  BLAKISTON'S  SON  &•  CO.'S 


Gordinier.  The  Gross  and  Minute  Anatomy  of  the  Central  Nervous 
System.  261  Illustrations. 

By  H.  C.  Gordinier,  a.m.,  m.d.,  Professor  of  Physiology  and  of  the  Anatomy  of 
the  Nervous  System  in  the  Albany  Medical  College  ; Member  American  Neurological 
Association.  With  48  Full-page  Plates  and  213  other  Illustrations,  a number  of 
which  are  printed  in  Colors  and  many  of  which  are  original.  Large  8vo. 

Handsome  Cloth,  $6.00  ; Sheep,  $7. 00  ; Half  Russia,  $8.00 

***  It  is  universally  acknowledged  that  for  a proper  comprehension  of  the  normal 
and  abnormal  activities  of  an  organ  a thorough  knowledge  of  its  anatomy  is  absolutely 
essential.  This  is  particularly  true  of  diseases  of  the  central  nervous  system,  for  in  no 
other  way  can  the  disease-symptoms  be  explained.  Without  this  knowledge,  clinical 
and  pathological  observations  are  of  little  avail.  This  book  is  not  a theoretic  and  tech- 
nical student’ s book,  but  a useful  working  supplement  to  all  works  upon  general  practice 
and  neurology,  and  as  such  is  destined  to  mark  an  epoch  in  medical  literature. 

*£*  The  illustrations,  of  which  there  are  a large  number,  are  chiefly  from  the 
author’s  own  preparations.  They  have  been  reproduced  in  the  very  best  manner,  the 
publishers’  aim  being  to  give  results  that  are  scientifically  correct  and  at  the  same  time 
pleasing  to  the  eye.  In  order  that  certain  pictures  may  be  more  faithfully  shown,  they 
have  been  printed  in  colors  ; this  will  bring  out  the  details  perfectly,  and  enable  the 
student  to  quickly  recognize  their  relative  value.  Those  illustrations  borrowed  from 
others  have  generally  been  remade,  so  that  they  will  harmonize  with  the  general  style 
adopted  for  the  work.  In  some  cases  these  have  been  improved  upon  in  details  which 
the  originals  failed  to  make  clear. 

“ This  is  an  excellent  book  on  a fascinating  subject,  and  the  author  deserves  the  thanks  of  the 
English-speaking  medical  world  for  his  labor  in  getting  it  up.  There  are  works  enough  on  general 
anatomy,  and  dry  enough  they  are,  as  we  all  remember  only  too  well ; but  the  anatomy  of  the 
nervous  system  alone  is  another  matter  entirely,  for  it  is  one  of  the  most  interesting  of  all  subjects 
of  medical  study  at  the  same  time  that  it  is  one  of  the  most  difficult.  For  both  of  these  reasons 
the  subject  is  deserving  of  a treatise  by  itself,  and  should  not  be  briefly  discussed  in  a few  pages  of 
a general  work  on  anatomy  or  in  an  introductory  chapter  of  a treatise  on  diseases  of  the  nervous 
system.” — The  New  York  Medical  Record. 

Gorgas’  Dental  Medicine. 

A Manual  of  Materia  Medica  and  Therapeutics.  By  Ferdinand  J.  S.  Gorgas,  m.d., 
d.d.s.,  Professor  of  the  Principles  of  Dental  Science,  Oral  Surgery,  and  Dental 
Mechanism  in  the  Dental  Department  of  the  University  of  Maryland.  Sixth  Edition, 
Revised  and  Enlarged,  with  many  Formulae.  8vo. 

Cloth,  $4.00;  Sheep,  $5.0 c> ; Half  Russia,  $6.00 

Greene.  The  Medical  Examination  for  Life  Insurance 

and  its  Associated  Clinical  Methods.  With  Chapters  on  the  Insurance  of  Sub- 
standard Risks  and  Accident  Insurance.  By  Charles  Lyman  Greene,  m.d.,  of  St. 
Paul,  Clinical  Professor  of  Medicine  and  Physical  Diagnosis  in  the  University  of  Min- 
nesota. With  99  Illustrations,  many  of  which  are  original,  several  being  printed 
in  Colors.  Octavo.  Just  Ready.  Cloth,  $4.00 

Griffith’s  Graphic  Clinical  Chart. 

Designed  by  J.  P.  Crozer  Griffith,  m.d.,  Instructor  in  Clinical  Medicine  in  the 
University  of  Pennsylvania.  Printed  in  three  colors.  Sample  copies  free. 

Put  up  in  loose  packages  of  50,  .50 

Price  to  Hospitals:  500  copies,  $4.00;  1000  copies,  $7. 50.  With  name  of  Hos- 
pital printed  on,  50  cents  extra. 

Groff.  Materia  Medica  for  Nurses. 

With  Questions  for  Self-examination  and  a very  complete  Pronouncing  Glossary. 
By  John  E.  Groff,  Pharmacist  to  the  Rhode  Island  Hospital,  Providence.  i2mo. 
235  pages.  Cloth,  #1.25 


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17 


Groves  and  Thorp.  Chemical  Technology. 

A New  and  Complete  Work.  The  Application  of  Chemistry  to  the  Arts  and  Manu- 
factures. Edited  by  Charles  E.  Groves,  f.r.s.,  and  Wm.  Thorp,  n.sc.,  f.i.c., 
assisted  by  many  experts.  With  numerous  Illustrations.  Each  volume  sold  separately. 
Vol.  I.  Fuel  and  Its  Applications.  607  Illustrations  and  4 Plates.  Octavo. 

Cloth,  $5.00;  Mor.,  $6.50 
Vol.  II.  Lighting.  Candles,  Oils,  Lamps,  etc.  By  W.  Y.  Dent,  L.  Field, 
Boverton  Redwood,  and  D.  A.  Louis.  Illustrated. 
Octavo.  Cloth,  #4.00;  y2  Mor.,  $5.50 

Vol.  III.  Gas  Lighting.  By  Charles  Hunt,  Manager  of  the  Birmingham 
Gasworks.  Illustrated.  Octavo. 

Cloth,  #3.50;  ]/2  Mor.,  $4.50 
Vol.  IV.  Electric  Lighting  and  Photometry.  By  Arthur  G.  Cooke,  m.a. 

(Cantab.),  Lecturer  on  Physics  and  Electric  Engineering 
at  the  Battersea  (London)  Polytechnic  ; and  W.  J.  Dibdin, 
f.i.c.,  f.c.s.,  late  Chemist  and  Superintending  Gas  Ex- 
aminer, London  County  Council.  In  Press. 

Gowers.  Manual  of  Diseases  of  the  Nervous  System. 

A Complete  Text-Book.  By  William  R.  Gowers,  m.d.,  f.r.s.,  Physician  to  Na- 
tional Hospital  for  the  Paralyzed  and  Epileptic  ; Consulting  Physician,  University 
College  Hospital ; formerly  Professor  of  Clinical  Medicine,  University  College,  etc. 
Revised  and  Enlarged.  With  many  new  Illustrations.  Two  volumes.  Octavo. 

Vol.  I.  Diseases  of  the  Nerves  and  Spinal  Cord. 

Third  Edition.  Cloth,  $4.00  ; Sheep,  $5.00  ; Half  Russia,  $6.00 

Vol.  II.  Brain  and  Cranial  Nerves;  General  and  Functional 
Diseases. 

Second  Edition.  Cloth,  $4.00;  Sheep,  $5.00;  Half  Russia,  $6.00 

***  This  book  has  been  translated  into  German,  Italian,  and  Spanish.  It  is  pub- 
lished in  London,  Milan,  Bonn,  Barcelona,  and  Philadelphia. 

Syphilis  and  the  Nervous  System. 

Being  a Revised  Reprint  of  the  Lettsomian  Lectures  for  1890,  delivered  before 
the  Medical  Society  of  London.  i2mo.  Cloth,  $1.00 

Medical  Ophthalmoscopy. 

A Manual  and  Atlas,  with  Colored  Autotype  and  Lithographic  Plates  and  Wood- 
cuts,  comprising  Original  Illustrations  of  the  changes  of  the  Eye  in  Diseases  of 
the  Brain,  Kidney,  etc.  Third  Edition,  Revised,  with  the  assistance  of  R. 
Marcus  Gunn,  f.r.c.s.,  Surgeon  Royal  London  Ophthalmic  Hospital,  Moor- 
fields.  Octavo.  Cloth,  $4.00 

Clinical  Lectures. 

A Volume  of  Essays  on  the  Diagnosis,  Treatment,  etc.,  of  Diseases  of  the 
Nervous  System.  Cloth,  $2.00 

Epilepsy  and  Other  Chronic  Convulsive  Diseases. 

Second  Edition.  In  Press. 

Haig.  Causation  of  Disease  by  Uric  Acid.  Fifth  Edition. 

A Contribution  to  the  Pathology  of  High  Arterial  Tension,  Headache,  Epilepsy, 
Mental  Depression,  Gout,  Rheumatism,  Diabetes,  Bright’s  Disease,  Anaemia,  etc. 
By  Alexander  Haig,  m.a.,  m.d.  (Oxon.),  f.r.c.p.,  Physician  to  Metropolitan  Hos- 
pital, London.  75  Illustrations.  Fifth  Edition.  8vo.  846  pages.  Cloth,  $ 3.00 

Diet  and  Food. 

Considered  in  Relation  to  Strength  and  Power  of  Endurance.  Third  Edition, 
Revised.  Just  Ready.  Cloth,  $1.00 


18 


P.  BLAKISTON'S  SON  CO.'S 


Hale.  On  the  Management  of  Children 

in  Health  and  Disease.  Cloth,  .50 

Hall.  Diseases  of  the  Nose  and  Throat. 

By  F.  de  Havilland  Hall,  m.d.,  f.r.c.p.  (Lond.),  Physician  to  the  Westminster 
Hospital ; President  of  the  Laryngological  Society  of  London  ; Joint  Lecturer  on  the 
Principles  and  Practice  of  Medicine  at  the  Westminster  Hospital ; and  Herbert 
Tilley,  m.d.,  b.s.  (Lond.),  f.r.c.s.  (Eng.),  Surgeon  to- the  Throat  Hospital,  Golden 
Square  ; Lecturer  on  Diseases  of  the  Nose  and  Throat,  London  Post-Graduate  College 
and  Polyclinic.  Second  Edition,  Thoroughly  Revised,  with  2 Plates  and  80  Illustra- 
tions. Cloth,  $2.75 

Hamilton.  Lectures  on  Tumors 

from  a Clinical  Standpoint.  By  John  B.  Hamilton,  m.d.,  ll.d.,  late  Professor  of 
Surgery  in  Rush  Medical  College,  Chicago  ; Professor  of  Surgery,  Chicago  Polyclinic  ; 
Surgeon  Presbyterian  Hospital,  etc.  Third  Edition,  Revised.  With  New  Illustra- 
tions. i2mo.  Cloth,  $1.25 

Hansell  and  Reber.  Muscular  Anomalies  of  the  Eye. 

By  Howard  F.  Hansell,  a.m.,  m.d.,  Clinical  Professor  of  Ophthalmology,  Jefferson 
Medical  College  ; Professor  of  Diseases  of  the  Eye,  Philadelphia  Polyclinic,  etc. ; and 
Wendell  Reber,  m.d.,  Instructor  in  Ophthalmology,  Philadelphia  Polyclinic,  etc. 
With  1 Plate  and  28  other  Illustrations.  i2mo.  Cloth,  $1.50 

Hansell  and  Bell.  Clinical  Ophthalmology. 

By  Howard  F.  Hansell,  a.m.,  m.d.,  and  James  H.  Bell,  m.d.  With  Colored  Plate 
of  Normal  Fundus  and  120  Illustrations.  i2mo.  Cloth,  $1.50 

Hare.  Mediastinal  Disease. 

The  Pathology,  Clinical  History,  and  Diagnosis  of  Affections  of  the  Mediastinum 
other  than  those  of  the  Heart  and  Aorta.  By  H.  A.  Hare,  m.d.,  Professor  of 
Materia  Medica  and  Therapeutics  in  Jefferson  Medical  College.  8vo.  Illustrated. 

Cloth,  $2.00 

Harlan.  Eyesight 

and  How  to  Care  for  It.  By  George  C.  Harlan,  m.d.,  Professor  of  Diseases  of 
the  Eye,  Philadelphia  Polyclinic.  Illustrated.  Cloth,  .40 

Harris'  Principles  and  Practice  of  Dentistry. 

Including  Anatomy,  Physiology,  Pathology,  Therapeutics,  Dental  Surgery,  and 
Mechanism.  By  Chapin  A.  Harris,  m.d.,  d.d.s.,  late  President  of  the  Baltimore 
Dental  College;  Author  of  “Dictionary  of  Medical  Terminology  and  Dental  Sur- 
gery.” Thirteenth  Edition,  Revised  and  Edited  by  Ferdinand  J.  S.  Gorgas, 
a.m.,  m.d.,  d.d.s.,  Author  of  “Dental  Medicine;”  Professor  of  the  Principles  of 
Dental  Science,  Oral  Surgery,  and  Dental  Mechanism  in  the  University  of  Maryland. 
1250  Illustrations.  1180  pages.  8vo. 

Cloth,  $ 6.00  ; Leather,  $7. 00  ; Half  Russia,  $8.00 

Dictionary  of  Dentistry. 

Including  Definitions  of  such  Words  and  Phrases  of  the  Collateral  Sciences  as 
Pertain  to  the  Art  and  Practice  of  Dentistry.  Sixth  Edition,  Rewritten,  Re- 
vised, and  Enlarged.  By  Ferdinand  J.  S.  Gorgas,  m.d.,  d.d.s.,  Author  of 
“ Dental  Medicine  ;”  Editor  of  Harris’  “Principles  and  Practice  of  Dentistry  ;” 
Professor  of  Principles  of  Dental  Science,  Oral  Surgery,  and  Prosthetic  Dentistry 
in  the  University  of  Maryland.  Octavo.  Cloth,  $5.00  ; Leather,  $6.00 


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Harris  and  Beale.  Treatment  of  Pulmonary  Consumption. 

By  Vincent  Dormer  Harris,  m.d.,  f.r.c.p.,  Physician  to  the  City  of  London  Hos- 
pital for  Diseases  of  the  Chest,  and  E.  Clifford  Beale,  m.a.,  f.r.c.p.,  Physician  to 
the  City  of  London  Hospital  for  Diseases  of  the  Chest,  etc.  i2mo.  Cloth,  $2.50 

Hartridge.  Refraction. 

The  Refraction  of  the  Eye.  A Manual  for  Students.  By  Gustavus  Hartridge, 
f.r.c.s.,  Senior  Surgeon  Royal  Westminster  Ophthalmic  Hospital  ; Ophthalmic 
Surgeon  to  St.  Bartholomew’s  Hospital,  etc.  105  Illustrations  and  Sheet  of  Test 
Types.  Tenth  Edition,  Revised  and  Enlarged  by  the  Author.  Cloth,  $1.50 

On  the  Ophthalmoscope. 

A Manual  for  Physicians  and  Students.  Third  Edition.  With  Colored  Plates 
and  68  Wood-cuts.  i2mo.  Cloth,  $1.50 

Hartshorne.  Our  Homes. 

Their  Situation,  Construction,  Drainage,  etc.  By  Henry  Hartshorne,  m.d.  Illus- 
trated. Cloth,  .40 

Hatfield.  Diseases  of  Children. 

By  Marcus  P.  Hatfield,  Professor  of  Diseases  of  Children,  Chicago  Medical  Col- 
lege. With  a Colored  Plate.  Second  Edition.  Being  No.  14  ? Quiz- Comp  end  ? 
Series.  i2mo.  Cloth,  .80;  Interleaved  for  the  Addition  of  Notes,  $1.00 

“ Dr.  Hatfield  seems  to  have  most  thoroughly  appreciated  the  needs  of  students,  and  most 
excellently  has  he  condensed  his  matter  into  available  form.  It  is  in  accord  with  the  most  recent 
teachings,  and  while  brief  and  concise,  is  surprisingly  complete.  . . . It  is  free  from  irritating 

repetition  of  questions  and  answers  which  mars  so  many  of  the  compends  now  in  use.  Written  in 
systematic  form,  the  consideration  of  each  disease  begins  with  its  definition,  and  proceeds  through 
the  usual  subheadings  to  prognosis  and  treatment,  thus  furnishing  a complete,  readable  text-book.  ’ ’ 
— Annals  of  Gynecology  and  Pediatry. 

Heath.  Minor  Surgery  and  Bandaging. 

By  Christopher  Heath,  f.r.c.s.,  Holme  Professor  of  Clinical  Surgery  in  Univer- 
sity College,  London.  Eleventh  Edition,  Revised  and  Enlarged.  With  176  Illus- 
trations, Formulae,  Diet  List,  etc.  i2mo.  Cloth,  $1.25 

Practical  Anatomy. 

A Manual  of  Dissections.  Eighth  London  Edition.  300  Illus.  Cloth,  $4.25 

Injuries  and  Diseases  of  the  Jaws. 

Fourth  Edition,  Edited  by  Henry  Percy  Dean,  m.s.,  f.r.c.s.,  Assistant  Sur- 
geon London  Hospital.  With  187  Illustrations.  8vo.  Cloth,  $4.50 

Hedley.  Therapeutic  Electricity  and  Practical  Muscle  Testing. 

By  W.  S.  Hedley,  m.d.,  m.r.c.s.,  in  charge  of  the  Electrotherapeutic  Department 
of  the  London  Hospital.  99  Illustrations.  Octavo.  Cloth,  $2.50 

Heller.  Essentials  of  Materia  Medica,  Pharmacy,  and  Prescription 
Writing. 

By  Edwin  A.  Heller,  m.d.,  Quiz-Master  in  Materia  Medica  and  Pharmacy  at  the 
Medical  Institute,  University  of  Pennsylvania.  i2mo.  Cloth,  $1.50 

Henry.  Anaemia. 

A Practical  Treatise.  By  Fred’k  P.  Henry,  m.d.,  Physician  to  Episcopal  Hospital, 
Philadelphia.  Haif  Cloth,  .50 


20 


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Hemmeter.  Diseases  of  the  Stomach.  Second  Edition. 

Their  Special  Pathology,  Diagnosis,  and  Treatment.  With  Sections  on  Anatomy, 
Analysis  of  Stomach  Contents,  Dietetics,  Surgery  of  the  Stomach,  etc.  By  John  C. 
Hemmeter,  m.d.,  philos. d.,  Professor  in  the  Medical  Department  of  the  University 
of  Maryland  ; Consultant  to  the  University  Hospital ; Director  of  the  Clinical  Labor- 
atory, etc. ; formerly  Clinical  Professor  of  Medicine  at  the  Baltimore  Medical  College, 
etc.  Second  Edition,  Enlarged  and  Thoroughly  Revised  and  in  parts  Rewritten. 
Colored  and  other  Illustrations.  Cloth,  $6.00  ; Leather,  $7.00  ; Half  Russia,  $8.00 

Diseases  of  the  Intestines. 

A Complete  Systematic  Treatise  on  Diseases  of  the  Intestines,  including  the 
Surgical  Aspects  of  the  subject.  Assisted  by  several  contributors  on  special 
subjects.  With  many  Full-page  Plates  and  other  Illustrations,  most  of  which 
are  Original.  Two  volumes.  Octavo.  Nearly  Ready. 

The  Section  on  Anatomy  has  been  prepared  by  Dr.  J.  Holmes  Smith,  Associate 
Professor  and  Demonstrator  of  Anatomy,  and  Lecturer  on  Clinical  Surgery,  University 
of  Maryland,  Baltimore.  The  Section  on  Bacteria  of  the  Intestines  has  been 
prepared  by  Dr.  Wm.  Royal  Stokes,  Associate  Professor  of  Pathology  and  Bacteriology, 
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Adler,  Demonstrator  of  Clinical  Pathology,  University  of  Maryland,  Baltimore.  The 
Illustrations  form  a most  useful  and  practical  series  of  pictures, — nearly  all  have  been 
reproduced  from  pathological  preparations  and  original  drawings,  a few  being  printed  in 
several  colors. 

Hewlett.  Manual  of  Bacteriology. 

By  R.  T.  Hewlett,  m.d.,  m.r.c.p.,  Assistant  Bacteriologist  British  Institute  of  Pre- 
ventive Medicine,  etc.  With  75  Illustrations.  Octavo.  Cloth,  $3.00 

Hollopeter.  Hay  Fever  and  Its  Successful  Treatment. 

By  W.  C.  Hollopeter,  a.m.,  m.d.,  Clinical  Professor  of  Pediatrics  in  the  Medico- 
Chirurgical  College  of  Philadelphia  ; Physician  to  the  Methodist  Episcopal,  Medico- 
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Cloth,  $1.00 

Holden's  Anatomy.  Seventh  Edition. 

A Manual  of  the  Dissections  of  the  Human  Body.  By  John  Langton,  f.r.c.s., 
Surgeon  to,  and  Lecturer  on  Anatomy  at,  St.  Bartholomew’s  Hospital.  Carefully 
Revised  by  A.  Hewson,  m.d.,  Demonstrator  of  Anatomy,  Jefferson  Medical  College, 
Philadelphia,  etc.  300  Illustrations.  Two  small  compact  volumes.  1 2mo.  Just  Ready. 

Vol.  I.  Scalp,  Face,  Orbit,  Neck,  Thorax,  Upper  Extremity.  435  pages.  153 
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Oil  Cloth,  $1,50 

Human  Osteology. 

Comprising  a Description  of  the  Bones,  with  Colored  Delineations  of  the  Attach- 
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its  Development.  Eighth  Edition,  Carefully  Revised.  Edited  by  Charles 
Stewart,  f.r.s.,  and  R.  W.  Reid,  m.d.,  f.r.c.s.  With  Lithographic  Plates 
and  Numerous  Illustrations.  Cloth,  $5.25 

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and  the  Milk.  Illustrated. 

Memoranda  (Chemical  and  Microscopical)  for  Laboratory  Use.  By  J.  W.  Holland, 
m.d.,  Professor  of  Medical  Chemistry  and  Toxicology  in  Jefferson  Medical  College 
of  Philadelphia.  Sixth  Edition,  Enlarged.  Illustrated  and  Interleaved.  i2mo. 

Cloth,  $1.00 

Horwitz’s  Compend  of  Surgery. 

Including  Minor  Surgery,  Amputations,  Bandaging,  Fractures,  Dislocations,  Surgical 
Diseases,  and  the  Latest  Antiseptic  Rules,  etc.,  with  Differential  Diagnosis  and 
Treatment.  By  Orville  Horwitz,  b.s.,  m.d.,  Professor  of  Genito-Urinary  Dis- 
eases, late  Demonstrator  of  Surgery,  Jefferson  Medical  College.  Fifth  Edition,  very 
much  Enlarged  and  Rearranged.  Over  300  pages.  167  Illustrations  and  98  For- 
mulae. i2mo.  No.  9 ? Quiz-  Compend  ? Series. 

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Horsley.  The  Brain  and  Spinal  Cord, 
the  Structure  and  Functions  of.  By  Victor  A.  Horsley,  m.b.,  f.r.s.,  etc.,  As- 
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Hovell.  Diseases  of  the  Ear  and  Naso-Pharynx. 

A Treatise  including  Anatomy  and  Physiology  of  the  Organ,  together  with  the  treat- 
ment of  the  affections  of  the  Nose  and  Pharynx  which  conduce  to  aural  disease.  By 
T.  Mark  Hovell,  f.r.c.s.  (Edin.),  m.r.c.s.  (Eng.),  Aural  Surgeon  to  the  London 
Hospital  for  Diseases  of  the  Throat,  etc.  128  Illus.  Second  Edition.  Cloth,  $5.50 

Humphrey.  A Manual  for  Nurses.  Seventeenth  Edition. 

Including  General  Anatomy  and  Physiology,  Management  of  the  Sick-room,  etc.  By 
Laurence  Humphrey,  m.a.,  m.b.,  m.r.c.s.,  Assistant  Physician  to,  and  Lecturer  at, 
Addenbrook’s  Hospital,  Cambridge,  England.  Seventeenth  Edition.  i2mo.  Illus- 
trated. Cloth,  $1.00 

Hughes.  Compend  of  the  Practice  of  Medicine.  Sixth  Edition. 

Giving  the  Synonyms,  Definition,  Causes,  Symptoms,  Pathology,  Prognosis,  Diag- 
nosis, Treatment,  etc.,  of  each  Disease.  The  Treatment  is  especially  full  and  a 
number  of  valuable  Prescriptions  have  been  incorporated.  Sixth  Edition,  Revised 
and  Enlarged.  By  Daniel  E.  Hughes,  m.d.,  Chief  Resident  Physician  Philadel- 
phia Hospital ; formerly  Demonstrator  of  Clinical  Medicine  at  Jefferson  Medical 
College,  Philadelphia.  Being  Nos.  2 and  3 ? Quiz-  Comp  end?  Series. 

Quiz-Compend  Edition,  in  two  Parts. 

Part  I. — Continued,  Eruptive,  and  Periodical  Fevers,  Diseases  of  the  Mouth, 
Stomach,  Intestines,  Peritoneum,  Biliary  Passages,  Liver,  Kidneys,  Blood,  etc., 
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System,  Diseases  of  the  Brain  and  Nervous  System,  Mental  Diseases,  etc. 

Price  of  each  Part,  in  Cloth,  .80  ; Interleaved  for  the  Addition  of  Notes,  $1.00 

Physicians’  Edition. 

In  one  volume,  including  the  above  two  parts,  a Section  on  Skin  Diseases,  and 
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Ireland.  The  Mental  Affections  of  Children. 

Idiocy,  Imbecility,  Insanity,  etc.  By  W.  W.  Ireland,  m.d.  (Edin.),  of  the  Home 
and  School  for  Imbeciles,  Mavisbush,  Scotland  ; late  Medical  Supt.  Scot.  National 
Institute  for  Imbecile  Children  ; Author  of  “The  Blot  on  the  Brain,”  etc.  Second 
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22 


P.  BLAKISTON'S  SON  &*  CO.'S 


Jacoby.  Electrotherapy.  Illustrated. 

See  Cohen,  Physiologic  Therapeutics,  page  9. 

Jacobson.  Operations  of  Surgery. 

By  W.  H.  A.  Jacobson,  b.a.  (Oxon.),  f.r.c.s.  (Eng.),  Assistant  Surgeon  Guy’s 
Hospital ; Surgeon  at  Royal  Hospital  for  Children  and  Women,  etc.  With  over  200 
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By  Walter  H.  H.  Jessop,  m.d.  (Cant.),  f.r.c.s.,  Ophthalmic  Surgeon  to,  and 
Lecturer  on  Ophthalmic  Medicine  and  Surgery  at,  St.  Bartholomew’s  Hospital,  Lon- 
don. 5 Colored  Plates,  Test  Types,  and  1 10  other  Illustrations.  i2mo.  Cloth,  $3.00 

Jones.  Medical  Electricity.  Third  Edition. 

A Practical  Handbook  for  Students  and  Practitioners  of  Medicine.  By  H.  Lewis 
Jones,  m.a.,  m.d.,  f.r.c.p.,  Medical  Officer,  in  Charge  Electrical  Department,  St. 
Bartholomew’s  Hospital.  Third  Edition  of  Steavenson  and  Jones’  Medical  Elec- 
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Keen.  Clinical  Charts. 

A Series  of  Seven  Outline  Drawings  of  the  Human  Body,  on  which  may  be  marked 
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Authorized  Translation By  William  Wotkyns  Seymour,  a.b.  (Yale),  m.d.  (Harvard), 
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Kirkes’  Physiology.  Sixteenth  Edition. 

( The  only  Authorized  Edition.  i2mo.  Dark  Red  Cloth.)  A Handbook  of  Phy  siology. 
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in  many  parts  Rewritten.  671  Illustrations,  a number  of  which  are  printed  in  Colors. 
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the  revisions  and  additions  of  Dr.  Halliburton,  and  the  new  and  original  illustrations  included  at 
his  suggestion.  This  edition  has  been  carefully  and  thoroughly  revised. 

Kenwood.  Public  Health  Laboratory  Work. 

By  H.  R.  Kenwood,  m.b.,  d.p.h.,  f.c.s.,  Instructor  in  Hygienic  Laboratory,  Univer 
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Kleen.  Handbook  of  Massage. 

By  Emil  Kleen,  m.d.,  ph.d.,  Stockholm  and  Carlsbad.  Authorized  Translation  from 
the  Swedish  by  Edward  Mussey  Hartwell,  m.d.,  ph.d.,  Director  of  Physical 
Training  in  the  Public  Schools  of  Boston.  With  an  Introduction  by  Dr.  S.  Weir 
Mitchell.  Illustrated.  8vo.  Cloth,  $2.25 


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23 


Kleen.  Diabetes  Mellitus  and  Glycosuria. 

Their  Diagnosis  and  Treatment.  See  preceding  title.  Octavo.  Cloth,  $2.50 

Knight.  Diseases  of  the  Throat. 

A Manual  for  Students.  By  Charles  E.  Knight,  m.d.,  Professor  of  Laryngology, 
Cornell  University  Medical  College  ; Surgeon  to* Throat  Department,  Manhattan  Eye 
and  Ear  Hospital,  etc.  Illustrated.  Nearly  Ready. 

Knopf.  Pulmonary  Tuberculosis.  Its  Modern  Prophylaxis  and  the 
Treatment  in  Special  Institutions  and  at  Home. 

By  S.  A.  Knopf,  m.d.,  Physician  to  the  Lung  Department  of  the  New  York  Throat 
and  Nose  Hospital ; former  Assistant  Physician  to  Professor  Dettweiler,  Falkenstein 
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By  Richard  Lake,  f.r.c.s.,  Surgeon  Laryngologist,  North  London  Hospital  for 
Consumption,  etc. ; Surgeon,  Metropolitan  Ear  and  Throat  Hospital ; Surgeon,  Royal 
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47  Illustrations.  No.  5 ? Quiz- Compend  ? Series. 

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quirements of  Practical  Medicine.  By  Dr.  L.  Landois,  Professor  of  Physiology  and 
Director  of  the  Physiological  Institute  in  the  University  of  Greifswald.  Fifth  Ameri- 
can translated  from  the  last  German  Edition,  with  Additions,  by  Wm.  Stirling, 
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versity of  Oxford,  England.  With  845  Illustrations,  many  of  which  are  printed  in 
' Colors.  8vo.  In  Press. 

Lane.  Surgery  of  the  Head  and  Neck. 

By  L.  C.  Lane,  a.m.,  m.d.,  m.r.c.s.  (Eng.),  Professor  of  Surgery  in  Cooper  Medical 
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Lazarus-Barlow.  General  Pathology. 

By  W.  S.  Lazarus-Barlow,  m.d.,  Demonstrator  of  Pathology  at  the  University  of 
Cambridge,  England.  795  pages.  Octavo.  Cloth,  $5.00 

Lee.  The  Microtomist’s  Vade  Mecum.  Fifth  Edition. 

A Handbook  of  the  Methods  of  Microscopic  Anatomy.  By  Arthur  Bolles  Lee, 
formerly  Assistant  in  the  Russian  Laboratory  of  Zoology  at  Villefranche-sur-Mer  (Nice). 
894  Articles.  Enlarged,  Revised,  and  Rearranged.  532  pages.  8vo.  Just  Ready. 

Cloth,  $4.00 

Leffmann  and  Beam.  Food  Analysis.  Illustrated. 

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delphia ; Vice-President  (1901)  Society  Public  Analysts,  etc.;  and  William  Beam, 
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Leffmann.  Compend  of  Medical  Chemistry. 

Inorganic  and  Organic.  Including  Urine  Analysis.  By  Henry  Leffmann,  m.d., 
Professor  of  Chemistry  in  the  Woman’s  Medical  College  of  Pennsylvania  and  in  the 
Wagner  Free  Institute  of  Science,  Philadelphia  ; Pathological  Chemist  Jefferson  Medi- 
cal College  Hospital ; Vice-Presidept,  1901,  Society  of  Public  Analysts,  etc.  No.  10 
? Quiz-  Compend ? Series.  Fourth  Edition,  Rewritten. 

Cloth,  .80  ; Interleaved  for  the  Addition  of  Notes,  $1.00 

The  Coal-Tar  Colors. 

With  Special  Reference  to  their  Injurious  Qualities  and  the  Restrictions  of  their 
Use.  A Translation  of  Theodore  Weyl’s  Monograph.  i2mo.  Cloth,  $1.25 

Examination  of  Water 

for  Sanitary  and  Technical  Purposes.  Fourth  Edition,  Enlarged.  Illustrated. 
i2mo.  Cloth,  $1.25 

Analysis  of  Milk  and  Milk  Products. 

Arranged  to  suit  the  needs  of  Analytical  Chemists,  Dairymen,  and  Milk  Inspec- 
tors. Second  Edition,  Revised  and  Enlarged.  Illustrated.  i2mo.  Cloth,  $1.25 

Handbook  of  Structural  Formulae 
for  the  Use  of  Students,  containing  180  Structural  and  Stereo-chemic  Formulae. 
i2mo.  Interleaved.  Cloth,  $1.00 

Lewers.  On  the  Diseases  of  Women. 

A Practical  Treatise.  By  Dr.  A.  H.  N.  Lewers,  Assistant  Obstetric  Physician  to 
the  London  Hospital.  146  Engravings.  Fifth  Edition,  Revised.  Cloth,  $2.50 

Lewis  (Bevan).  Mental  Diseases. 

A Text-Book  having  Special  Reference  to  the  Pathological  Aspects  of  Insanity.  By 
Bevan  Lewis,  l.r.c.p.,  m.r.c.s.,  Medical  Director  West  Riding  Asylum,  Wake- 
field, England.  26  Lithograph  Plates  and  other  Illustrations.  Second  Edition,  Re- 
vised and  Enlarged.  8vo.  Cloth,  $7.00 

Lincoln.  School  and  Industrial  Hygiene. 

By  D.  F.  Lincoln,  m.d.  Cloth,  .40 

Longley’s  Pocket  Medical  Dictionary. 

Giving  the  Definition  and  Pronunciation  of  Words  and  Terms  in  General  Use  in 
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Used  in  Prescriptions,  etc.  By  Elias  Longley.  Cloth,  .75  ; Tucks  and  Pocket,  $.1.00 

Macalister’s  Human  Anatomy.  816  Illustrations. 

Systematic  and  Topographical,  including  the  Embryology,  Histology,  and  Mor- 
phology of  Man.  With  Special  Reference  to  the  Requirements  of  Practical  Surgery 
and  Medicine.  By  Alex.  Macalister,  m.d.,  f.r.s.,  Professor  of  Anatomy  in  the 
University  of  Cambridge,  England.  816  Illustrations.  Octavo. 

Cloth,  $5.00  ; Leather,  $6.00 

Mackenzie.  The  Pharmacopoeia  of  the  London  Hospital  for  Dis- 
eases of  the  Throat. 

By  Sir  Morell  Mackenzie,  m.d.  Fifth  Edition,  Revised  and  Improved  by  F.  G. 
Harvey,  Surgeon  to  the  Hospital.  Cloth,  #1.00 


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Macready.  A Treatise  on  Ruptures. 

By  Jonathan  F.  C.  H.  Macready,  f.r.c.s.,  Surgeon  to  the  Great  Northern  Central 
Hospital ; to  the  City  of  London  Hospital  for  Diseases  of  the  Chest ; to  the  City  of 
London  Truss  Society,  etc.  24  Full-page  Plates  and  Wood  Engravings.  Octavo. 

Cloth,  $6.00 

Mann.  Forensic  Medicine  and  Toxicology. 

By  J.  Dixon  Mann,  m.d.,  f.r.c.p.,  Professor  of  Medical  Jurisprudence  and  Toxi- 
cology in  Owens  College,  Manchester  ; Examiner  in  Forensic  Medicine  in  University 
of  London,  etc.  Illustrated.  Octavo.  Cloth,  $6.50 

Mann’s  Manual  of  Psychological  Medicine 

and  Allied  Nervous  Diseases.  Their  Diagnosis,  Pathology,  Prognosis,  and  Treat- 
ment, including  their  Medico-Legal  Aspects.  With  Chapter  on  Expert  Testimony  and 
an  Abstract  of  the  Laws  Relating  to  the  Insane  in  all  the  States  of  the  Union.  By 
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stration before  the  Class.  By  John  Marshall,  f.r.s.,  f.r.c.s.,  Professor  of 
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etc.  In  Sheets,  $40.00  ; Backed  with  Muslin  and  Mounted  on  Rollers,  $60.00 

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Maxwell.  Terminologia  Medica  Polyglotta. 

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Maylard.  The  Surgery  of  the  Alimentary  Canal. 

By  Alfred  Ernest  Maylard,  m.b.,  b.s.,  Senior  Surgeon  to  the  Victoria  Infirmary, 
Glasgow.  Second  Edition.  97  Illustrations.  Octavo.  Cloth,  $3.00 

Mays’  Theine  in  the  Treatment  of  Neuralgia. 

By  Thomas  J.  Mays,  m.d.  i6mo.  y2  bound,  .50 

McBride.  Diseases  of  the  Throat,  Nose,  and  Ear. 

A Clinical  Manual  for  Students  and  Practitioners.  By  P.  McBride,  m.d.,  f.r.c.p. 
(Edin.),  Surgeon  to  the  Ear  and  Throat  Department  of  the  Royal  Infirmary  ; Lec- 
turer on  Diseases  of  Throat  and  Ear,  Edinburgh  School  of  Medicine,  etc.  With 
Colored  Illustrations  from  Original  Drawings.  Third  Edition.  Thoroughly  Revised 
and  Enlarged.  Octavo.  Just  Ready.  Handsome  Cloth,  Gilt  Top,  $7.00 


26 


P.  B LA K IS T ON  ' S SON  CO.'S 


McCook.  American  Spiders  and  Their  Spinning  Work. 

A Natural  History  of  the  Orbweaving  Spiders  of  the  United  States.  By  Henry  C. 
McCook,  d.d.,  Vice-President  of  the  Academy  of  Natural  Sciences  of  Philadelphia  ; 
Member  Entomological  Society  ; Author  of  “The  Agricultural  Ants  of  Texas,”  etc. 
Three  volumes.  Handsomely  Illustrated.  Cloth,  $50.00 

McNeill.  The  Prevention  of  Epidemics  and  the  Construction  and 
Management  of  Isolation  Hospitals. 

By  Dr.  Roger  McNeill,  Medical  Officer  of  Health  for  the  County  of  Argyll. 
With  Numerous  Plans  and  other  Illustrations.  Octavo.  Cloth,  $3.50 

Meigs.  Milk  Analysis  and  Infant  Feeding. 

The  Examination  of  Human  and  Cow’s  Milk,  Cream,  Condensed  Milk,  etc.,  and 
Directions  as  to  the  Diet  of  Young  Infants.  By  Arthur  V.  Meigs,  m.d.  i2mo. 

Cloth,  .50 

Memminger.  Diagnosis  by  the  Urine. 

The  Practical  Examination  of  Urine,  with  Special  Reference  to  Diagnosis.  By 
Allard  Memminger,  m.d.,  Professor  of  Chemistry  and  Hygiene  ; Clinical  Professor 
of  Urinary  Diagnosis  in  the  Medical  College  of  the  State  of  South  Carolina  ; Visiting 
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Revised.  24  Illustrations.  i2mo.  Cloth,  $1.00 

Montgomery.  A Text-Book  of  Practical  Gynecology. 

By  Edward  E.  Montgomery,  m.d.,  Professor  of  Gynecology  in  Jefferson  Medical 
College,  Philadelphia  ; Gynecologist  to  the  Jefferson  and  St.  Joseph’s  Hospitals,  etc.  ; 
527  Illustrations,  many  of  which  are  from  original  sources.  800  pages.  Octavo. 
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***  This  is  a systematic  modern  treatise  on  Diseases  of  Women.  The  author’s 
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been  drawn  by  special  artists  who,  for  a number  of  months,  have  devoted  their  sole 
attention  to  this  work. 

Morris.  Text-Book  of  Anatomy.  Second  Edition.  790  Illustra- 
tions, many  in  Colors. 

A Complete  Text-Book.  Edited  by  Henry  Morris,  f.r.c.s.,  Surgeon  to,  and  Lee-  j 
turer  on  Anatomy  at,  Middlesex  Hospital,  assisted  by  J.  Bland  Sutton,  f.r.c.s.,  ] 
J.  H.  Davies-Colley,  f.r.c.s.,  Wm.  J.  Walsham,  f.r.c.s.,  H.  St.  John  Brooks,  ] 
m.d.,  R.  Marcus  Gunn,  f.r.c.s.,  Arthur  Hensman,  f.r.c.s.,  Frederick  Treves,  | 
f.r.c.s.,  William  Anderson,  f.r.c.s.,  Arthur  Robinson,  m.d.,  m.r.c.s.,  and  ; 
Prof.  W.  H.  A.  Jacobson.  One  Handsome  Octavo  Volume,  with  790  Illustrations,  J 
of  which  many  are  printed  in  Colors.  Thumb  Index  in  each  Copy.  ^ 

Cloth,  $6.00  ; Leather,  $7.00  ; Half  Russia,  $8.00  j 

“ Of  all  the  text-books  of  moderate  size  on  human  anatomy  in  the  English  language,  Morris  j 
is  undoubtedly  the  most  up-to-date  and  accurate.  . . . For  the  student,  the  surgeon,  or  for  the 

general  practitioner  who  desires  to  review  his  anatomy,  Morris  is  decidedly  the  book  to  buy.” — 
The  Philadelphia  Medical  Journal. 

Handsome  circular,  with  sample  pages  and  colored  illustrations,  will  be  sent  free 
to  any  address. 

Renal  Surgery. 

With  Special  Reference  to  Stone  in  the  Kidney  and  Ureter,  and  to  the  Surgical 
Treatment  of  Calculous  Anuria,  together  with  a Critical  Examination  of  Sub- 
parietal  Injuries  of  the  Ureter.  Illustrated.  8vo.  Cloth,  $ 2.00 

Mitchell  and  Gulick.  Mechanotherapy.  9 

See  Cohen,  Physiologic  Therapeutics,  page  10. 


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27 


Morton  on  Refraction  of  the  Eye. 

Its  Diagnosis  and  the  Correction  of  its  Errors.  With  Chapter  on  Keratoscopy  and 
Test  Types.  By  A.  Morton,  m.b.  Sixth  Edition,  Revised.  Cloth,  $1.00 

Moullin.  Surgery.  Third  Edition,  by  Hamilton. 

A Complete  Text-Book.  ByC.  W.  Mansell  Moullin,  m.a.,  m.d.  (Oxon.),  f.r.c.s., 
Surgeon  and  Lecturer  on  Physiology  to  the  London  Hospital ; formerly  Radcliffe 
Traveling  Fellow  and  Fellow  of  Pembroke  College,  Oxford.  Third  American 
Edition,  Revised  and  Edited  by  the  late  John  B.  Hamilton,  m.d.,  ll.d.,  Professor 
of  the  Principles  of  Surgery  and  Clinical  Surgery,  Rush  Medical  College,  Chicago  ; 
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Oettel.  Practical  Exercises  in  Electro-Chemistry. 

By  Dr.  Felix  Oettel.  Authorized  Translation  by  Edgar  F.  Smith,  m.a.,  Professor 
of  Chemistry,  University  of  Pennsylvania.  Illustrated.  Cloth,  .75 

Introduction  to  Electro-Chemical  Experiments. 

Illustrated.  By  same  Author  and  Translator.  Cloth,  .75 

Ohlemann.  Ocular  Therapeutics  for  Physicians  and  Students. 

By  M.  Ohlemann,  m.d.,  late  Physician  in  the  Ophthalmological  Clinical  Institute, 
Royal  Prussian  University  of  Berlin,  etc.  Translated  and  Edited  by  Charles  A. 
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to  the  Philadelphia  and  to  the  Presbyterian  Hospitals.  i2mo.  Cloth,  $1.75 

Ormerod.  Diseases  of  Nervous  System. 

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Paralyzed  and  Epileptic,  London.  66  Wood  Engravings.  i2mo.  Cloth,  $1.00 


28 


P.  BLAKISTON'S  SON  CO.'S 


Osgood.  The  Winter  and  Its  Dangers. 

By  Hamilton  Osgood,  m.d.  Cloth,  .40 

Osier  and  McCrae.  Cancer  of  the  Stomach. 

A Clinical  Study.  By  William  Osler,  m.d.,  and  Thomas  McCrae,  m.b.  (Tor.),  of 
the  Johns  Hopkins  Hospital,  Baltimore.  With  Illustrations.  8vo.  Just  Ready. 

Cloth,  $2.00 

Osier.  Chorea  and  Choreiform  Affections. 

By  William  Osler,  m.d.,  f.r.c.p.  (Lond.),  Professor  of  Medicine,  Johns  Hopkins 
University,  etc.  8vo.  Cloth,  $2.00 

Ostrom.  Massage  and  the  Original  Swedish  Movements. 

Their  Application  to  Various  Diseases  of  the  Body.  A Manual  for  Students,  Nurses, 
and  Physicians.  By  Kurre  W.  Ostrom,  from  the  Royal  University  of  Upsala, 
Sweden,  Instructor  in  Massage  and  Swedish  Movements  in  the  Hospital  of  the 
University  of  Pennsylvania  and  in  the  Philadelphia  Polyclinic  and  College  for  Gradu- 
ates in  Medicine,  etc.  Fourth  Edition,  Enlarged.  105  Illustrations,  many  of  which 
were  drawn  especially  for  this  purpose.  i2mo.  Cloth,  $1. 00 

“ In  this  volume  the  author  gives  an  excellent  description  of  the  methods  of  massage  and 
Swedish  movements,  together  with  their  applicability  to  various  diseased  conditions  of  the  body. 
The  methods  are  rapidly  becoming  popularized  in  our  own  country,  and  the  perusal  of  such  a book 
as  Mr.  Ostrom  has  written  will  be  of  great  advantage  to  physicians,  for  whose  use  it  is  mainly 
intended.” — The  Journal  oj  the  American  Medical  Association. 

Packard's  Sea  Air  and  Sea  Bathing. 

By  John  H.  Packard,  m.d.  Cloth,  .40 

Parkes.  Hygiene  and  Public  Health. 

A Practical  Manual.  By  Louis  C.  Parkes,  m.d.,  d.p.h.  (Lond.  Univ.),  Lecturer 
on  Public  Health  at  St.  George’s  Hospital;  Medical  Officer  of  Health  and  Public 
Analyst,  Borough  of  Chelsea,  London,  etc.;  and  Henry  Kenwood,  m.b.,  f.c.s., 
Assistant  Professor  of  Public  Health,  University  College,  London,  etc.  Sixth  Edition, 
Enlarged  and  Revised.  85  Illustrations.  i2mo.  Just  Ready.  Cloth,  $3.00 

“ The  style  is  good ; dry  facts,  laws,  and  statistics  are  put  in  such  a way  that  the  reader  does 
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The  Elements  of  Health. 

An  Introduction  to  the  Study  of  Hygiene.  Illustrated.  Cloth,  $1.25 

Phillips.  Spectacles  and  Eyeglasses. 

Their  Prescription  and  Adjustment.  By  R.  J.  Phillips,  m.d.,  Instructor  in  Diseases 
of  the  Eye,  Philadelphia  Polyclinic  ; Ophthalmic  Surgeon,  Presbyterian  Hospital. 
Second  Edition,  Revised  and  Enlarged.  49  Illustrations.  i2mo.  Cloth,  $1. 00 

“ This  little  work  now  appears  in  the  form  of  a revised  second  edition.  It  is  of  convenient 
size  and  is  excellently  printed.  The  book  is  issued  as  an  aid  to  those  who  prescribe  and  who 
sell  eyeglasses  and  spectacles,  for  the  purpose  of  enabling  them  to  reach  the  most  satisfactory 
and  beneficial  results  in  the  adjustment  of  lenses  to  the  eyes  of  patients.  Since  the  proper  adjust- 
ment of  spectacles  and  eyeglasses  is  of  very  great  importance,  it  is  desirable  that  the  rules  and 
suggestions  contained  in  this  little  volume  should  be  familiar  to  every  oculist  and  optician.” — The 
Medical  Record l New  York. 

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on  the  subject  of  which  it  treats.  It  should  be  read  by  every  one  who  is  interested  in  that  most 
important  portion  of  the  ophthalmic  surgeon’s  work — the  supervision  of  the  proper  adjustment  of 
spectacles.  It  is  doubly  useful  for  those  practitioners  of  ophthalmology  who  are  unable  to  command 
the  services  of  a skilled  optician.” — The  American  Journal  of  the  Medical  Sciences , Philadelphia . 


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Potter.  A Handbook  of  Materia  Medica,  Pharmacy,  and  Thera- 
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30 


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Potter.  Speech  and  Its  Defects. 

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Preston.  Hysteria  and  Certain  Allied  Conditions. 

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Lectures  on  Practical  Pharmacy.  By  Barnard  S.  Proctor.  Third  Edition,  Re- 
vised. With  Elaborate  Tables  of  Chemical  Solubilities,  etc.  Illustrated.  Cloth,  $3.00 

Reese’s  Medical  Jurisprudence  and  Toxicology. 

A Text-Book  for  Medical  and  Legal  Practitioners  and  Students.  By  John  J.  Reese, 
m.d.,  Editor  of  “Taylor’s  Jurisprudence,”  formerly  Professor  of  the  Principles  and 
Practice  of  Medical  Jurisprudence,  including  Toxicology,  in  the  University  of  Pennsyl- 
vania Medical  Department.  Fifth  Edition,  Revised  and  Edited  by  Henry  Leffmann, 
m.d. , Pathological  Chemist,  Jefferson  Medical  College  Hospital ; Chemist,  State  Board 
of  Health  ; Professor  of  Chemistry,  Woman’s  Medical  College  of  Pennsylvania,  etc. 
i2mo.  645  pages.  Cloth,  $3.00;  Leather,  $3.50 

“To  the  student  of  medical  jurisprudence  and  toxicology  it  is  invaluable,  as  it  is  concise, 
clear,  and  thorough  in  every  respect.” — The  American  Journal  of  the  Medical  Sciences. 

Reeves.  Medical  Microscopy. 

Including  Chapters  on  Bacteriology,  Neoplasms,  Urinary  Examination,  etc.  By 
James  E.  Reeves,  m.d.,  ex-President  American  Public  Health  Association,  etc. 
Numerous  Illustrations,  some  of  which  are  printed  in  Colors.  i2mo.  Cloth,  $2.50 

Regis.  Mental  Medicine. 

A Practical  Manual.  By  Dr.  E.  Regis,  formerly  Chief  of  Clinique  of  Mental  Dis- 
eases, Faculty  of  Medicine  of  Paris  ; Physician  of  the  Maison  de  Sante  de  Castel 
d’Andorte.  With  a Preface  by  M.  Benjamin  Ball,  Clinical  Professor  of  Mental 
Diseases,  Faculty  of  Medicine,  Paris.  Authorized  Translation  by  H.  M.  Bannister, 
m.d.,  late  Senior  Assistant  Physician,  Illinois  Eastern  Hospital  for  the  Insane,  etc. 
With  an  Introduction  by  the  Author.  i2mo.  Cloth,  $2.00 

Richardson.  Long  Life 

and  How  to  Reach  It.  By  J.  G.  Richardson,  formerly  Professor  of  Hygiene,  Uni- 
versity of  Pennsylvania.  Cloth,  .40 


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31 


Richardson’s  Mechanical  Dentistry. 

A Practical  Treatise  on  Mechanical  Dentistry.  By  Joseph  Richardson,  d.d.s. 
Seventh  Edition,  Thoroughly  Revised  and  in  many  parts  Rewritten  by  Geo.  W. 
Warren,  a. m.,  d.d.s.,  Professor  of  Clinical  Dentistry  and  Oral  Surgery  ; Chief  of 
the  Clinical  Staff,  Pennsylvania  College  of  Dental  Surgery,  Philadelphia.  With  691 
Illustrations,  many  of  which  are  from  Original  Wood  Engravings.  Octavo.  675 
pages.  Cloth,  $5.00  ; Leather,  $6.00  ; Half  Russia,  $7.00 

Richter’s  Inorganic  Chemistry. 

A Text-Book  for  Students.  By  Prof.  Victor  von  Richter,  University  of  Breslau. 
Fifth  American  from  Tenth  German  Edition  by  Prof.  H.  Klinger,  University  of 
Konigsberg.  Authorized  Translation  by  Edgar  F.  Smith,  m.a.,  ph.d.,  Sc.d., 
Professor  of  Chemistry,  University  of  Pennsylvania  ; Member  of  the  Chemical  Society 
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Cloth,  $1.75 

Organic  Chemistry. 

The  Chemistry  of  the  Carbon  Compounds.  Third  American  Edition,  Translated 
from  Prof.  Anschutz’s  Eighth  German  Edition  by  Edgar  F.  Smith,  m.a., 
ph.d.,  Sc.d.,  Professor  of  Chemistry,  University  of  Pennsylvania.  Revised 
and  Enlarged.  Illustrated.  i2mo.  Two  volumes. 

Vol.  I.  Aliphatic  Series.  625  pages.  Cloth,  $3.00 

Vol.  II.  Carbocyclic  and  Heterocyclic  Series.  671  pages.  Cloth,  $3.00 

Robinson.  Latin  Grammar  of  Pharmacy  and  Medicine. 

By  D.  H.  Robinson,  ph.d.,  Professor  of  Latin  Language  and  Literature,  University 
of  Kansas.  Introduction  by  L.  E.  Sayre,  ph.g.,  Professor  of  Pharmacy  and 
Dean  of  the  Department  of  Pharmacy  in  University  of  Kansas.  Third  Edition, 
Revised  with  the  help  of  Prof.  L.  E.  Sayre,  of  University  of  Kansas,  and  Dr. 
Charles  Rice,  of  the  College  of  Pharmacy  of  the  City  of  New  York.  i2mo. 

Cloth,  $1.75 

“ This  method  of  preparing  medical  students  and  pharmacists  for  a practical  use  of  the  lan- 
guage is  in  every  way  to  be  commended.  . . . Pharmacists  should  know  enough  to  read  pre- 

scriptions readily  and  understanding^.” — Johns  Hopkins  Hospital  Bulletin. 

“ It  is  practical ; its  arrangement  shows  the  careful  and  thoughtful  genius  of  its  author,  who 
seems  to  have  comprehended  just  the  need  of  the  student,  and  put  it  in  such  genial  form  as  to  lead 
the  pupil  rapidly  to  an  understanding  of  what  he  had  feared  would  be  uninteresting  and  tedious.” 
— Pharmaceutical  Record. 

St.  Clair.  Medical  Latin. 

Designed  Expressly  for  the  Elementary  Training  of  Medical  Students.  By  W.  T. 
St.  Clair,  Instructor  in  Latin  in  the  Kentucky  School  of  Medicine  and  in  the  Louis- 
ville Male  High  School.  i2mo.  Cloth,  $1.00 

Sayre.  Organic  Materia  Medica  and  Pharmacognosy. 

An  Introduction  to  the  Study  of  the  Vegetable  Kingdom  and  the  Vegetable  and 
Animal  Drugs.  Comprising  the  Botanical  and  Physical  Characteristics,  Source, 
Constituents,  Pharmacopceial  Preparations  ; Insects  Injurious  to  Drugs,  and  Phar- 
macal  Botany.  By  L.  E.  Sayre,  b.s.,  ph.m.,  Dean  of  the  School  of  Pharmacy  and 
Professor  of  Materia  Medica  and  Pharmacy  in  the  University  of  Kansas  ; Member 
Committee  of  Revision  of  the  United  States  Pharmacopoeia,  etc.  With  Sections  on 
Histology  and  Microtechnique  by  William  C.  Stevens,  Professor  of  Botany  in  the 
University  of  Kansas.  Second  Edition,  Revised  and  Enlarged.  With  374  Illustra- 
tions, the  majority  of  which  are  from  Original  Drawings.  8vo.  Cloth,  $4.50 

Schamberg.  Compend  of  Diseases  of  the  Skin. 

By  Jay  F.  Schamberg,  Professor  of  Diseases  of  the  Skin,  Philadelphia  Polyclinic  ; 
Fellow  of  the  College  of  Physicians  of  Philadelphia  ; Quiz-Master  at  University  of 
Pennsylvania.  Second  Edition,  Revised  and  Enlarged.  105  Illustrations.  ? Quiz- 
Comp  end?  Series , No.  16.  Cloth,  .80;  Interleaved,  $1.00 


32 


P.  BLAKISTON'S  SON  <5-  CO.'S 


Schreiner.  Diet  List. 

Arranged  in  the  Form  of  a Chart  on  which  Articles  of  Diet  can  be  Indicated  for  any 
Disease.  By  E.  R.  Schreiner,  m.d.,  Assistant  Demonstrator  of  Physiology,  Uni- 
versity of  Pennsylvania.  Put  up  in  Pads  of  50  with  Pamphlet  of  Specimen  Dietaries. 

Per  Pad,  .75 

Scott.  The  Urine  : Its  Chemical  and  Microscopical  Examination. 
By  Lindley  Marcroft  Scott,  m.a.,  m.d.,  etc.  With  41  Colored  Plates  and  other 
Illustrations.  Quarto.  Cloth,  $5.00 

Scoville.  The  Art  of  Compounding.  Second  Edition. 

A Text-Book  for  Students  and  a Reference  Book  for  Pharmacists.  By  Wilbur  L. 
Scoville,  ph.g.,  Professor  of  Applied  Pharmacy  and  Director  of  the  Pharmaceutical 
Laboratory  in  the  Massachusetts  College  of  Pharmacy.  Second  Edition,  Enlarged 
and  Improved.  Cloth,  $2.50;  Sheep,  $3.50;  Half  Russia,  $4.50 

Self-Examination  for  Medical  Students. 

3500  Questions  on  Medical  Subjects,  with  the  proper  References  to  Standard  Books 
in  which  replies  may  be  found,  and  including  Complete  Sets  of  Questions  from  two 
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Just  Ready.  * Paper,  10  cents. 

Sheild.  Lectures  on  Nasal  Obstruction. 

By  A.  Marmaduke  Sheild,  m.b.  (Camb.),  f.r.c.s.  (Eng.),  Surgeon  to  St.  George’s 
Hospital,  London,  and  Surgeon-in-Charge  of  the  Throat  Department ; late  Assistant 
Surgeon,  Lecturer  on  Operative  Surgery,  and  Aural  Surgeon,  Charing  Cross  Hospital. 
With  1 Colored  Plate  and  27  Illustrations  in  the  Text.  Just  Ready.  Cloth,  $1.50 

Shuttleworth.  Mentally  Deficient  Children. 

Their  Treatment  and  Training.  By  George  E.  Shuttleworth,  m.d.,  m.r.c.s., 
Medical  Examiner  of  Defective  Children,  School  Board  of  London  ; late  Medical 
Superintendent  Royal  Albert  Asylum  for  Idiots,  etc.  Second  Edition,  Revised. 

Cloth,  $1.50 

Smith.  Abdominal  Surgery.  Sixth  Edition. 

Being  a Systematic  Description  of  all  the  Principal  Operations.  By  J.  Greig  Smith, 
m.a. , f.r.s.e.  , Surgeon  to  British  Royal  Infirmary.  224  Illustrations.  Sixth  Edition, 
Enlarged  and  Thoroughly  Revised  by  James  Swain,  m.d.  (Lond.),  f.r.c.s.,  Pro- 
fessor of  Surgery,  University  College,  Bristol,  etc.  Two  vols.  8vo.  Cloth,  $10.00 

Smith.  Electro-Chemical  Analysis. 

By  Edgar  F.  Smith,  m.a.,  ph.d.,  sc.d.,  Professor  of  Chemistry,  University  of 
Pennsylvania.  Second  Edition,  Revised  and  Enlarged.  27  Illustrations.  i2mo. 

Cloth,  $1.25 

***  This  book  has  been  translated  and  published  in  both  Germany  and  France. 

Smith  and  Keller.  Experiments. 

Arranged  for  Students  in  General  Chemistry.  By  Edgar  F.  Smith,  m.a.,  ph.d., 
Sc.d.,  Professor  of  Chemistry,  University  of  Pennsylvania,  and  Dr.  H.  F.  Keller, 
Professor  of  Chemistry,  Philadelphia  High  School.  Fourth  Revised  Edition.  8vo. 
Illustrated.  Just  Ready.  Cloth,  .60 

Smith.  Dental  Metallurgy. 

A Manual.  By  Ernest  A.  Smith,  f.c.s.,  Assistant  Instructor  in  Metallurgy,  Royal 
College  of  Science,  London.  Illustrated.  i2mo.  Cloth,  $1.75 

Smith.  Wasting  Diseases  of  Infants  and  Children. 

By  Eustace  Smith,  m.d.,  f.r.c.p.,  Physician  to  the  East  London  Hospital  for 
Children,  etc.  Sixth  Edition,  Revised.  Cloth,  $2.00 


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Starling.  Elements  of  Human  Physiology. 

By  Ernest  H.  Starling,  m.d.  (Lond.),  m.r.c.p.,  Joint  Lecturer  on  Physiology  at 
Guy’s  Hospital,  London,  etc.  With  ioo  Illus.  i2mo.  437  pages.  Cloth,  $1.00 

Starr.  The  Digestive  Organs  in  Childhood. 

The  Diseases  of  the  Digestive  Organs  in  Infancy  and  Childhood.  With  Chapters  on 
the  Investigation  of  Disease  and  the  Management  of  Children.  By  Louis  Starr, 
m.d. , late  Clinical  Professor  of  Diseases  of  Children  in  the  Hospital  of  the  University 
of  Pennsylvania ; Physician  to  the  Children’s  Hospital,  Philadelphia.  Third 
Edition.  Illustrated.  Octavo.  Preparing. 

The  Hygiene  of  the  Nursery. 

Including  the  General  Regimen  and  Feeding  of  Infants  and  Children,  and  the 
Domestic  Management  of  the  Ordinary  Emergencies  of  Early  Life,  Massage,  etc. 
Sixth  Edition,  Enlarged.  25  Illustrations.  i2mo.  Cloth,  $1.00 

***  General  and  specific  rules  for  feeding  are  given,  and  Diet  Lists  from  the  first 
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milk,  etc.  Directions  for  the  sterilization  of  milk,  substitutes  for  milk,  preparation  of 
food  for  both  well  and  sick  children,  nutritious  enemata,  etc.,  and  the  general  manage- 
ment of  the  Nursery. 

Stearns.  Lectures  on  Mental  Diseases. 

By  Henry  Putnam  Stearns,  m.d.,  Physician-Superintendent  at  the  Hartford  Retreat ; 
Lecturer  on  Mental  Diseases  in  Yale  University.  With  a Digest  of  Laws  of  the 
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By  Graham  Steel;  m.d.,  f.r.c.p.,  Physician  to  the  Manchester  Royal  Infirmary  ; 
Lecturer  on  Clinical  Medicine  and  on  Diseases  of  the  Heart  at  Owens  College. 
Illustrated.  Just  Ready.  Cloth,  #1.25 

Stevenson  and  Murphy.  A Treatise  on  Hygiene. 

By  Various  Authors.  Edited  by  Thomas  Stevenson,  m.d.,  f.r.c.p.,  Lecturer  on 
Chemistry  and  Medical  Jurisprudence  at  Guy’s  Hospital,  London,  and  Shirley  F. 
Murphy,  Medical  Officer  of  Health  to  the  County  of  London.  In  three  octavo 
volumes. 

Vol.  I.  With  Plates  and  Wood  Engravings.  Octavo.  Cloth,  $6.00 

Vol.  II.  With  Plates  and  Wood  Engravings.  Octavo.  Cloth,  $ 6.00 

Vol.  III.  Sanitary  Law.  Octavo.  Cloth,  $5.00 

***  Special  Circular  upon  application. 

Stewart’s  Compend  of  Pharmacy. 

Based  upon  “Remington’s  Text-Book  of  Pharmacy.”  By  F.  E.  Stewart,  m.d., 
ph.g.  , late  Quiz-Master  in  Chemistry  and  Theoretical  Pharmacy,  Philadelphia  College 
of  Pharmacy  ; Lecturer  on  Pharmacology,  Jefferson  Medical  College.  Fifth  Edition. 
Complete  Tables  of  Metric  and  English  Weights  and  Measures.  ? Quiz- Compend ? 
Series.  Cloth,  .80  ; Interleaved  for  the  Addition  of  Notes,  $1.00 

Stirling.  Outlines  of  Practical  Physiology. 

Including  Chemical  and  Experimental  Physiology,  with  Special  Reference  to  Practical 
Medicine.  By  W.  Stirling,  m.d.,  sc.d.,  Professor  of  Physiology  and  Histology, 
Owens  College,  Victoria  University,  Manchester  ; Examiner  in  Physiology,  Univer- 
sities of  Edinburgh  and  London.  Third  Edition.  289  Illustrations.  Cloth,  $2.00 

Outlines  of  Practical  Histology. 

368  Illustrations.  Second  Edition,  Revised  and  Enlarged.  With  new  Illustra- 
tions. i2mo.  Cloth,  *$2. 00 


34 


P.  B LA K IS T ON ' S SON  &>  CO.'S 


Stohr.  Text-Book  of  Histology,  Including  the  Microscopical 
Technic.  301  Illustrations. 

By  Dr.  Philip  Stohr,  Professor  of  Anatomy  at  University  of  Wurzburg.  Author- 
ized Translation  by  Emma  L.  Bilstein,  m.d.,  formerly  Demonstrator  of  Histology, 
Woman’s  Medical  College  of  Penna.  Edited,  with  Additions,  by  Dr.  Alfred 
Schaper,  Professor  of  Anatomy,  University  of  Breslau;  formerly  Demonstrator  of 
Histology,  Harvard  Medical  School,  Boston.  Third  American  from  the  Eighth  German 
Edition,  Enlarged  and  Revised.  301  Illustrations.  Octavo.  Cloth,  $3.00 

“ This  edition  of  an  already  well-known  student’s  manual  requires  little  but  favorable  com- 
ment. Its  other  editions  have  made  it  well  and  favorably  known,  and  this  one  only  makes  the 
work’s  position  more  secure.  The  book  is  not  only  a useful  one  for  the  student,  but  makes  a very 
good  work  of  reference  for  its  subject,  and  is  thus  entitled  to  a place  upon  the  shelves  of  the  prac- 
titioner.”— The  Medical  Record , New  York. 

Sturgis.  Manual  of  Venereal  Diseases.  Seventh  Edition. 

By  F.  R.  Sturgis,  m.d.,  Sometime  Clinical  Professor  of  Venereal  Diseases  in  the 
Medical  Department  of  the  University  of' the  City  of  New  York;  formerly  one  of 
the  Visiting  Surgeons  to  Charity  Hospital,  Blackwells  Island,  Department  of  Vene- 
real Diseases  ; Member  of  the  American  Association  of  Genito-Urinary  Surgeons,  etc. 
Seventh  Edition,  Revised  and  in  part  Rewritten  by  F.  R.  Sturgis,  m.d.,  and  Follen 
Cabot,  m.d.,  Instructor  in  Genito-Urinary  and  Venereal  Diseases  in  the  Cornell  Uni- 
versity Medical  College  ; Genito-Urinary  Out-Patient  Surgeon  to  Bellevue  Hospital ; 
Visiting  Dermatologist  to  the  New  York  City  (Charity)  Hospital ; Lecturer  on  Genito- 
Urinary  and  Venereal  Diseases,  University  of  Vermont,  1900.  i2mo.  200  pages. 
Just  Ready.  Cloth,  $1.25 

Sutton's  Volumetric  Analysis. 

A Systematic  Handbook  for  the  Quantitative  Estimation  of  Chemical  Substances  by 
Measure,  Applied  to  Liquids,  Solids,  and  Gases.  Adapted  to  the  Requirements  of 
Pure  Chemical  Research,  Pathological  Chemistry,  Pharmacy,  Metallurgy,  Photog- 
raphy, etc.,  and  for  the  Valuation  of  Substances  Used  in  Commerce,  Agriculture, 
and  the  Arts.  By  Francis  Sutton,  f.c.s.  Eighth  Edition,  Revised  and  Enlarged. 
With  1 16  Illustrations.  8vo.  Just  Ready.  Cloth,  $5.00 

Swain.  Surgical  Emergencies. 

Together  with  the  Emergencies  Attendant  on  Parturition  and  the  Treatment  of  Poison- 
ing. By  William  Paul  Swain,  f.r.c.s.,  Surgeon  to  the  South  Devon  and  East 
Cornwall  Hospital,  England.  Fifth  Edition.  149  Illustrations.  i2mo. 

Cloth,  $1.75 

Swanzy.  Diseases  of  the  Eye  and  their  Treatment. 

A Handbook  for  Physicians  and  Students.  By  Henry  R.  Swanzy,  a.m.,  m.b., 
f.r.c.s. 1.,  Examiner  in  Ophthalmology,  University  of  Dublin  ; Surgeon  to  the  National 
Eye  and  Ear  Infirmary  ; Ophthalmic  Surgeon  to  the  Adelaide  Hospital,  Dublin. 
Seventh  Edition,  Thoroughly  Revised  and  Enlarged.  165  Illustrations,  one  Plain 
Plate,  and  a Zephyr  Test  Card.  i2mo.  Cloth,  $2.50 

“ Is  without  doubt  the  most  satisfactory  manual  we  have  upon  diseases  of  the  eye.  It  occu- 
pies the  middle  ground  between  the  students’  manuals,  which  are  too  brief  and  concise,  and  the 
encyclopedic  treatises,  which  are  too  extended  and  detailed  to  be  of  special  use  to  the  general 
practitioner.” — Chicago  Medical  Recorder. 

Symonds.  Manual  of  Chemistry 
for  Medical  Students.  By  Brandreth  Symonds,  a.m.,  m.d.,  Assistant  Physician 
Roosevelt  Hospital,  Out-Patient  Department,  New  York.  Second  Edition.  i2mo. 

Cloth,  $2.00 

Taft.  Index  of  Dental  Periodical  Literature. 

By  Jonathan  Taft,  d.d.s.  8vo. 


Cloth,  $2.00 


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35 


Tanner’s  Memoranda  of  Poisons 

and  their  Antidotes  and  Tests.  By  Thos.  Hawkes  Tanner,  m.d.  Eighth  Edition, 
Revised  by  Henry  Leffmann,  m.d.,  Professor  of  Chemistry,  Woman’s  Medical  Col- 
lege of  Penna. ; Vice-President  Society  of  Public  Analysts.  i2mo.  Cloth,  .75 

Taylor.  Practice  of  Medicine. 

By  Frederick  Taylor,  m.d.,  Physician  to,  and  Lecturer  on  Medicine  at,  Guy’s 
Hospital,  London  ; Physician  to  Evelina  Hospital  for  Sick  Children.  Fifth  Edition. 

Cloth,  #4.00 

Taylor  and  Wells.  Diseases  of  Children.  Illustrated.* 

A Manual  for  Students  and  Physicians.  By  John  Madison  Taylor,  a.b.,  m.d., 
Professor  of  Diseases  of  Children,  Philadelphia  Polyclinic  ; Pediatrist  to  the  Philadel- 
phia Hospital ; Assistant  Physician  to  the  Children’s  Hospital  and  to  the  Orthopedic 
Hospital  ; Consulting  Physician  to  the  Elwyn  and  the  Vineland  Training  Schools  for 
Feeble-minded  Children;  Neurologist  to  the  Howard  Hospital,  etc.;  and  William 
H.  Wells,  m.d.,  Adjunct  Professor  of  Obstetrics' and  Diseases  of  Infancy  in  the 
Philadelphia  Polyclinic  ; Demonstrator  of  Clinical  Obstetrics,  Jefferson  Medical  Col- 
lege ; Chief  Gynecologist,  Mt.  Sinai  Hospital.  With  Numerous  Illustrations.  Second 
Edition,  Revised  and  Enlarged.  Octavo.  Just  Ready.  Cloth,  $4. 50 

Temperature  Charts 

for  Recording  Temperature,  Respiration,  Pulse,  Day  of  Disease,  Date,  Age,  Sex, 
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Thayer.  Compend  of  Pathology. 

Specially  adapted  for  Medical  Students  and  Physicians.  By  A.  E.  Thayer,  m.d., 
Assistant  Instructor  in  Pathology,  Cornell  Medical  School ; Pathologist  to  the  City 
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Cloth,  .80;  Interleaved  for  Notes,  $1.00 

Thorington.  Retinoscopy.  Fourth  Edition. 

(The  Shadow  Test)  in  the  Determination  of  Refraction  at  One  Meter  Distance  with 
the  Plane  Mirror.  By  James  Thorington,  a.m.,  m.d.,  Professor  of  Diseases  of  the 
Eye  in  the  Philadelphia  Polyclinic  ; Ophthalmologist  to  the  Elwyn,  Vineland,  and 
New  Jersey  State  Training  Schools  for  Feeble-minded  Children  ; Lecturer  on  the 
Anatomy,  Physiology,  and  Care  of  the  Eyes  in  the  Philadelphia  Manual  Training 
Schools,  etc.  51  Illustrations,  several  of  which  are  Colored.  Fourth  Edition,  En- 
larged. i2mo.  Just  Ready.  Cloth,  $1.00 

Refraction  and  How  to  Refract.  Second  Edition. 

With  200  Illustrations,  most  of  which  are  made  from  Original  Drawings,  and 
13  of  which  are  in  Colors.  Second  Edition,  Revised.  i2mo.  Cloth,  $1.50 
Synopsis  of  Contents. — I.  Optics.  II.  The  Eye  ; The  Standard  Eye  ; 
Cardinal  Points  ; Visual  Angle  ; Minimum  Visual  Angle  ; Standard  Acuteness  of 
Vision  ; Size  of  Retinal  Image,  Accommodation  ; Mechanism  of  Accommoda- 
tion ; Far  and  Near  Point  ; Determination  of  Distant  Vision  and  Near  Point ; 
Amplitude  of  Accommodation  ; Convergence  ; Angle  Gamma  ; Angle  Alpha. 
III.  Ophthalmoscope  ; Direct  and  Indirect  Method.  IV.  Emmetropia  ; Hyper- 
opia ; Myopia.  V.  Astigmatism  or  Curvature  Ametropia  ; Tests  for  Astigma- 
tism. VI.  Retinoscopy.  VII.  Muscles.  VIII.  Cycloplegics  ; Cycloplegia  ; 
Asthenopia ; Examination  of  the  Eyes.  IX.  How  to  Refract.  X.  Applied 
Refraction.  XI.  Presbyopia ; Aphakia ; Anisometropia ; Spectacles.  XII. 
Lenses  ; Spectacle  and  Eye  Glass  Frames  ; How  to  Take  Measurements  for 
Them  and  How  They  Should  be  Fitted.  Index. 


36 


R.  BLAKISTON'S  SON  CO.’S 


Thorne.  The  Schott  Methods  of  the  Treatment  of  Chronic  Dis- 
eases of  the  Heart. 

With  an  Account  of  the  Nauheim  Baths  and  of  the  Therapeutic  Exercises.  By  W. 
Bezly  Thorne,  m.d.,  m.r.c.p.  With  Plates  and  Numerous  other  Illustrations. 
Third  Edition,  Revised  and  Enlarged.  Octavo.  Cloth,  $1.75 

Tissier.  Pneumatotherapy  and  Inhalation  Methods. 

See  Cohen,  Physiologic  Therapeutics,  page  10. 

Tomes’  Dental  Anatomy. 

A Manual  of  Dental  Anatomy,  Human  and  Comparative.  By  C.  S.  Tomes,  d.d.s. 
263  Illustrations.  Fifth  Edition.  i2mo.  Cloth,  $4.00 

Dental  Surgery. 

A System  of  Dental  Surgery.  By  John  Tomes,  f.r.s.  Fourth  Edition,  Thor- 
oughly Revised  by  C.  S.  Tomes,  d.d.s.  With  289  Illustrations.  i2mo.  717 
pages.  Cloth,  $4.00 

Treves.  German-English  Medical  Dictionary. 

By  Frederick  Treves,  f.r.c.s.,  assisted  by  Dr.  Hugo  Lang,  b.a.  (Munich). 
i2mo.  Half  Calf,  $3.25 

Physical  Education  : Its  Effects,  Value,  Methods,  etc.  8vo. 

Cloth,  .75 

Tuke.  Dictionary  of  Psychological  Medicine. 

Giving  the  Definition,  Etymology,  and  Synonyms  of  the  Terms  used  in  Medical  Psy- 
chology, with  the  Symptoms,  Pathology,  and  Treatment  of  the  Recognized  Forms  of 
Mental  Disorders,  together  with  the  Law  of  Lunacy  in  Great  Britain  and  Ireland. 
Edited  by  D.  Hack  Tuke,  m.d.,  ll.d.,  Examiner  in  Mental  physiology  in  the  Uni- 
versity of  London.  Two  volumes.  Octavo.  Cloth,  $10.00 

“ A comprehensive,  standard  book.” — The  British  Medical  Journal. 

“It  is  vastly  more  than  a Dictionary.  It  is  an  elaborate  and  complete  Encyclopaedia  of 
Psychological  Medicine ; in  fact,  a small  library  in  itself  on  that  subject.  The  high  expectations 
which  Dr.  Tuke’s  work  in  this  field  had  raised  are  more  than  fulfilled.  ...  It  will  be  found 
to  be  a most  useful  reference  handbook  for  the  alienist  and  student.  The  general  physician  also 
cannot  fail  to  find  the  book  exceedingly  useful  in  special  cases.” — Boston  Medical  and  Surgical 
Journal. 

“We  believe  that  the  student  might  obtain. a better  knowledge  of  insanity  from  this  work  than 
from  most  of  the  text-books,  besides  a great  deal  of  interesting  and  valuable  information  nowhere 
else  accessible.” — American  Journal  of  Insanity.  - 

Traube.  Physico-Chemical  Methods. 

By  Dr.  J.  Traube,  Privatdocent  in  the  Technical  High  School  of  Berlin.  Author- 
ized Translation  by  W.  D.  Hardin,  Harrison  Senior  Fellow  in  Chemistry,  University 
of  Pennsylvania.  With  97  Illustrations.  8vo.  Cloth,  $1.50 

Thresh.  Water  and  Water  Supplies. 

By  John  C.  Thresh,  d.sc.  (Lond.),  m.d.,  d.p.h.  (Cambridge),  Medical  Officer  of 
Health  to  the  Essex  County  Council  ; Lecturer  on  Public  Health,  King’s  College, 
London  ; Fellow  of  the  Institute  of  Chemistry  ; Member  Society  Public  Analysts, 
etc.  Second  Edition,  Revised.  Illustrated.  438  pages.  i2mo.  Cloth,  $2.00 

Turnbull’s  Artificial  Anesthesia. 

A Manual  of  Anesthetic  Agents  in  the  Treatment  of  Diseases,  also  their  Employment 
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Tests  of  Purity  ; Treatment  of  Asphyxia  ; Spasms  of  the  Glottis  ; Syncope,  etc.  By 
Laurence  Turnbull,  m.d.,  ph.g.,  Aural  Surgeon  to  Jefferson  College  Hospital,  etc. 
Fourth  Edition,  Revised.  54  Illustrations.  i2mo.  Cloth,  $2.50 


MEDICAL  AND  SCIENTIFIC  PUBLICATIONS. 


37 


Tuson.  Veterinary  Pharmacopoeia. 

Including  the  Outlines  of  Materia  Medica  and  Therapeutics.  By  Richard  V. 
Tuson,  late  Professor  at  the  Royal  Veterinary  College.  Fifth  Edition,  Edited  by 
James  Bayne,  f.c.s.,  Professor  of  Chemistry  and  Toxicology  at  the  Royal  Veterinary 
College.  i2mo.  Cloth,  $2.25 

Tyson.  The  Practice  of  Medicine.  Second  Edition.  Just  Ready. 

A Text-Book  for  Physicians  and  Students,  with  Special  Reference  to  Diagnosis  and 
Treatment.  By  James  Tyson,  m.d.,  Professor  of  Medicine  in  the  University  of 
Pennsylvania;  Physician  to  the  University  and  to  the  Philadelphia  Hospitals,  etc. 
With  Colored  Plates  and  many  other  Illustrations.  Second  Edition,  Revised  and 
Enlarged.  127  Illustrations.  8vo.  1222  pages. 

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***  This  edition  has  been  entirely  reset  from  new  type.  The  author  has  revised  it 
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' “ Represents  the  outcome  of  much  well-directed  labor,  and  constitutes  a reliable  and  useful 
text-book.” — The  London  Lancet. 

“ Few  teachers  in  the  country  can  claim  a longer  apprenticeship  in  the  laboratory  and  at  the 
bedside,  none  a more  intimate  acquaintance  with  students,  since  in  one  capacity  or  another  he  has 
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Guide  to  the  Examination  of  Urine. 


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Third  Edition,  Revised  and  Enlarged.  With  Colored  and  other  Illustrations. 
278  pages.  i2mo.  Cloth,  $1.50 

Cell  Doctrine. 

Its  History  and  Present  State.  Second  Edition.  Cloth,  $1.50 

United  States  Pharmacopoeia. 

Seventh  Decennial  Revision.  Cloth,  $2.50  (Postpaid,  $2.77);  Sheep,  $3.00  (Post- 
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only,  unbound,  $3.50  (Postpaid,  $3. 90). 

Select  Tables  from  the  U.  S.  P. 


Being  Nine  of  the  Most  Important  and  Useful  Tables,  printed  on  Separate 
Sheets.  Carefully  put  up  in  Patent  Envelope.  .25 

Ulzer  and  Fraenkel.  Introduction  to  Chemical-Technical  Analysis. 
By  Prof.  F.  Ulzer  and  Dr.  A.  Fraenkel,  Directors  of  the  Testing  Laboratory  of 
the  Royal  Technological  Museum,  Vienna.  Authorized  Translation  by  Hermann 
Fleck,  nat.sc.d.,  Instructor  in  Chemistry  and  Chemical  Technical  Analysis  in  the 
John  Harrison  Laboratory  of  Chemistry,  University  of  Pennsylvania,  with  an 
Appendix  by  the  Translator  relating  to  Food  Stuffs,  Asphaltum,  and  Paint.  12  Illus- 
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P.  BLAKISTON'S  SON  CO.'S 


Van  Nliys  on  the  Urine. 

Chemical  Analysis  of  Healthy  and  Diseased  Urine,  Qualitative  and  Quantitative.  By  • 
T.  C.  Van  Nuys.  39  Illustrations.  Octavo.  Cloth,  $1.00 

Van  Harlingen  on  Skin  Diseases. 

A Practical  Manual  of  Diagnosis  and  Treatment,  with  Special  Reference  to  Differential 
Diagnosis.  By  Arthur  Van  Harlingen,  m.d.,  Emeritus  Professor  of  Diseases  of 
the  Skin  in  the  Philadelphia  Polyclinic  ; Dermatologist  to  the  Children’s  Hospital. 
Third  Edition,  Revised  and  Enlarged.  With  Formulae  and  Illustrations,  several  being 
in  Colors.  580  pages.  Cloth,  $2.75 

As  would  naturally  be  expected  from  the  author,  his  views  are  sound,  his  information 
extensive,  and  in  matters  of  practical  detail  the  hand  of  the  experienced  physician  is  everywhere 
visible.” — The-  Medical  News. 

Virchow’s  Post-mortem  Examinations. 

A Description  and  Explanation  of  the  Method  of  Performing  them  in  the  Dead- 
House  of  the  Berlin  Charite  Hospital,  with  Especial  Reference  to  Medico-Legal 
Practice.  By  Professor  Virchow.  Translated  by  Dr.  T.  P.  Smith.  Illustrated. 
Third  Edition.  Cloth,  .75 

Voswinkel.  Surgical  Nursing. 

A Manual  for  Nurses.  By  Bertha  M.  Voswinkel,  Graduate  Episcopal  Hospital, 
Philadelphia;  late  Nurse-in-Charge  Children’s  Hospital,  Columbus,  O.  Second 
Edition,  Revised  and  Enlarged,  ill  Illustrations.  i2mo.  Cloth,  $1.00 

Walker.  Students’  Aid  in  Ophthalmology. 

By  Gertrude  A.  Walker,  a.b.,  m.d.,  Clinical  Instructor  in  Diseases  of  the  Eye  at 
Woman’s  Medical  College  of  Pennsylvania.  40  Illustrations  and  Colored  Plate. 
i2mo.  Cloth,  $1.50 

Walsham.  Surgery  : Its  Theory  and  Practice.  Seventh  Edition. 

For  Students  and  Physicians.  By  Wm.  J.  Walsham,  m.d.,  f.r.c.s.,  Senior  Assist- 
ant Surgeon  to,  and  Demonstrator  of  Practical  Surgery  in,  St.  Bartholomew’s  Hospital ; 
Surgeon  to  Metropolitan  Free  Hospital,  London.  Seventh  Edition,  Revised  and  En- 
larged by  100  pages.  With  483  Illustrations  and  28  Skiagrams.  Just  Ready. 

Cloth,  $3.50 

Ward.  Notes  on  Massage. 

Including  Elementary  Anatomy  and  Physiology.  By  Jessie  M.  Ward,  Instructor  in 
Massage  in  the  Pennsylvania,  Philadelphia,  Jefferson,  and  Woman’s  Hospitals,  etc. 
i2mo.  Interleaved.  Paper  Cover,  $1.00 

Warren.  Compend  of  Dental  Pathology  and  Dental  Medicine. 

Containing  all  the  most  Noteworthy  Points  of  Interest  to  the  Dental  Student  and  a 
Chapter  on  Emergencies.  By  George  W.  Warren,  d.d.s.,  Professor  of  Clinical 
Dentistry  and  Oral  Surgery  ; Clinical  Chief,  Pennsylvania  College  of  Dental  Surgery, 
Philadelphia.  Third  Edition,  Enlarged.  Illustrated.  Being  No.  ij  ? Quiz- Com- 
pend? Series.  i2mo.  Cloth,  .80  ; Interleaved  for  the  Addition  of  Notes,  #1.00 

Dental  Prosthesis  and  Metallurgy. 

129  Illustrations.  Cloth,  $1.25 

Weber  and  Hinsdale.  Climatology — Health  Resorts — Mineral 

Springs. 

See  Cohen,  Physiologic  Therapeutics,  page  10. 


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39 


Wells.  Compend  of  Gynecology. 

By  Wm.  H.  Wells,  m.d.,  Demonstrator  of  Clinical  Obstetrics,  Jefferson  Medical 
College,  Philadelphia  ; Chief  Gynecologist  Mt.  Sinai  Hospital  ; Fellow  of  the  College 
of  Physicians  of  Philadelphia.  Second  Edition,  Revised.  140  Illustrations.  Being 
No.  7 ? Quiz- Comp  end?  Series.  i2mo.  Cloth,  .80;  Interleaved  for  Notes,  $1.00 

Wethered.  Medical  Microscopy. 

A Guide  to  the  Use  of  the  Microscope  in  Practical  Medicine.  By  Frank  J.  Weth- 
ered, m.d. , m.r.c.p.,  Demonstrator  of  Practical  Medicine,  Middlesex  Hospital  Med- 
ical School ; Assistant  Physician,  late  Pathologist,  City  of  London  Hospital  for 
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Weyl.  Sanitary  Relations  of  the  Coal-Tar  Colors. 

By  Theodore  Weyl.  Authorized  Translation  by  Henry  Leffmann,  m.d.,  ph.d. 

i2mo.  Cloth,  $1.25 

Whitacre.  Laboratory  Text-Book  of  Pathology. 

By  Horace  J.  Whitacre,  m.d.,  Demonstrator  of  Pathology,  Medical  College  of 
Ohio,  Cincinnati.  Illustrated  with  12 1 Original  Drawings  and  Microphotographs. 
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White.  The  Mouth  and  Teeth.  Illustrated. 

By  J.  W.  White,  m.d.,  d.d.s.  Cloth,  .40 

White  and  Wilcox.  Materia  Medica,  Pharmacy,  Pharmacology,  and 
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A Handbook  for  Students.  By  W.  Hale  White,  m.d.,  f.r.c.p.,  etc.,  Physician  to, 
and  Lecturer  on  Materia  Medica  and  Therapeutics,  Guy’s  Hospital  ; Examiner  in 
Materia  Medica  to  the  Conjoint  Board,  etc.  Fourth  American  Edition,  Revised  by 
Reynold  W.  Wilcox,  m.a.,  m.d.,  ll.d.,  Professor  of  Clinical  Medicine  and  Thera- 
peutics at  the  New  York  Post-Graduate  Medical  School  and  Hospital ; Visiting  Phy- 
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Williams.  Manual  of  Bacteriology.  Second  Edition. 

By  Herbert  U.  Williams,  m.d.,  Professor  of  Pathology  and  Bacteriology,  Medical 
Department,  University  of  Buffalo.  Second  Edition,  Revised.  90  Illus.  i2mo. 

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wickshire, England.  With  Illustrations.  Eighth  Edition.  i2mo.  Cloth,  $3.00 

Wilson.  The  Summer  and  its  Diseases. 

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Medicine,  Jefferson  Medical  College,  Philadelphia.  Cloth,  .40 

Wilson.  System  of  Human  Anatomy. 

Eleventh  Revised  Edition,  Edited  by  Henry  Edward  Clark,  m.d.,  m.r.c.s.  492 
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Winckel.  Text-Book  of  Obstetrics. 

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Authorized  Translation  by  J.  Clifton  Edgar,  a.m.,  m.d.,  Professor  of  Obstetrics 
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40 


P.  BLAKISTON'S  SON  & CO.' S PUBLICATIONS. 


Windle.  Surface  Anatomy  and  Landmarks. 

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and  other  Illustrations.  i2mo.  Cloth,  $1.00 

Winternitz.  Hydrotherapy — Thermotherapy — Balneology. 

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Woody.  Essentials  of  Medical  and  Clinical  Chemistry. 

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istry and  Diseases  of  Children  in  the  Medical  Department,  Kentucky  University, 
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“ The  fact  that  Prof.  Woody’s  little  book  has  reached  a third  edition  in  such  a short  time  is 
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material  and  its  plan  of  presentation,  resulting  from  the  author’s  large  experience  as  a practitioner 
and  teacher  of  medical  chemistry,  is  well  intended  to  offer  to  the  student  that  which  is  really  essen- 
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A Text-Book  by  John  W.  Wright,  a.m.,  m.d.,  Professor  of  Ophthalmology  and 
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THE  STANDARD  TEXT=BOOK 

Morris’  Anatomy 

Second  Edition,  Enlarged  and  Improved 

790  Illustrations,  of  which  214  are  Colored 

Octavo.  1274  Pages.  Cloth,  $6.00 ; Leather,  $7.00 

“ Morris’  Anatomy”  was  published  at  a time  when  methods  of  teaching, 
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and  made  it  from  the  day  of  publication  a standard  authority. 

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endeavor  to  enhance  its  value.  The  text  has  been  thoroughly  revised  and 
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colors,  while  the  typographical  appearance  has  been  improved  in  several 
particulars. 

The  illustrations,  in  correctness  and  excellence  of  execution,  are  equaled 
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? Quiz-Compends  ?.  They  are  well  arranged,  full,  and  concise,  and  are  really  the  best  line  of  text- 
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BLAKISTON’S  ?QUIZ-COMPENDS? 

The  Best  Series  of  Manuals  for  the  Use  of  Students. 

Price  of  each,  Cloth,  .80.  Interleaved  for  taking  Notes,  81.00. 

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professors,  and  are  kept  constantly  revised,  so  that  they  may  thoroughly  represent  the  present  state 
of  the  subject  upon  which  they  treat.  The  authors  have  had  large  experience  as  Quiz-Masters 
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wherever  they  could  be  used  to  advantage.  Can  be  used  by  students  of  any  college,  and  contain 
information  nowhere  else  collected  in  such  a condensed  practical  shape. 

ILLUSTRATED  CIRCULAR  FREE. 

No.  1.  HUMAN  ANATOMY.  Sixth  Revised  and  Enlarged  Edition.  Including  Vis- 
ceral Anatomy.  Can  be  used  with  either  Morris’s  or  Gray’s  Anatomy.  1 1 7 Illustrations  and 
16  Lithographic  Plates  of  Nerves  and  Arteries,  with  Explanatory  Tables,  etc.  By  Samuel 
O.  L.  Potter,  m.d.,  formerly  Professor  of  the  Practice  of  Medicine,  Cooper  Medical  College, 
San  Francisco;  Major  and  Brigade  Surgeon,  U.  S.  Vol. 

No.  2.  PRACTICE  OF  MEDICINE.  Part  I.  Sixth  Edition,  Revised,  Enlarged,  and 
Improved.  By  Dan’l  E.  Hughes,  M.d.,  Physician -in-Chief,  Philadelphia  Hospital;  late 
Demonstrator  of  Clinical  Medicine,  Jefferson  Medical  College,  Philadelphia. 

No.  3.  PRACTICE  OF  MEDICINE.  Part  II.  Sixth  Edition,  Revised,  Enlarged,  and 
Improved.  Same  author  as  No.  2. 

No.  4.  PHYSIOLOGY.  Tenth  Edition,  with  new  Illustrations.  Enlarged  and  Revised. 
By  A.  P.  Brubaker,  m.d.,  Professor  of  Physiology  in  the  Pennsylvania  College  of  Dental 
Surgery;  Adjunct  Professor  of  Physiology,  Jefferson  Medical  College,  Philadelphia. 

No.  5.  OBSTETRICS.  Sixth  Edition.  By  Henry  G.  Landis,  m.d.  Revised  and  Edited 
by  Wm.  H.  Wells,  m.d.,  Instructor  of  Obstetrics,  Jefferson  Medical  College,  Philadelphia. 
Enlarged.  3 Plates  and  47  other  Illustrations. 

No.  6.  MATERIA  MEDIC  A,  THERAPEUTICS,  AND  PRESCRIPTION 
WRITING.  Sixth  Revised  Edition.  Same  author  as  No.  1. 

No.  7.  GYNECOLOGY.  Second  Edition.  By  Wm.  H.  Wells,  m.d.,  Instructor  of  Obstet- 
rics, Jefferson  Medical  College,  Philadelphia.  140  Illustrations. 

No.  8.  DISEASES  OF  THE  EYE  AND  REFRACTION.  Second  Edition.  Includ- 
ing Treatment  and  Surgery  and  a Section  on  Local  Therapeutics.  By  George  M.  Gould, 
M.d.,  Editor  Philadelphia  Medical  Journal,  and  W.  L.  Pyle,  M.D. , Assistant  Surgeon,  Wills 
Eye  Hospital.  With  Formulae,  Glossary,  several  useful  Tables,  and  109  Illustrations. 

No.  9.  SURGERY,  Minor  Surgery,  and  Bandaging.  Fifth  Edition,  Enlarged  and  Im- 
proved. By  Orville  Horwitz,  b.s.,  m.d.,  Clinical  Professor  of  Genito-Urinary  Surgery 
and  Venereal  Diseases  in  Jefferson  Medical  College  ; Surgeon  to  Philadelphia  Hospital,  etc. 
With  98  Formulae  and  167  Illustrations. 

No.  10.  MEDICAL  CHEMISTRY.  Fourth  Edition.  Including  Urinalysis,  Chemistry  of 
Milk,  Blood,  etc.  By  Henry  Leffmann,  m.d.,  Professor  of  Chemistry  in  Pennsylvania 
College  of  Dental  Surgery  and  in  the  Woman’s  Medical  College,  Philadelphia. 

No.  11.  PHARMACY.  Fifth  Edition.  Based  upon  Professor  Remington’s  Text-Book  of 
Pharmacy.  By  F.  E.  Stewart,  m.d.,  ph.g.,  late  Quiz-Master  in  Pharmacy  and  Chemistry, 
Philadelphia  College  of  Pharmacy;  Lecturer  at  Jefferson  Medical  College. 

No.  12.  VETERINARY  ANATOMY  AND  PHYSIOLOGY.  Illustrated.  By  Wm. 
R.  Ballou,  m.d.,  Professor  of  Equine  Anatomy  at  New  York  College  of  Veterinary  Sur- 
geons; Physician  to  Bellevue  Dispensary,  etc.  With  29  graphic  Illustrations. 

No.  13.  DENTAL  PATHOLOGY  AND  DENTAL  MEDICINE.  Third  Edition, 
Illustrated.  By  George  W.  Warren,  d.d.S.,  Pennsylvania  College  of  Dental  Surgery. 

No.  14.  DISEASES  OF  CHILDREN.  Colored  Plate.  By  Marcus  P.  Hatfield, 
Professor  of  Diseases  of  Children,  Chicago  Medical  College.  Second  Edition,  Enlarged. 
No.  15.  GENERAL  PATHOLOGY.  Illustrated.  By  A.  E.  Thayer,  m.d.,  etc.  Preparing. 
No.  16.  DISEASES  OF  THE  SXIN.  By  Jay  F.  Schamberg,  m.d,  Professor  of  Skin 
Diseases,  "Philadelphia  Polyclinic.  Second  Edition,  Revised.  105  Illustrations. 

No.  17.  HISTOLOGY.  Illustrated.  By  H.  H.  Cushing,  m.d.  Preparing. 

41 


JUST  READY,  ONE  VOLUME 


A Cyclopedia  of  Practical 
Medicine  and  Surgery 

A CONCISE  REFERENCE  BOOK,  ALPHABETICALLY 
ARRANGED 

OF 

MEDICINE,  SURGERY,  OBSTETRICS,  MATERIA  MEDICA,  THERAPEUTICS, 
AND  THE  VARIOUS  SPECIALTIES,  WITH  PARTICULAR 
REFERENCE  TO  DIAGNOSIS  AND  TREATMENT 

COMPILED  UNDER  THE  EDITORIAL  SUPERVISION  OF 

GEORGE  M*  GOULD,  MJX  AND  WALTER  L.  PYLE,  M.D. 

Author  of  **  An  Illustrated  Dictionary  of  Medicine ? ” Assistant  Surgeon  Wills  Eye  Hospital?  formerly 

Editor  **  Philadelphia  Medical  Journal,”  etc.  Editor  **  International  Medical  Magazine,”  etc. 

AND  SEVENTY-TWO  SPECIAL  CONTRIBUTORS 

WITH  MANY  ILLUSTRATIONS 


LARGE  SQUARE  OCTAVO.  TO  CORRESPOND  WITH  GOULD'S  “ ILLUSTRATED 

DICTIONARY.”  FULL  SHEEP  OR  HALF  DARK-GREEN  LEATHER,  $10.00? 

WITH  THUMB  INDEX,  $H.00?  HALF  RUSSIA,  THUMB  INDEX,  $12.00,  NET 

The  great  success  of  Dr.  Gould’ s * ‘ Illustrated  Dictionary  of  Medicine  ’ * suggested 
the  preparation  of  this  companion  volume,  which  should  be  to  the  physician  the  same 
trustworthy  handbook  in  the  broad  field  of  general  information  that  the  Dictionary  is 
in  the  more  special  one  of  the  explanation  of  words  and  the  statement  of  facts.  The 
aim  has  been  to  provide  in  a one-volume  book  all  the  material  usually  contained  in 
the  large  systems  and  much  which  they  do  not  contain.  Instead  of  long  discursive 
papers  on  special  subjects  there  are  short,  concise,  pithy  articles  alphabetically 
arranged,  giving  the  latest  methods  of  diagnosis,  treatment,  and  operating — a working 
book  in  which  the  editors  and  their  collaborators  have  condensed  all  that  is  essential 
from  a vast  amount  of  literature  and  personal  experience. 

The  illustrations  have  been  selected  with  care,  only  those  having  been  used  that  are 
of  practical  value  ; no  effort  has  been  made  to  overload  the  book  with  useless  pictures. 

The  seventy-two  special  contributors — the  names  of  whom  are  given  on  the 
following  page — have  been  selected  from  all  parts  of  the  country  in  accordance 
with  their  fitness  for  treating  special  subjects  about  which  they  may  be  considered 
expert  authorities.  They  are  all  men  of  prominence,  teachers,  investigators,  and 
writers  of  experience,  who  give  to  the  book  a character  unequaled  by  any  other  work 
of  the  kind. 

V LARGE  DESCRIPTIVE  CIRCULAR  UPON  APPLICATION 

42 


GOULD  AND  PYLE’S 

CYCLOPEDIA  OF  MEDICINE 


LIST  OF  CONTRIBUTORS 


Samuel  W.  Abbott,  A.M.,  M.D.,  Boston. 
James  M.  Anders,  M.D.,  LL.D.,  Phila. 
Joseph  D.  Bryant,  M.D.,  New  York. 

James  B.  Bullitt,  M.D.,  Louisville. 

Charles  H.  Burnett,  A.M.,  M.D.,  Phila. 

J.  Abbott  Cantrell,  M.D.,  Philadelphia. 
Archibald  Church,  M.D.,  Chicago. 

L.  Pierce  Clark,  M.D.,  Sonyea,  N.  Y. 
Solomon  Solis-Cohen,  M.D.,  Philadelphia. 
Nathan  S.  Davis,  Jr.,  M.D.,  Chicago. 
Theodore  Diller,  M.D.,  Pittsburg. 
Augustus  A.  Eshner,  M.D.,  Philadelphia. 
J.  T.  Eskridge,  M.D.,  Denver,  Col. 

J.  McFadden  Gaston,  A. B.,  M.D.,  Atlanta, 
Ga. 

J.  McFadden  Gaston,  Jr.,  A.M.,  M.D.,  At- 
lanta, Ga. 

Virgil  P.  Gibney,  M.D.,  New  York. 

George  M.  Gould,  A.M.,  M.D.,  Phila. 

W.  A.  Hardaway,  A.M.,  M.D.,  St.  Louis. 
John  C.  Hemmeter,  M.B.,  M.D.,  Baltimore. 
Barton  Cooke  Hirst,  M.D.,  Philadelphia. 
Bayard  Holmes,  M.D.,  Chicago. 

Orville  Horwitz,  B.S.,  M.D.,  Philadelphia. 
Daniel  E.  Hughes,  M.D.,  Philadelphia. 
James  Nevins  Hyde,  A.M.,  M.D.,  Chicago. 
E.  Fletcher  Ingals,  A.M.,  M.D.,  Chicago. 
Abraham  Jacobi,  M.D.,  New  York. 
William  W.  Johnston,  M.D.,  Washington, 
D.  C. 

Wyatt  Johnston,  M.D.,  Montreal. 

Allen  A.  Jones,  M.D.,  Buffalo. 

William  W.  Keen,  M.D.,  LL.D.,  Phila. 
Howard  S.  Kinne,  M.D.,  Philadelphia. 
Ernest  Laplace,  M.D.,  Philadelphia. 
Benjamin  Lee,  M.D.,  Philadelphia. 
Charles  L.  Leonard,  M.D.,  Philadelphia. 
James  Hendrie  Lloyd,  A.M.,  M.D.,  Phila. 
J.  W.  MacDonald,  M.D.  (Edin.),  F.R.C.S. 

Ed.,  Minneapolis. 

L.  S.  McMurtry,  M.D.,  Louisville. 

G.  Hudson  Makuen,  Philadelphia. 


Matthew  D.  Mann,  M.D.,  Buffalo. 

Henry  O.  Marcy,  A.M.,  M.D.,  LL.D., 
Boston. 

Rudolph  Matas,  M.D.,  New  Orleans. 
Joseph  M.  Mathews,  M.D.,  Louisville. 
John  K.  Mitchell,  M.D.,  Philadelphia. 
Harold  N.  Moyer,  M.D.,  Chicago. 

John  H.  Musser,  M.D.,  Philadelphia. 

A.  G.  Nicholls,  M.D.,  Montreal. 

A.  H.  Ohmann-Dusmesnil,  M.D.,  St. 
Louis. 

William  Osier,  M.D.,  Baltimore. 

Samuel  O.  L.  Potter,  A.M.,  M.D.,  M.R. 

C.P.  (London),  San  Francisco. 

Walter  L.  Pyle,  A.M.,  M.D.,  Philadelphia. 

B.  Alexander  Randall,  A.M.,  M.D.,  Phila. 
Joseph  Ransohoff,  M.D.,  F.R.C.S.  (Eng.), 

Cincinnati. 

Jay  F.  Schamberg,  A.M.,  M.D.,  Phila. 
Nicholas  Senn,  M.D.,  LL.D.,  Chicago. 
Richard  Slee,  M.D.,  Swiftwater,  Pa. 

S.  E.  Solly,  M.D.,  M.R.C.S.,  Colorado 
Springs,  Col. 

Edmond  Souchon,  M.D.,  New  Orleans. 
Ward  F.  Sprenkel,  M.D.,  Philadelphia. 
Charles  G.  Stockton,  M.D.,  Buffalo. 

John  Madison  Taylor,  A.M.,  M.D.,  Phila. 
William  S.  Thayer,  M.D.,  Baltimore. 
James  Thorington,  A.M.,  M.D.,  Phila. 
Martin  B.  Tinker,  M.D.,  Philadelphia. 
James  Tyson,  M.D.,  Philadelphia. 

J.  Hilton  Waterman,  M.D.,  New  York. 

H.  A.  West,  M.D.,  Galveston,  Texas. 

J.  William  White,  M.D.,  PH.D.,  Phila. 
Reynold  W.  Wilcox,  M.A.,  M.D.,  LL.D., 
New  York. 

George  Wilkins,  M.D.,  Montreal. 
DeForest  Willard,  M.D.,  Philadelphia. 
Alfred  C.  Wood,  M.D.,  Philadelphia. 
Horatio  C.  Wood,  M.D.,  LL.D.,  Phila. 
Albert  Woldert,  PH.G.,  M.D.,  Phila. 
James  K.  Young,  M.D.,  Philadelphia. 


43 


Deaver'S  Surgical  Anatomy 

A Treatise  on  Human  Anatomy- 
in  its  Application  to  the  Practice 
of  Medicine  and  Surgery  & & 

By  JOHN  B.  DEAVER,  M.D. 

Surgeon-in- Chief  to  the  German  Hospital , Philadelphia  ; Surgeon  to  the  Children' s Hospital; 
Consulting  Surgeon  to  St.  Agnes',  St.  Timothy' s , and  Germantown 
Hospitals;  formerly  Assistant  Professor  of  Applied 
» Anatomy,  University  of  Pennsylvania,  etc. 

In  Three  Royal  Octavo  Volumes,  containing  about  Four  Hundred  and  Fifty  Full-page  Plates, 
nearly  all  from  dissections  made  for  the  purpose 


Handsome  Cloth,  $21.00 ; Full  Sheep,  $24.00;  Half  Green  Morocco, 
Marbled  Edges,  $24.00  ; Half  Russia,  Gilt,  Marbled  Edges,  $27.00  net. 


SYNOPSIS  OF  CONTENTS 

VOLUME  L — Upper  Extremity — Back  of  Neck,  Shoulder,  and  Trunk — Cranium — Scalp — 
Face. 

VOLUME  IL — Neck — Mouth,  Pharynx,  Larynx,  Nose— Orbit — Eyeball — Organ  of  Hearing — 
Brain — Female  Perineum — Male  Perineum. 

VOLUME  IIL — Abdominal  Wall — Abdominal  Cavity — Pelvic  Cavity — Chest — Lower  Ex- 
tremity. 

The  book  is  designed  to  aid  the  general  practitioner  and  surgeon  in  his 
everyday  work.  The  text  is  excellently  clear,  succinct,  and  systematically  arranged, 
and  contains  a wealth  of  illustrations  far  in  advance  of  the  usual  text-book.  It  is  not 
intended  merely  for  the  surgeon — though  to  him  it  will  prove  invaluable — but  for  the 
general  physician,  who,  while  called  upon  to  cope  with  innumerable  emergencies  and 
special  cases,  has  not  the  means  or  the  hospital  facilities  by  which  he  can  readily 
acquaint  himself  with  every  phase  of  anatomy — superficial  and  deep — as  applied  to 
disease  and  the  most  modern  methods  of  treatment  of  injuries. 

To  the  specialist  it  will  prove  of  great  value.  The  anatomy  of  the  head  and 
neck,  the  spinal  cord,  the  organs  of  sense,  and  the  throat  appeals  directly  to  the 
ophthalmologist,  aurist,  rhinologist,  laryngologist,  and  neurologist,  while  those  sections 
devoted  to  the  abdomen  and  pelvic  cavity  will  give  the  gynecologist  and  specialist 
on  diseases  of  the  urinary  organs,  rectum,  etc.,  material  regarding  the  relations  of  the 
parts  and  the  operations  thereon,  unique  in  many  ways,  and  in  a manner  never  before 
so  exactly  and  concisely  stated.  To  those  devoted  to  these  specialties  it  will  prove  a 
supplement  to  other  text-books  that  omit  special  anatomy,  and  which  do  not  attempt 
to  show  the  applied  anatomy* 


44 


Deaver’s  Surgical  Anatomy 


The  illustrations,  which  at  the  first  glance  appear  as  the  prominent  feature  of 
the  book — but  which  in  reality  do  not  overshadow  the  text — consist  of  a series  of 
pictures  absolutely  unique  and  fresh.  They  will  bear  comparison  from  an  artistic  point 
of  view  with  any  other  work,  while  from  a practical  point  of  view  there  is  no  other 
volume  or  series  of  volumes  to  which  they  can  be  compared.  When  originally  an- 
nounced, the  book  was  to  contain  two  hundred  illustrations.  As  the  work  of  prepara- 
tion progressed,  this  number  gradually  increased  until  it  is  estimated  that  there  will  now 
be  more  than  four  hundred  full-page  plates,  many  of  which  contain  more  than  one 
figure.  With  the  exception  of  a few  minor  pictures  made  from  preparations  in  the 
possession  of  the  author,  they  have  all  been  drawn  by  special  artists  from  dissections 
made  for  the  purpose  in  the  dissecting-rooms  of  the  University  of  Pennsylvania.  Their 
accuracy  cannot  be  questioned,  as  each  drawing  has  been  submitted  to  the  most  careful 
scrutiny. 

From  The  Medical  Record,  New  York, 

44  The  reader  is  not  only  taken  by  easy  and  natural  stages  from  the  more  superficial  to  the 
deeper  regions,  but  the  various  important  regional  landmarks  are  also  indicated  by  schematic 
tracing  upon  the  limbs*  Thus  the  courses  of  arteries,  veins,  and  nerves  are  indicated  in  a way  that 
makes  the  lesson  strikingly  impressive  and  easily  learned.  No  expense,  evidently,  has  been 
spared  in  the  preparation  of  the  work,  judging  from  the  number  of  full-page  plates  it  contains,  not 
counting  the  smaller  drawings.  Most  of  these  have  been  ‘ drawn  by  special  artists  from  dissections 
made  for  the  purpose  in  the  dissecting-rooms  of  the  University  of  Pennsylvania.’  In  summing  up 
the  general  excellences  of  this  remarkable  work,  we  can  accord  our  unqualified  praise  for  the 
accurate,  exhaustive,  and  systematic  manner  in  which  the  author  has  carried  out  his  plan,  and  we 
can  commend  it  as  a model  of  its  kind,  which  must  be  possessed  to  be  appreciated.” 

From  The  Philadelphia  Medical  Journal. 

“ Many  members  of  the  profession  to  whom  Dr.  Deaver  is  well  known  either  personally  or  by 
reputation  as  a surgeon,  writer,  teacher,  and  practical  anatomist,  have  awaited  the  appearance  of 
his  Surgical  Anatomy  with  the  expectation  of  finding  in  it  a guide  in  this  difficult  branch  of  medi- 
cine of  much  more  than  ordinary  practical  value,  and  their  expectations  will  not  be  disappointed  ♦” 

From  The  Journal  of  the  American  Medical  Association. 

“In  order  to  show  its  thoroughness,  it  is  only  necessary  to  mention  that  no  less  than  twelve 
full-page  plates  are  reproduced  in  order  to  accurately  portray  the  surgical  anatomy  of  the  hand, 

and  it  is  doubtful  whether  any  better  description  exists  in  any  work  in  the  English  language.” 

From  The  Southern  California  Practitioner. 

“ Aside  from  the  merit  of  this  great  work,  it  will  be  a delight  to  the  lover  of  books.  Its  gen 
eral  make-up  shows  the  highest  development  of  the  book-making  art.  The  bibliophile,  when 
holding  one  of  these  volumes  in  his  hands,  would  be  as  careful  with  it  as  though  he  were  handling 
an  infant,  and  to  drop  it  would  cause  him  the  keenest  pain.  The  illustrations,  the  print,  and  the 
paper  and  binding  are  each  and  all  delightful  in  themselves,  and  yet  the  text  is  concise  and  clear, 
and  taken  with  the  illustrations  make  a remarkably  good  substitute  for  the  dissecting-room.  To 
have  these  three  volumes  on  his  library  shelves  will  be  a source  of  pride  and  joy  and  profit  to 
every  practitioner.  Dr.  Deaver  has  in  these  volumes  conferred  a boon  upon  the  medical  profession 
which  has,  at  least,  never  been  surpassed  by  any  one.” 

From  The  New  Orleans  Medical  and  Surgical  Journal. 

“ While  the  needs  of  the  undergraduate  have  been  fully  kept  in  view,  it  has  been  the  aim  of 
the  author  to  provide  a work  which  would  be  sufficient  for  reference  for  use  in  actual  practice.  We 
believe  the  book  fulfils  both  requirements.  The  arrangement  is  systematic  and  the  discussion  erf 
surgical  relations  thorough.” 

Large  Descriptive  Circular  will  be  sent  upon  application 

45 


Hemmeter.  Diseases  of  the  Stomach*  Second 
Edition,  Enlarged.  Illustrated. 

Their  Special  Pathology,  Diagnosis,  and  Treatment.  With  Sections  on  Anatomy, 

Analysis  of  Stomach  Contents,  Dietetics,  Surgery  of  the  Stomach,  etc.  By  John 

C.  Hemmeter,  m.d.,  philos. d.,  Professor  in  the  Medical  Department  of  the 

University  of  Maryland  ; Consultant  to  the  University  Hospital ; Director  of  the 

Clinical  Laboratory,  etc.  Second  Revised  Edition.  With  Colored  and  other 

Illustrations.  Octavo.  890  pages. 

Cloth,  $ 6.00  ; Leather,  $7.00  ; Half  Russia,  $8.00 

***  The  rapid  sale  of  the  first  edition  of  this  book  has  encouraged  the  author  to 
revise  it  very  thoroughly  and  to  add  much  new  material  (about  100  pages)  and  a num- 
ber of  new  illustrations.  About  two-thirds  of  the  book  has  been  actually  reconstructed. 
The  section  on  Dietetics  will  be  found  particularly  useful. 

“ A second  enlarged  and  revised  edition  appearing  in  a little  over  a year  from  the  date  of  the 
original  publication  speaks  for  the  popularity  and  value  of  the  work.  This  book  easily  occupies 
the  first  place  among  its  sort  in  the  English  language  and  is  particularly  free  from  that  enthusiastic 
hobby  riding  which  is  not  unknown  among  gastro-enterologists.  The  bibliographical  references 
are  very  full  and  complete,  and  the  work  is  one  of  the  highest  order  as  well  as  one  of  the  utmost 
practical  value.” — Chicagp  Medical  Recorder. 

“ This  edition  of  Hemmeter’s  work  on  ‘ Diseases  of  the  Stomach  ’ contains  much  new  and 
important  material.  The  following  articles  have  been  added  : Hypertrophic  stenosis  of  the  pylorus, 
obstruction  of  the  orifices,  the  use  and  abuse  of  rest  and  exercise  in  the  treatment  of  digestive  dis- 
eases. Part  of  the  chapter  on  motor  insufficiency,  electro-diaphany,  hemorrhage  from  the  stomach, 
and  the  articles  on  gastroptosis  and  enteroptosis  have  been  entirely  rewritten.  The  present  edition 
will  undoubtedly  gain  as  many  friends  as  the  first  edition.  ” — The  Medical  Record , New  York. 

“ Dr.  Hemmeter  certainly  provides  a book  which  is  well  worthy  of  a careful  study.  ...  It 
treats  of  many  subjects  in  an  original  manner,  and  is  not  only  based  on  a considerable  personal 
experience,  but  takes  due  notice  of  the  labors  of  other  well-known  workers  in  this  field.” — British 

Medical  Journal. 

“ Completely  scientific,  modern,  accurate,  and  creditable.  . . . We  commend  it.” — Journal 
oj  the  American  Medical  Association. 

“We  know  of  no  work  from  which  the  physician  may  gain  more  information  than  this.” — 
Australian  Medical  Gazette. 

“ The  consideration  of  the  general  methods  of  clinical  examination  of  the  stomach  is  thor- 
oughly adequate.” — Boston  Medical  and  Surgical  Journal. 

“ We  part  from  Dr.  Hemmeter’s  book  with  the  sense  that  it  embodies  the  best  knowledge  of 
the  time.” — London  Lancet. 

“ We  wish  to  express  unqualified  approval  of  the  tendency  which  is  shown  to  emphasize  the 
simple  and  more  practical  methods  of  diagnosis.” — New  York  Medical  Journal. 

“The  best  contemporary  treatise  on  diseases  of  the  stomach  which  we  possess,  not  only  in 
America,  but  in  the  whole  world.’ f — Prof.  L.  Boas , of  Berlin. 


In  Preparation  by  the  same  Author 

Diseases  of  the  Intestines.  Original  Illustrations 

A Complete,  Systematic  Treatise,  Including  the  Surgical  Aspects  of  the  Subject. 

46 


Gordinier.  The  Gross  and  Minute  Anatomy 
of  the  Central  Nervous  System.  Colored 
Illustrations. 

By  H.  C.  Gordinier,  a.m.,  m.d.,  Professor  of  Physiology  and  of  the  Anatomy 
of  the  Nervous  System  in  the  Albany  Medical  College  ; Member  American  Neuro- 
logical Association.  With  48  Full-page  Plates  and  213  other  Illustrations,  a 
number  of  which  are  printed  in  Colors  and  many  of  which  are  original.  Large 
8vo.  Cloth,  $ 6.00  ; Sheep,  $ 7.00  ; Half  Russia,  $8.00. 

***  It  is  universally  acknowledged  that  for  a proper  comprehension  of  the  normal 
and  abnormal  activities  of  an  organ  a thorough  knowledge  of  its  anatomy  is  absolutely 
essential.  This  is  particularly  true  of  diseases  of  the  central  nervous  system,  for  in  no 
other  way  can  the  disease  symptoms  be  explained.  Without  this  knowledge,  clinical 
and  pathologic  observations  are  of  little  avail.  This  book  is  not  a theoretic  and  tech- 
nical student’s  book,  but  a useful  working  supplement  to  all  works  upon  general  practice 
and  neurology,  and  as  such  is  destined  to  mark  an  epoch  in  medical  literature. 

“ This  is  an  excellent  book  on  a fascinating  subject,  and  the  author  deserves  the  thanks  of  the 
English-speaking  medical  world  for  his  labor  in  getting  it  up.  There  are  works  enough  on  general 
anatomy,  and  dry  enough  they  are,  as  we  all  remember  only  too  well ; but  the  anatomy  of  the 
nervous  system  alone  is  another  matter  entirely,  for  it  is  one  of  the  most  interesting  of  all  subjects 
of  medical  study,  at  the  same  time  that  it  is  one  of  the  most  difficult.  For  both  of  these  reasons 
the  subject  is  deserving  of  a treatise  by  itself,  and  should  not  be  briefly  discussed  in  a few  pages 
of  a general  work  on  anatomy,  or  in  an  introductory  chapter  of  a treatise  on  diseases  of  the  ner- 
vous system.” — Medical  Record,  New  York. 

“ The  author  has  made  an  honest  attempt  to  place  in  the  hands  of  the  English  student  a 
comprehensive  and  accurate  text-book,  devoid  of  the  many  intricacies  of  modern  thought  and 
speculation.  For  the  average  man  the  work  will  appeal  strongly ; the  facts  that  he  can  use  are 
readily  found.” — The  Journal  of  Nervous  and  Mental  Diseases , New  York. 

“ Throughout  the  book  the  descriptions  of  the  gross  and  minute  anatomy  are,  as  a rule,  clear, 
objective,  and  as  easy  of  comprehension  as  could  be  expected  of  so  difficult  a subject.  The  state- 
ments are  most  of  them  quite  didactically  made,  but  this  we  consider  an  advantage  rather  than  a 
defect,  especially  in  a text-book  for  students  as  well  as  practitioners.  . . . The  chapter  on 
cerebral  localization  is  carefully  written,  and  gives  the  most  recent  results  on  the  subject.” — The 
American  Journal  of  Insanity , Baltimore. 

“ Represents  much  painstaking  research,  and  bears  also  the  stamp  of  original  investigation. 
It  is  unusually  well  written,  and  the  illustrations,  many  of  which  are  original,  are  well  chosen.  It 
is  destined  to  take  its  place  among  the  standard  books  of  its  class.” — New  York  Medical  Journal. 

“ This  book  will  be  welcomed  by  teachers,  practitioners,  and  students.  It  will  save  teachers 
and  writers  on  the  nervous  system  the  necessity  of  accompanying  their  lectures  and  books  on 
diseases  of  the  nervous  system  with  chapters  on  anatomy.  It  is  really  the  first  thoroughly  system- 
atic work  on  the  anatomy  of  the  central  nervous  system  that  has  appeared  in  the  English  language. 
The  work  is  the  more  necessary  because  diseases  of  the  central  nervous  system  are  becoming  more 
and  more  recognized,  and  because  the  works  on  general  anatomy  do  not  pretend  to  describe  the 
minute  anatomy  of  the  central  nervous  system.  Authors  of  books  on  neurology  recognize  the  fact 
that  their  readers  cannot  understand  the  descriptions  of  the  diseases  of  the  central  nervous  system 
without  a knowledge  of  the  anatomy  of  the  parts  involved.  The  subject  is  a difficult  one  at  best, 
but  the  student  who  will  make  an  earnest  effort  to  master  the  details  cannot  fail  to  do  so  with  the 
aid  of  this  work.  The  author’s  descriptions  are  clear,  concise,  comprehensive,  and  profusely  and 
beautifully  illustrated.” — Pacific  Medical  Journal , San  Francisco. 

“ As  there  can  be  no  accurate  understanding  of  the  diseases  of  the  nervous  system  without  a 
thorough  knowledge  of  the  anatomy,  it  is  no  wonder  that  the  average  practitioner  is  as  ignorant  of 
neurology  as  is  unfortunately  the  case.  The  present  volume  is  a praiseworthy  attempt  to  remove 
the  approach  that  has  thus  far  rested  upon  English  and  American  neurology.” — Boston  Medical 
and  Surgical  Journal. 

“ We  commend  Gordinier’s  chapter  on  cerebral  localization.  This  will  be  especially  helpful  to 
clinicians,  although  all  the  views  expressed  in  it  are  not  yet  outside  of  the  domain  of  controversy. 
We  should  like  to  say  more  about  Gordinier’s  book,  but  space  forbids.  It  is  handsomely  printed 
and  copiously  illustrated,  and  we  can  recommend  it  as  a good  text-book  of  nervous  anatomy.” 
— Philadelphia  Medical  Journal. 


47 


JUST  READY 


PRACTICAL  GYNECOLOGY 


A Modern  Comprehensive  Text-Book 


By  E.  E.  MONTGOMERY,  M.D. 

Professor  of  Gynecology,  Jefferson  Medical  College?  Gynecologist  to  the  Jefferson  Medical 
College  and  St.  Joseph's  Hospitals?  Consulting  Gynecologist  to 
the  Philadelphia  Lying-in  Charity 


WITH  FIVE  HUNDRED  AND  TWENTY-SEVEN 
ILLUSTRATIONS 

Nearly  all  of  which  have  been  Drawn  and  Engraved  Specially  for  this 
Work,  for  the  most  part  from  Original  Sources 

OCTAVO*  819  PAGES 

CLOTH,  $5.00 ; LEATHER,  $6.00 ; HALF  RUSSIA,  $7.00 


EXTRACT  FROM  THE  PREFACE 

This  work  has  been  under  consideration  for  the  past  fifteen  years,  and  much  of  it 
has  been  several  times  rewritten.  An  effort  has  been  made  to  make  it  a comprehensive 
work  upon  the  subject,  giving  the  experience  and  methods  of  the  most  careful  men, 
while  my  own  experience  has  been  utilized  to  indicate  that  which  I have  found  most 
useful  and  worthy  of  acceptance. 

Each  general  subject  is  considered  with  reference  to  its  influence  upon  the  entire 
genital  tract,  and  the  work  is  divided  into  sections  rather  than  chapters.  This  course, 
although  a departure  from  the  ordinary  text-book  arrangement,  is  that  which  experience 
has  demonstrated  to  be  most  effective  in  impressing  the  subject  upon  the  student,  and 
would  seem  to  me  preferable  to  him  who  uses  the  book  to  refresh  his  knowledge  upon 
some  particular  subject.  The  illustrations  are  arranged  solely  with  the  purpose  of 
rendering  clear  the  text  and  to  promote  the  work  of  diagnosis  and  treatment.  For  the 
excellence  and  character  of  the  illustrations  I am  greatly  indebted  to  the  generosity  of 
the  publishers  and  to  the  skill  and  patience  of  their  artists,  Messrs.  Shannon  and  Von 
du  Lancken.  To  the  kindly  oversight  of  Dr.  Robert  L.  Dickinson  is  due  much  of  the 
exactness  of  the  drawings.  Acknowledgment  is  due  Miss  Eleanor  A.  Cantner  for  her 
ability  in  the  preparation  of  preliminary  sketches  and  of  the  index. 

Should  it  be  the  means  of  lightening  the  work  of  the  student,  of  making  more 
clear  the  pathway  of  the  busy  practitioner,  and,  most  of  all,  of  benefiting  suffering 
women  through  improved  methods  of  diagnosis  and  treatment,  I shall  feel  well  repaid 
for  the  many  days  and  nights  of  labor  which  it  has  cost. 

48 


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